Professional Documents
Culture Documents
D. Seetharam Prasad
As partial fulfillment of post graduation degree
Ayurveda Vachaspati M.D. (Kayachikitsa)
Under Rajeev Gandhi University of Health Sciences, Bangalore, Karnataka
Guide
Reader in Kayachikitsa
Post graduation and research center, Kayachikitsa
Co-Guides
Lecturer in Kayachikitsa
Post graduation and research center, Kayachikitsa
Assistant Professor
Department of Dermatology
Karnataka Institute of Medical Sciences, Hubli
This is to certify that the contents of this thesis entitled Evaluation of the efficacy of
Ojovardhini Yoga in Ojokshaya (with special reference to HIV infection) has been
worked out by D. SEETHARAM PRASAD, under my supervision with close guidance.
Even though this disease, Ojokshaya has been mentioned in Ayurvedic texts, the
aetiology, pathogenesis etc., needs further evaluation and research. It is as developed and
explained by D. SEETHARAM PRASAD is unique and scientific and will definitely help in
elucidation of this disease in Ayurvedic and Modern scientific parlance and further planning
with the management.
This study is not an ersatz, not produced just for any Degree, Diploma or Titles. This
work is applied, scientific and an original contribution in the field of research in Ayurveda.
I am fully satisfied with the work and recommend the dissertation to be put before the
M.D. (Ayurveda Vachaspathi) Kayachikitsa panel of Rajiv Gandhi University of Health
Sciences, Bangalore for adjudication.
Guide
Certificate
I have immense pleasure to certify that D. Seetharam Prasad under my Co-guidance
has carried out present work entitled Evaluation of the efficacy of Ojovardhini Yoga in
Ojokshaya (with special reference to HIV infection). He has completed this clinical study
very sincerely and methodically. I am fully satisfied with his study, which is being presented
as a dissertation for the award of M.D. (Ayurveda Vachaspathi) Kayachikitsa of Rajiv Gandhi
University of Health Sciences, Bangalore.
This study bears ample evidences of original thoughts and expressions and this
dissertation has not been formed previously for the award of any Degree /Diploma or titles.
I am recommending this dissertation to be submitted before the adjudicators for
assessment and approval.
J.S.V.V. SAMSTHES
Certificate
This is to certify that D. SEETHARAM PRASAD has worked for his thesis on the
topic entitled Evaluation of the efficacy of Ojovardhini Yoga in Ojokshaya
(with
We here with forward this thesis for the evaluation and adjudication.
(Dr. G. B. Patil)
Acknowledgements
I am deeply indebted to several people who have helped me during the study.
With a deep sense of gratitude, I thank my guide Dr. K. Siva Rama Prasad, Reader, PostGraduate and Research Center in Kayachikitsa, D.G.M.A.M.C, Gadag for his much-valued
guidance, constant support and encouragement throughout the study.
I am grateful to my Co-guide Dr. Ashok Kumar panda, lecturer, Post-Graduate and
Research Center in Kayachikitsa, D.G.M.A.M.C, Gadag for inspiring me to take up this
dissertation subject and supporting me with timely guidance and encouragement
I am thankful to my co-guide Dr. Keloji Hanumanthayya, Assistant Professor, Department of
Dermatology, Karnataka Institute of Medical Sciences, Hubli, for his teaching, guidance and
help in managing severe cases.
I acknowledge my sincere gratitude to Dr. V. Varadacharyulu, H.O.D. Post-Graduate and
Research Center in Kayachikitsa, D.G.M.A.M.C, Gadag, for his expert comments, critical
analysis and affectionate encouragement, throughout the study.
Words are poor substitutes for my immense feelings of gratitude for Dr. G. B. Patil, Principal,
DGMAMC, Gadag. I thank him for his ever inspiring encouragement, facilities provided and
for his personal interest in overall supervision of this study.
I extend my immense gratitude to Dr. M.C. Patil, Dr. Shashidhar Doddamani, Dr.
Raghavadra Shetter and Dr. Kuber. S,, lecturers, Post-Graduate and Research Center in
Kayachikitsa, D.G.M.A.M.C, Gadag. I scenically remember the co-operation and support
extended by Dr. G.S. Hiremath, Dr. B.G. Swamy and Dr. U. V. Purad, and all the staff or
DGMAMC. I thank all my colleges for their constant support and co-operation.
I sincerely thank Mr. P.M. Nandakumar, statistician, for the statistical analysis of the results.
I am deeply indebted to M/S Om Pharmaceuticals Ltd., for preparing the Ojovardhiniyoga
with good manufacturing practices. I am grateful to Shree Dhootapapeswar Research
Foundation for carrying out the analytical study and toxicity test with drug standardization.
I am thankful to Karnataka state council for science and technology for the financial support
provided, for this study.
With deep sense of gratitude I thank all the subjects who participated in this study.
D. Seetharam Prasad
Index
Pages
1. Introduction
1-5
2. Literary review
A. Ayurveda perspective
6 - 26
a) Shareera
b) Nidana
c) Chikitsa
B. Modern perspective
27 - 54
(a) Immunology
(b) Aetiology
(c) Patho-physiology
(d) Management and Prevention
3. Drug review
55 - 82
Ojovardhini Yoga
I.
II.
III.
IV.
V.
VI.
VII.
VIII.
Mrutunjaya Rasa
IX.
Swarnamakshika Bhasma
83 - 91
5. Master Charts
92 104
105 - 120
121 - 140
Summary
Bibliography
Appendix case sheet
141 - 144
Master charts
Chart
number
Description
Demography chart
Chief complaints
Associated complaints
Ojo Kshaya
10
11
12
13
14
15
16
17
Tables
Table
number
Description
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
Graphs
Table
number
Description
Source of Infection
Presenting complaints
10
Chronicity of disease
11
Tridosha status
12
13
Manasika Nidana
14
Status of Ojas
15
16
17
18
List of Photographs
Chart
number
Description
Page
number
47
48
49
52
56
60
63
67
71
10
74
11
77
12
79
13
80
=tzni: Ex xi xSx xi : *
Oh! Rising sun let your rays kill the microorganisms, which cause diseases
Man is a creature composed of millions of cells. A microbe is composed of only one,
yet throughout the ages, the two have been in ceaseless conflict. The disparity in size
between man and microbe is so tremendous that our minds and imaginations are usually
unequal to the task of grasping their difference. Yet, throughout the ages, the microbes have
had the upper hand in their ceaseless conflict with man. Even though the modern scientific
world believes that existence of these micro organisms were known to man only since 2-3
centuries, the above narrated verse from Atharvaveda which dates back to 5000 years,
reveals the knowledge of man about microbes as early as Vedic period.
Even now, nobody believes that Ayurveda the mother science of all medical
knowledges of world has authentic information about microbes and diseases caused by
them.
Infectious diseases are the main causes of deaths world wide and they contribute
more than 70% of total number of diseases found in human beings. Even though Ayurveda
gives more importance to host factor in the prevention and management of these diseases,
the specific anti microbial therapy is also part of management modalities explained in
different classical texts of Ayurveda.
Sankramana or Upasarga denote infection and krimi, raksha, rakshasa,
yathudhana, pishacha, gandharva, bhoota, nishachara represents different types of
microbes. Many diseases like Rajayakshma, (tuberculosis) Abhishyanda,(conjuctvites) kusta
(leprosy) jwara (fever) upadamsha (syphilis) pooyameha (gonorrhea) apatantraka (tetanus),
visarpa (erysipelas) masoorika (smallpox) rohini (diphtheria) are some examples of
infectious diseases. Coming to the mode of infection, Sushrutha explains all common modes
of infection what we notice today, such as sexual intercourse, physical contact, droplet
infection, food and water born infection, sharing the bed, cloth ornaments etc.
The pioneering work of stalwarts of modern medical science, such as Louis Pasteur,
Robert Koch and Joseph Lister made us aware of bacteria. Then at the beginning of 20th
century we became aware of microbes smaller than bacteria such as virus, which means
poison in Latin. These viruses have caused many diseases such as smallpox and polio that
have ravaged human race.
HIV the new epidemic
The last two decades have seen the sudden emergence of new epidemics, which is
popularly known as AIDS, which is caused by a virus, called HIV. This has left trails of
human devastation and misery from Sydney to Seattle, from Mumbai to Mombasa. Over 60
million have been infected since the start of epidemic and about 22 million are dead. The
rest carry virus within them like a tickling time bomb, although many of these people look
apparently healthy. United nations has reported in 1999, that AIDS has become the leading
cause of death from are infectious disease and will remain so for at least 2 more decades if
the spread of disease is checked effectively.
In India, till now 25 lakh people have died and every year another 3 lakh are dying. In
southern India, nearly 2% of adult population are said to be HIV carriers. India has a
national AIDS control program, which started in 1987. National AIDS control organization
monitors over all surveillance, awareness programs and targeted intervention. But with all
these programs HIV has spread by leaps and bounds. Karnataka is one of the high HIV
prevalent states. Almost all districts have reported HIV cases. Dharwad, Gadag, Bellary and
near by districts show high incidence of HIV in rural parts. Low literacy coupled with rapid
urbanization has caused this drastic spread.
Need of the study
Even though the scenario is very grave, the modern medical science, which is the
mainstay of medical practice, is yet to come out with a cure for this disease. Even though,
thousands of researches going on worldwide to synthesize a molecule or two, which can
totally irradiate HIV, the future of already infected ones is still gloomy as scientists feel,
discovery of a cure is not possible in near future.
In the mean time, many exploit the situation in the name of Ayurveda, who claim to
have sure shot-cure for HIV/AIDS. Newspapers across the country carry attractive
advertisements even though not ethical, in which quacks claim to have time tested, miracle
cure for AIDS. On the other hand Ayurvedic fraternity has not taken the situation seriously
and turned Nelsons eye to this condition. It is a fact that no one has ever cured HIV
infection, but it doesnt mean to say that it is not possible. We have many examples of high
success rates in the management of many viral conditions being treated with Ayurvedic
medicines, the common example being viral Hepatitis.
With this backdrop, an attempt has been made here to understand the HIV infection
and AIDS in terms of Ayurveda, as understanding is increasingly essential for physician, for
infected ones, their relatives and the society at large. The modern medical understanding
gives us a picture of one side of coin whereas, we get a clear picture of any condition, when
we analyze the whole subject with Ayurvedic point of view. After the WHO recognition as an
authentic medical science, Ayurveda has to prove itself as a comprehensive system which is
useful in management of al types of diseases, very specifically infectious diseases.
Understanding of HIV/AIDS has given new meaning to already known terminology of
Ayurveda. Ojokshaya is one such condition, which has been in lime light in recent days. As
immunological disorders, role of genetics, in causation of disease is increasingly becoming
more important in recent days, the focus of Ayurvedic physician is shifting to these basic
concepts of Ayurveda.
Charaka doctrines classified Balam (immunity) in to three categories, i.e. Sahaja
(innate), Kalaja (seasonal) and Yuktikrita (acquired). Chakrapani commented, as Vyadhi
Kshamatwam is a force antagonistic to virulence of disease causative factors1. Susruta
clarified further stating Balam is Ojas2.
Ojokshaya is a broad understanding of immuno deficiency, depilated vigor and
vitality. Charaka while explaining the causes of Ojokshaya has given emphasis to
Bhootapaghata or infection, which has kindled our interest to do research on Ojokshaya,
with special reference to HIV infection.
Understanding a disease will not end with that knowledge. It is the basis for
developing its management modalities. Usually it is a trend to try the established drug,
which has a reference in Ayurvedic classics. In recent years, as there are thousands of
research updates are available on Ayurvedic medicinal herbs and minerals, Ayurvedic
physicians have a responsibility of developing new drugs in the light of emergence of new
disease. It is in line with principles of Ayurveda to develop new drugs, of course not
deviating from basic principles.
So a rational combination was made to tackle cause of disease and management of
resultant condition. The Ojovardhini-yoga, which has Ojovardhaka, Ama pachaka,
jwarahara, and krimigna drugs in it. Recent researchers have proved all the properties of
individual drugs also. An attempt has been made to develop non-pharmacopeal methods of
SHAREERA
Ayurveda describes human body as seat of Chetana (consciousness) and a product
of panchabhoutic vikara, existing in equilibrium. When this equilibrium gets disturbed, that
results in defective bodily tissues. This is the beginning of any disease4. The normal healthy
state of such a body requires normalcy of several factors. They are Dosha, Agni, Dhatu, and
Mala along with peaceful disposition of Atma, Indriya and Mana5.
constitutions are equally capable of resisting the diseases. As long as the Dhatu are strong
and healthy and are conducting their normal functions with their essence i.e. Ojas being
both qualitatively and quantitatively effective, the body will be strong enough to resist and
counter the decay and degeneration caused by either the natural processes or disease.
Sleshma in normal state apart from other confers10
1. Weight and bulk
2. Strength to perform work and resist disease and decay
3. Promotes durability (preserves the body from decay)
4. Promotes healing process (Ropanam) and
5. Promotes tissue building.
The functions of Kapha11
The important functions, attributed to the Sleshma by the different Acharyas are
1. It is responsible for growth, weight and bulk of the body i.e. Brumhanam,
Gauravam.
2. It is vrishya a function relates to sexual stamina and productivity
3. Sthairya- it imparts stability and durability to the body and strength to the
limbs.
4. It confers strength required to perform labours physical activity i.e.
Vyayama shakti
5. It also provides the power to resist and overcome forces or factors, which
bring about disease and decay popularly known as Vyadikshamatvata viz.
Vyadhi Bala viroditva Vyadhi Utpadaka Hetu Pratibhandhakatvam.
6. Ropana promotes healing process
also increases along with the growth of the body elements i.e. Sapta Dathus. It
comprehends both sharira and satwa i.e. body and mind.
2. Kalaja Bala15: This type of Bala is influenced by the factors like seasonal variations and
age of the individuals. Thus Kalaja Bala is supposed to be dissipated at its lowest level
in the Adana kala comprising of shishira, vasanta and greeshma ritus. On other hand
Bala is stated to be conserved and at its high peak level in the visarga kala, increasing
over Varsha, Sharat and Hemanta ritus, which are known as Sheeta kala or cooler
period.
3. Yuktikrita16: This type of Bala refers to the bodys resistance against diseases, which
can be enhanced by appropriate nutrition such as meat, ghee etc. Restorative and
rasayana therapy in keeping with the seasonal requirements, adoption of Swastha Vritta
principles of Ayurveda along with Achara rasayana also contributes the growth of
Yuktikrita Bala.
Dalhana in his commentary on Bala Lakshanas as explained by Susruta, observes Ojas
and Bala as synonyms, especially with Chikitsa point of view. However they are distinct in
the sense the former is the essence of all the Dhatus and it has physical properties like
Roopa Rasa Veerya etc. The later is to be determined from the power to lift heavy weight
and the capacity to bear heavy loads etc. it doesnt possess physical properties17.
OJAS
The term Ojas has been stated in Ayurvedic classics represents not only Sleshma
but also for Rasa and Rakta18. It is seen that Chakrapani has made a reference to two kinds
of Ojas viz. Ardhanjali Ojas19 and Astabindu Ojas20. Para Ojas permeates through Rasa in
entire body and nourishes entire body21. Ojas is the essence of all Dhatus22. These are
important and significant in the context of Vyadhi kshamatva, interpreted both as Vyadhi
Bala viroditva and Vyadhi utapadaka vibandakatva23. These two types of Ojas have a direct
bearing on bodys defense against decay degeneration and infection.
Sharangadhra says Ojas is all pervading in the body, and has gunas like Sheeta,
Snigdha and Stihara. This somatmaka dravya is bala pusti kara in nature24. Kashyapa says
excluding Sleshma there is a dravya, which is of reddish yellow or white in colour and its
seat as Hridaya. Further he says the increase in Ojas results in Vriddhi of Bala, Varna, Agni,
Medha, Ayu and Sukha. And the decrease results in Kshaya25.
Charaka has made a mention of Slishmika Ojas26, which according to Chakrapani is
different from Astabindu Ojas27. It is transported through the Ojovaha dhamanis28. It is
Ardhanjali in quantity. Charaka has also described further two kinds of Ojas i.e. Para and
Apara in the chapter Arthedashamahamuliya. In this context Chakrapani says while
commenting that the quantity of Para Ojas is 8 drops (Astabindu) and it is located in
Hridaya. The seat of apara Ojas (Ardhanjali) on the other hand is the ten dhamanis
connected with Hridaya29.
Nirukti (etymology)
Ojas word has its root in Uj or Vaj dhatu30, which means confer or strong (Ugra).
Ojas is the subanta pratyaya of word Ojas, which means Deepti, Prakashah and Balam31.
Kalidasa in Raghuvamsha kavya writes Rudraoujasa with reference to the potency of lord
Shiva.
Paribhasha (Definition)
Ojas is the essence of all the seven Dhatus. Ojas is nothing but the Bala or strength
of the body, which is the ultimate end product of the seven Dhatus32 starting from Rasa and
ending at Shukra. Some people consider Ojas as Upadhatu33. But Chakrapani contradicts
this opinion and says Ojas sustains the body but doesnt nourish it.
10
11
latters initial formation and is permanently located there, sustaining the life of the foetus.
Loss of Ojas amounts to the loss of life itself. Chakrapani comments that the above function
pertains to both the Ojas and further explains that Ojas plays a role in three different stages
of the life of the foetus.
1. At the time of conception it is the essence of Shukra and Shonita.
2. In the second stage it is the essence of the Rasa Sara, which provides nutrition to the
embryo.
3.
In the third stage, when there is formation of various organs, Ojas manifests with its own
action.
12
NIDANA OF OJOKSHAYA
The pathological state of Ojas is called as Ojokshaya41. Charaka and all other
classics have described this Ojo vikriti as Ojokshaya. Where as Susruta has classified this
condition in to three different stages42 as 1) Ojovishramsha 2) Ojovyapat and 3)
Ojokshaya.
The Nidana, which cause depletion of any Dhatu, can also cause depletion in the
Ojas qualitatively and quantitatively. But exclusively some aetiology has been attributed to
perpetuate the condition of Ojokshaya. The factors influencing the Ojokshaya are as follows.
Nidana43 (Etiological factors)
1. Ahara karana
2. Vihara karana
3. Manasika karana
4. Agantu karana
Ahara karana: alpashana (malnutrition), anashana (starvation) are the two important
causes related it food.
Vihara karana: vatatapasevana (exposure to extreme heat of sun and blows of winds),
ativyayama (indulging in heavy work beyond once capacity), ati vyavaya (indulging in
excessive sex), sonita ativartana (loss of blood due to hemorrhage, injuries, excess
menstrual bleeding etc.), and prajagara (keeping awake in the night) are the important
causes related to Vihara.
Manasika karana: kopa (anger) shoka (grief) chinta (worry) bhaya (phobia) are the
important psychological causes.
Agantu karana: These are the external causes like Bhutopaghata due to bhuta, pishacha,
rakshasa etc. Charaka has mentioned that the Ojas is the Ahara for rakshasa and if they
13
consume the Ojas, it causes depletion of Ojas. Here rakshas i.e. Rajarichara, can be
correlated to infectious organisms which spreads through Prasanga (sexual contact), Gatra
samsparsha (physical touch), Niswasa (droplet infection), Sahabhojana (eating together)
and Sahashayyasana (sharing bed, furniture etc.).
Nidanarthakara Rogas:
Rajayakshma44, Prameha45, Pandu46, Raktarsha, Raktatisara, Kshayaja Kasa, Kshataja
kasa, Sannipata Jwara47, are the diseases in which in their later stage lead to Ojokshaya.
Sushrutha hinted such possibility while dealing Abhinyasajwara, wherein he used the
term Hataujasa48 indicating the rundown or deranged condition of Ojas. The clinical features
are low or even sub normal temperature. Sub-comatose state, loss of voice, cracked
tongue, dryness of throat, suppression of stools, perspiration, micturition, hardness of chest,
aversion to food, dull complexion, difficulty in breathing and delirium. Further Susruta, made
a clear cut observation while dealing Sannipata Jwara in which the distribution of Ojas to the
various parts of the body is affected either due to leakage or loss or obstruction to the Ojas
carrying tiny srotases. Such a condition is termed as Oja-nirodhaja Sannipata. The
symptoms of such Sannipata Jwara are inertness of the limbs, chills, fits, loss of
consciousness, delirium etc.
The acute condition referred above illustrates how the pronounced loss of Ojas
contributes to an extra-ordinary state of susceptibility to increased microbial / viral activity
and to toxins produced by these agents. Other clinical conditions, which are slow in
progression, chronic in nature and cause profound Dhatu Kshaya (wasting of body tissues)
occur due to metabolic abnormalities leading to diminished production of Ojas. This will
happen due to loss of structural integrity of Dhatuvaha Srotas and obstruction in the supply
14
system. Such other disease syndromes are Rajayakshma Madhumeha, Ojomeha49, Pandu,
Sannipata Jwara etc.
Charaka has enumerated the pathological sequences very clearly while explaining the
Samprapti of Rajayakshma in Charaka Chikitsa. After explaining the manner in which
nutrient materials are normally metabolized and assimilated by the dathus he elaborates it
further. Due to the obstruction of srotas as a result of a deficiency of nutrients of raktadi
dathus, lowered functioning of dhatwagnis and catabolic events, the food ingested, which
undergoes pachana in the kosta is changed into malas.
Madhumeha is one such condition in which while explaining the Samprapti Charaka
observes; Vata by its ruksha Guna transforms the Ojas, sweet in taste to astringent and
transports it to the mutrashaya leading to the causation of the condition known as
madhumeha. Here the Ojas produced in this person itself is vitiated50.
The case of Pandu Roga the Samprapti is dominated by Pitta. The aggravated Dosha
vitiates the Dhatus, which in turn loose their integrity and lose of normal varna, Bala
(resistance) and sneha, which are the gunas of Ojas are depleted by the Dosha-Dhatu
sammurchana resulting the clinical features; impoverished Rakta and Medo Dhatus, leading
shitilendriya and vaivarnyata.
Prameha, the urinary disorder is of two types. One caused due to endogenous factors
like Vatadi Doshas, another one caused by exogenous or Agantuja factors like indulgence in
sex with the unfit and diseased partners. There are twenty types of prameha originating from
Vata, Pitta and Kapha Doshas. However they were silent on the second variety of infectious
prameha in their works. Since it appears that in those days of samhita kala every one used
to live responsibly, there was no scope for transmission of UTI and STD. Agantuja prameha
disease appeared in India soon after the invasion by foreigners, who carried the infection
15
along with them. Therefore these disease entities were included in the later works like
Sharangadhara samhita, Bhavaprakasha etc. Agantuja (acquired) prameha is infectious and
communicable disease, transmitted through agamya and dushita yoni samsarga (Sexually
transmitted). This acquired prameha appears differently in different people in accordance
with Lakshanas /Dosha - Dushya sammurchana and other Samprapti ghatakas as well as
Bala of the individual. The principle varieties are
1. Aupasargika meha (Puyameha)
2.
Ojomeha
16
The further advancement of the disease leads to depletion of Ojas both quantitatively and
qualitatively.
Visesha Samprapti: bhutopaghata janya Ojokshaya manifests in a different manner. The
infectious organisms (Bhuta) cause cell damage and entry of pathogen in to the cell
(Bhutabhishanga) is the hallmark of this process. These pathogens cause srotorodha, which
leads to Vata Vriddhi and vitiation of other Doshas. From this stage onwards the
pathological processes continue like samanya Samprapti.
Sankhya Samprapti53
There are three types of Ojas vitiation mentioned as Ojo-visramsa, Ojovyapat and
Ojokshaya. Even though they are explained as the types of Ojo vikriti, practically they look
like the stages of Ojokshaya.
Ojo-visramsa: Ojas mixes with Rasa Dhatu in Hridaya, from there it circulates through out
the body via various srotases. In this condition, the circulating Ojas leaks out or oozes out
from the tiny distributing channels as a result this vital substance may not reach certain
organs / parts of the body and leads to the following signs and symptoms.
OjoVyapat: it is a pathological condition of Ojas because of vitiation by the Doshas as a
result, the Ojas looses its physiological or normal qualities and properties as described to it
this vikruta Ojas produces the following Lakshanas.
Ojokshaya: This is the final stage of ojo-vikruti represents the loss and wasting of Ojas.
ROOPA (SYMPTOMATOGY)
Charaka has described the Ojokshaya Lakshanas as follows54.
Abheekshna (stressful)
Durmana (sorrowful)
17
18
ghee etc. the Dravyas having opposite qualities like ruksha, Ushna, Katu and Kashaya Rasa
Dravyas are Anupashaya.
Vyavachedaka Nidana
It is also possible that Lakshanas of Visramsa /Vyapat /Kshaya may be felt in various
other clinical conditions apart from Ojokshaya. Sannipataja Jwara, Vishama jwara,
Rajayakshma and Kshata ksheena are the differential diagnosis of Ojokshaya.
Samprapti gataka
Dosha
: Tridosha
Dooshya
: sapthadhatu, ojas
Agnidusti
Roga marga
19
CHIKITSA
The term Chikitsa is derived from root Kit Rogapanayane58 i.e. to adopt measures
calculated to remove the factors of the disease. Amarakosha ascribes it as Ruk
Pratikriya59. Susruta puts it in nut shell measures calculated to the removal of causative
factors. In a nut shell action against to the disease i.e. break down of Samprapti is Chikitsa.
Here it can be achieved by reinstitution Ojas by Ojaskarabhavas (Rasayana). And through
prevention by Sadvritta also. As the Bhutopaghata is also a cause of Ojokshaya, specific
Bhuta-vighata Chikitsa has to be incorporated viz. Apakarshana and prakriti vighata60.
) Krimihara Chikitsa
Apakarshana
Prakriti vighta
) Ojovardhaka Chikitsa
Rasayana
Vajikarana
Dravyas having specific krimigna property can achieve Krimi apakarshana and prakriti
vighata of Krimi. Drugs having Katu, Tiktha, Kashaya Rasa and Krimi hara Prabhava are
used here. Drugs like vidanga, nimba, yastimadhu and bhringaraja are some of the Krimi
hara Dravyas.
In the case of Ojo-visramsa and Vyapat, one has to treat with rejuvenating treatment,
which will not cause digestive disorders or indigestion. Persons with totally depleted Ojas
have to be left out of active treatment, as it will not respond to any treatment. If timely
treatment is initiated these cases respond positively and Agni in each Dhatu gets back to its
normal state. Because of Ojovardhaka bhavas or rejuvenators, they get proper nourishment
and sneha Guna or the Ojas in its natural form gets regenerated. As and when Ojas gets
20
replenished the person gets softness of the skin, youth, fine hairs gets regenerated and he
will get back interest in life and gets enthusiasm. His eyesight will improve and digestive
capacity regained, body gets re-infused with luster. And again for these patients there are
many restrictions in diet and activities. Ojas gets depleted if he indulges in Kashaya
(astringent), Tiktha (bitter), Sheeta (cold), controlling natural urges, excessive indulgence in
sex and exhaustive physical activities and in the event of any other debilitating diseases61.
In Ojo-visramsa there will be roughness of skin, change in complexion, pricking type of
pain. In Vyapat there will be emaciation of body, depletion of digestive secretions, diarrhea
or vomiting will manifest. In Ojokshaya diminution of sensory perception, excessive debility
and diminution of digestive capacity followed by death will occur. For these conditions are
intake of therapeutic unctuous substances Oleation, Sudation, medicinal baths followed by
easily digestible food are to be given. Depletion in Doshas, Dhatus and malas as well the
loss of vigor or strength or Ojas will make the person desire for such food or drink which will
increase the depleted once. Then he has to be provided with such foodstuffs, which will
enable to restoration of normally and he will regain his strength. Here as a last warning
Sushrutha says, if because of depleted body mass if the person has severe vitiation of Vata
Dosha then the person will become unconscious and one with complete loss of Ojas should
not be treated with active therapeutics as it will become futile.
If a person indulges again in Vata karaka dietetics, excessive exercises, indulges in too
much of sex, reading, gets afflicted by fear, worry insomnia, unquenched excessive thirst
hunger, loss of bodily tissues, unsatisfying, unwholesome food intake will lead to depletion
of Rasa Dhatu. This will cause malnutrition to other Dhatus, which will also get depleted
subsequently. If this weak person if not treated and continues to indulge in above said
causative factors, he will get breathlessness. Chronic cough, tuberculosis, spleeno-megaly,
21
ascetics, and Malabsorption syndrome, bleeding disorders and he will die due to these
diseases. As in this condition the strength of the patient is less and the strength of the
disease is more, he has to immediately stop indulging in causative factors. He has to be
treated with the rasayana drugs like, ashwagnadha, vidari, vidarigandha, shatavari, bala,
atibala, nagabala. He should also take milk and milk products, meat, rice grown in 60 days,
jovar, wheat and other products which are sweet in take. He should take rest and sleep in
daytime also, should not work or do any exercise, should take enemata which are
strengthening in nature and nourishing in nature.
All the seven Dhatus from Rasa to Shukra have particular cellular structure. Rasa Dhatu
is an exception which will be in liquid form and having no dense particles in it and devoid of
samhata Guna or the solidifying nature. As it nourishes all the Dhatus separately coming in
direct contact with them. It is considered as a part of kosha. The other 6 Dhatus have dense
particles in it and property of getting solidified. The first three are considered as shakshas.
The latter three i.e. as the Majja and Shukra are considered as marmas because any
disease related these Dhatus are difficult to treat. It is included in meadhyama roga marga.
For this reason the finest end product of dhatuwagnipaka. The Ojas has been considered as
seat of prana and diseases pertaining to Ojas are not only difficult to treat they are fatal also.
So Ojas is also considered as madhyama roga marga.
Ojavridhikara bhavas62
The factors responsible for good status of Ojas in its natural form
1. Birth in a country where people are naturally strong.
2. Birth at a time when people naturally gain strength
3. Favorable disposition of time i.e. pleasant and moderate climate
4. Excellence of qualities of sperm and ovum (that of parents )
22
23
2. Rest (sleep and relaxation): A burst of findings is now beginning to shed light on the
ultimate purpose of the sleep and in particular, on the convoluted interplay between
sleep and the immune system. Experiments suggest that the immune system is some
how repaired as bolstered during sleep and that in turn has a role in regulating sleep.
Researchers have reported that sleep serves many purposes such as regulates body
temperature organizes memories and replenishes the immune system.
Ayurveda rounded up all these so called latest research findings on sleep in a two line
stanza in astanga hrudayam which says timely sleep provuces sukha, pusti (strength) bala
(immunity) vrushata (sex power) jnana (knowledge) and jeevitham (life activities). Whereas
in the absence of sleep, quick opposite clinical picture may emerge like dukha
(unhappiness), krushata (emaciation) and nirbalata (loss of strength) Kleebata (impotency)
agnana (lack of knowledge) and mruthyu (death).
On the close observation of the Lakshanas attributed in the Ayurvedic classics for
Ojokshaya. (shukra kshaya and nidra kshaya ) one can notice the similarity of the
symptoms. Further these signs and symptoms very closely resemble and correlate with the
clinical picture on infected subjects.
3. Brahmacharya: Resistance is a function of several factors like emotional and physical
fitness. The more emotionally fit individual is more resistant to infections. Natural
immunity which identifies and destroys disease-causing organisms. The more often one
is exposed to infections organisms, the higher is the chances of becoming ill. One can
act to reduce exposure to viruses like HIV. Limiting the number of sexual partners or
practicing monogamy will not only protect from HIV but also from other sankramika
Vyadhi. All this is possible only when one, adopts responsible life practices
Brahmacharya the main pillar of good health.
24
Achara rasayana measures in the long run prevent the psychosomatic illnesses and help
in total recovery from various shareera rogas (somatic diseases) and promote the health
swasthasya swasthya rakshanam. The term Achara rasayana refers to certain regimen
one should follow in his daily life. Those are satyabhashana (specking truth), akrodha
(control anger), nivrutham madya maithunat (giving up alcohol and over indulgence in sex),
ahimsa (non violence) anayasam(giving up sedentary habits) prashantam (peace of mind),
priya vadinam (pleasant talk), japa (meditation) shoucha param(cleaniliness), dheeram
(courage) dana (sharing) etc.
Swasthavritta practices
The striking feature of Ayurvedic out look is that it never takes the causes and ways of
treatment mechanically, instead it views from the social. Ecological factors man is a social
organism, therefore is interaction and relationship is very important, as such practice of
virtues. Good behavior in accordance with social circumstances and customs is important in
keeping good health. According to Charaka, diseases have their origin in mind. All diseases
are due to prajanaparadha. The influence of the season and corresponding changes in our
diet and ways of life naturally affects the condition of internal Doshas1. In greeshma i.e. summer Vata Dosha accumulates and in rainy season it is aggravated.
2. In rainy (varsha) season Pitta accumulates and in autumn it is provoked
3. In winter we have good strength and health. But by the end of winter Kapha accumulates
but not provoked as it but in vasanta it melts and creates trouble.
In view of all these natural changes and their effects, the seasonal routine is stated in
Ayurveda. The important step is to keep the body clean and pure. For this purpose
Shodhana measures i.e. purificatory measures are prescribed at the confluence of the
seasons.
25
Vasti is advised immediately before or during the rainy season to pacify Vata. Virechana
before the beginning of autumn, Vamana, Nasya at the end of winter and before spring are
advocated. In disease conditions also if the Doshas are in excess and the patient is strong
enough to undergo shodhanas the purifactory treatment is the best choice
The urges for releasing the flatus, urine faces etc re the natural impulses either to be
prevented or forcibly induced. It is such conscious or unconscious anti-natural misdeeds that
cause all diseases. In the modern sense, all these impulses follow the natural efforts of
organism to maintain the homeostasis which is disturbed due to the biological process going
on in the system by accumulation of wastes, increase of crbon-di-oxide or up setting the
hormonal system. The impulses are due to the reflex mechanism of the organism.
Therefore, interfering I its functions strains the nervous system and biological functions and
the root cause of all disease production.
Dina charya64 the daily routine. Vagbhata stated that actions that are beyond ones
strength or over actions are so irrational if one restores to them it destroys him like a ling
trying to drag an elephant. The irrational actions such as exercise, sleeplessness,
indulgence I sex etc. these should be done within the limits. Adherence to good morals in
life is very essential for healthy life without diseases. These good moral practices are
encapsulated in short in Vagbhata. Always restore to wholesome diets and congenial
movements acting only after due deliberations avoid indulgence in sensual pleasures one
who is generous, equable of mind, truthful, patient and follower of great men becomes free
from diseases.
26
The human defense system is divided in to two major categories immune and nonimmune. Immunity is characterized by an antigen specific response to a foreign antigen or
pathogen and generally takes several days or longer to materialize. A key feature of
immunity is memory for the antigen such that subsequent exposure leads to more rapid and
often a vigorous response. A non-immune host defense is not antigen specific. And is an
immediate response system (beginning with in minutes of an insult) with out memory for the
eliciting
stimulus.
The
non-immune
process
is
called
inflammation.
Neutrophils,
Eosionophils, Basophils, Natural Killer cells, Monocytes and Macrophages are the mediators
of this immediate response system. The dual limbs of the immune system consist of cellular
and humoral immunity. The principal effector of cellular immunity is the thymus-derived (T)
lymphocyte and of humoral immunity is the bone marrow derived (B) lymphocyte. Both B
and T lymphocyte derive from common stem cell of bone marrow.
BONE MARROW
The bone marrow is actually one of the largest organs in the body, approaching the
size and weight of the liver. It is also one of the most active tissues of the body. Normally,
27
75% of the cells in the marrow belong to the white blood cell-producing myeloid series, and
only 25% are maturing red cells, even though there are over 500 times as many red cells in
the circulation as there are white cells. This difference in the marrow probably reflects the
fact that the average life span of white cells is short, whereas that of red cells is long.
The bone marrow contains multi potent uncommitted stem cells that differentiate into
committed stem cells, and the committed stem cells differentiate into the various
differentiated cell types found in marrow and blood. The multi potent uncommitted stem cells
are few in number but are capable of completely replacing the bone marrow when injected
into a host, whose own bone marrow has been completely destroyed. It appears likely that
the bone marrow contains separate pools of committed stem cells for megakaryocytes,
lymphocytes, erythrocytes, eosinophils, and basophils, whereas neutrophils and monocytes
arise from a common precursor.
Immune mechanisms
Lymphocytes are key constituents of the immune system. In mammals, this system
has the remarkable ability to produce antibodies against many millions of different foreign
agents that invade the body. In addition, the immune system "remembers," and a second
exposure to a foreign substance produces a more rapid and greater Humoral immunity is
immunity due to circulating antibodies in the globulin fraction of the plasma proteins. It is a
major defense against bacterial infections. Cellular immunity is responsible for delayed
allergic reactions and rejection of transplants of foreign tissue.
It constitutes a major
defense against infections due to viruses, fungi, and a few bacteria such as the tuberculus
bacillus. It also helps to defend against tumors. There have been spectacular advances in
immunology in recent years, and the field is now large and complex. Only the fundamentals
are presented here.
28
Unlike other
29
Cellular immunity is mediated by T8, cells. These cells are activated when they are
presented with antigens and MHC-1 proteins on the surfaces of antigen presenting cells.
When also exposed to interleukin-2 (see below), they proliferate and differentiate into
cytotoxic T cells. The cytotoxic T cells attack and destroy cells that have the antigen, which
activated them. They kill by inserting pore-forming molecules (perforins) in the membranes
of their target cells in the same fashion as the complement system does. They may also act
by inducing within the cells an as yet undefined change that leads to death. Suppressor T
cells, which develop more slowly than cytotoxic T cells, help terminate the immune response
30
helper/inducer cells.
To ensure maximal specific T cell response the antigen is linked to molecular
components of the HLA system (by B cells, dendritic cells and macrophages) and presented
to the T cell.
The transformed blast cell undergoes progressive mitotic division and each cell of the
resulting clone has the same specific immune potential. The subsequent T cell activities
tend to remain local at the site of the antigen concentration and this cell-mediated immunity
(CMI) is delayed, i.e. at least 24 hours are required for a significant local concentration of
sensitised T cells.
T cell functions and mechanisms
1.
Overall regulation of the immune response and reactions - This is effected by helper T
cells which promote, and suppressor T cells which inhibit immune reactions. In the
peripheral blood, 2/3 of the T lymphocytes are helper and 1/3 suppressor.
Using
monoclonal antibodies, helper cells carry the CD4 surface antigen and suppressor cells
the CD8.
2.
31
(b) Natural killer cells, again cause lysis by direct cell to cell contact but usually the
killing action is non-specific.
(c) Delayed hypersensitivity reactions are mediated by the release of lymphokines
from the specifically activated T cells.
activity associated with the promotion and control of the immune response and the
inflammatory reaction.
Lymphokines. However, since other cells produce them as well, it seems more appropriate
to call them Cytokines. This field is growing very rapidly, and most of the Cytokines are
initially named for other actions, e.g., B cell-differentiating factor, B cell-stimulating factor 2.
There is a convention that once the amino acid sequence of a factor in humans is known its
32
name is changed to interleukin. Thus, for example, the name of B cell-differentiating factor
was changed to interleukin-4.
33
PATHOLOGY
The acquired immune deficiency syndrome (AIDS) was first recognized in the United
States in the summer of 1981, when the Centers for Disease Control and prevention (CDC)
reported the unexplained occurrence of two diseases. Pneumocystis carinii pneumonia in
five previously healthy homosexual men in Los Angeles was reported first. Soon after
Kaposi's sarcoma in 26 previously healthy homosexual men in New York, and Los Angeles
were reported. Within months, the disease became recognized in male and female Injection
Drug Users (IDUs) and soon after, in recipients of blood transfusions and in hemophiliacs.
As the epidemiological pattern of the disease was unfolded, it became clear that a microbe
transmissible by sexual contact or blood and blood products was the most likely etiologic
agent for the epidemic. In 1983, Human Immuno deficiency Virus (HIV) was isolated from a
patient with lymphadenopathy. In 1984 it was demonstrated clearly that this virus is the
causative agent of AIDS.
During the early years of 1980's the care of HIV-infected individuals in the United
States was confined to restricted groups of physicians and hospitals, in urban areas, of
north eastern and western seaboards. But today, every practicing physician in this country
and other parts of the world is required to have some degree of familiarity with the work up,
diagnosis, management, of HIV-infected individuals. HIV- infected individuals are presenting
in increasing numbers to family physicians, obstetricians, gynecologists, pediatricians and
surgeons with clinical problems that may be directly or indirectly related to their HIVinfection.
DEFINITION: Any HIV- infected individual with CD4+ T cell count of < 200/l had AIDS by
definition, regardless of the presence of symptoms or opportunistic diseases. The clinical
34
Glycoprotein
GP41
Fatty (Lipid
Bilayer
membrane
Protein
P18
Protein
P24
Reverse transcriptase
enzyme
35
Electron microscopy shows that the HIV virus is an icosahedral structure containing
numerous external spikes formed by the two major envelope proteins, the external gp 120
and the transmembrane gp41. The Virion buds from the surface of the infected cell
incorporates a variety of host proteins, including Major Histo-compatibility complex (MHC)
class I and II, antigens into its lipid bilayer.
Life cycle of HIV
HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNA
to DNA by the enzyme reverse transcriptase. The life cycle begins with the high affinity
binding of the gp 120 protein via a portion of its VI region near the N terminus to its receptor
on the host cell surface, the CD4 molecule. It has recently been demonstrated that the coreceptor that must be present together with the CD4 molecule for fusion and entry of T-cell
tropic strains of HIV-1 is a molecule termed CXCR4. The reverse transcriptase enzyme,
which is contained in the infecting Virions, then catalyzes the reverse transcription of the
genomic RNA into double-stranded DNA. The DNA translocates to the nucleus, where it is
integrated randomly into the host cell chromosomes through the action of another virally
encoded enzyme Integrase.
HIV genome: HIV-1 has genes that encode the structural proteins of the virus gag
encodes the proteins that form the core of the Virion (including p24 antigen) i pol encodes
the enzymes responsible for reverse transcription and integration and env encodes the
envelope glycoproteins.
Molecular heterogeneity of HIV-1: Molecular analysis of various HIV isolates reveals
sequence variation over many parts of the viral genome.
36
37
prolonged exposure of the vaginal and cervical mucosa and endometrium to infected
seminal fluid.
Transmission by blood and blood products: HIV can be transmitted by blood products,
both among individuals who share contaminated paraphernalia (needles and syringes) for
injection drug use and in those who receive transfusions of blood and blood products. It is
estimated that 90 to 100% individuals who were transfused with HIV-infected blood became
infected. Transfusions of whole blood, packed red blood cells, platelets, leukocytes, and
plasma are all capable of transmitting HIV infection. The precautionary measures taken to
check this: (1) the screening of all blood for p24 antigen and for HIV antibody body enzyme
linked immunosorbent assay (ELISA), with a confirmatory western blot where applicable; (2)
the self-deferral of donors on the basis of risk behavior.
Occupational transmission of HIV: There is a small but definite occupational risk of HIV
transmission among health care workers, laboratory personnel, and potentially others who
work with HIV infected specimens, particularly when sharp objects are used. It is estimated
that 250,000 to 1 million health care workers are stuck with needles or other sharp medical
instruments in each year large.
Maternal to fetal / infant transmission: (vertical) HIV infection can be transmitted from an
infected mother to her fetus during pregnancy or during delivery. This is an extremely
important form of transmission of HIV infection in developing countries, where the proportion
of infected women to infected men is approximately 1:1.
Transmission by other body fluids: There is no convincing evidence that saliva can
transmit HIV infection, either through kissing or through other exposures, such as
occupationally to health care workers.
38
EPIDEMIOLOGY
HIV infection and AIDS is a global pandemic, with cases reported virtually from every
country. The current estimate of the number of cases of HIV infection among adults
worldwide is approximately 22 million, and approximately 2.6 million HIV- infected children
have been born since the start of the HIV pandemic, and approximately one half of these
have developed AIDS and have died. The global projections for the total number of HIVinfected individuals by the year 2000 range from 40 to 100 million.
AIDS IN INDIA
The first case of HIV infection was identified in India in 1986 at Chennai. During
these early days it was limited to female sex workers. Focus was shifted from Chennai to
Mumbai as hundreds of female sex workers were found to have HIV infection. It is with truck
drivers, it stared spreading from big cities to smaller ones. People, who travel from cities to
city and those who travel from villages to cities, were found to be more susceptible because
of unprotected, non-marital sexual contact. Even though thousands of people got infected
through blood transfusion during the first decade of epidemic, the heterosexual contact is
the major cause of spread. Every year 3 lakh Indians die due to AIDS. AIDS deaths since
the beginning amounts to 25 lakhs. It is second highest figure among communicable
diseases, which cause death.
PATHOPHYSIOLOGY AND PATHGOGENESIS
The hallmark of HIV disease is a profound immunodeficiency resulting primarily from
a progressive quantitative and qualitative deficiency of the subset of T lymphocytes referred
to as helper or inducer T cells. This subset of T cells is defined phenotypicaly by the
presence on its surface of the CD4 molecule. This serve as the primary cellular receptor of
HIV it has recently been demonstrated that a co-receptor must be present together with CD4
39
for effective fusion and entry of HIV-1 into its target cells. It is important appreciate that the
pathogenic mechanisms of HIV disease are multi factorial and multi-phasic and are different
at different stages of the disease.
HIV has a number of mechanisms to evade elimination by the immune system. HIV
has an extraordinary ability to mutate, but this mechanism probably acts mainly after the
establishment of chronic infection and contributes to the maintenance of chronicity. Since
the transmitted virus and the virus that initially becomes established as a chronic infection
are relatively homogeneous, the initial escape from immune system control likely involves
other mechanisms. Molecular analysis of clonotypes has demonstrated that clones of CD8 +
Cytolytic T Lymphocytes (CTLs) that expand greatly during primary HIV infection and likely
represent the high -affinity clones that would be expected to be more efficient in eliminating
virus infected cells disappear after their initial burst of expansion.
Viral Dynamics
It was originally thought that very little virus replication occurred during clinical
latency. However studies of lymphoid tissue using PCR analysis for HIV RNA and in site
hybridization for individual virus expressing cells clearly demonstrated that HIV replication
40
occurs throughout the course of HIV infection, even during clinical latency. The availability of
sensitive PCR techniques led to the demonstration that plasma viremia present at all stages
of HIV disease.
The cytokine network in the HIV pathogenesis
On perturbation of the immune system by antigenic challenge, the expression of
cytokines increases to varying degrees. Cytokines that are important components of this
immune regulatory network have been demonstrated to play a major role in the regulation of
HIV expression in vitro. A number of in vitro model systems of chronically infected monocyte
or T cell lines, primary cultures of peripheral blood or lymph node mononuclear cells from
HIV-infected individuals, and acutely infected primary cell cultures have been used to
demonstrate the role of cytokines in the regulation of HIV expression. Potent modulation of
HIV expression has been demonstrated either by manipulating endogenous cytokines or by
adding exogenous cytokines to culture. Cytokines that induce HIV expression in one or
more of these systems include IL-1, IL-2, IL-3, IL-6, IL-12, TNF and TNF . Macrophage
colony stimulating factor (M-CSF), and granulocyte macrophage colony stimulating factor
(GM-CSF). Among these cytokines the most consistent and potent inducer of HIV
expression are the pro-inflammatory cytokines TNF , IL- and IL-6. Interferon (INF) and
(INF) , IL-4, IL-10 and INF can either induce or suppress HIV expression, depending on
the system involved.
Diagnosis of HIV infection
The diagnosis of HIV infection depends on the demonstration of antibodies to HIV
and or the direct detection of HIV or one of its components. The standard screening test for
HIV is the enzyme linked immuno sorbent assay (ELISA). This solid phase assay is an
extremely good screening test, with a sensitivity of over 99.5% most diagnostic laboratories
41
use a commercial ELISA kit that contains antigens from both HIV-1and HIV-2 and that will
detect either.
The most commonly used confirmatory test is the Western Blot. It takes advantage of
the fact that multiple HIV antigens, having different molecular weights elicit the production of
specific antibodies. These antigens can be separated on the basis of molecular weight, and
antibodies to each component can be detected as discrete bands on the western Blot. A
negative western blot is one in which no bands are present at molecular weights
corresponding to HIV gene products. In a patient with positive or indeterminate ELISA and a
negative western blot, one can conclude with certainty that the ELISA reactivity was a false
positive.
Evaluation of CD4 Count: The close relationship between clinical manifestations of HIV
infection and CD4+Tcell count has made measurement of the latter quantity a routine part of
the evaluation of HIV infected individuals. CD4+Tcells counts make a powerful set of tools
for determining prognosis and monitoring response to therapy while the CD4+Tcell count
provides information on the current immunologic status of the patient. This measurement is
done by Flow Cytometry method.
Patients with CD4+T cell counts below 200/ul are at high risk of infection with
preumocystis carini, while patients with CD4+T cell counts below 100/l are at high risk of
infection with cytomegalovirus and mycobacterium avium-intracellulare complex. Patients
with an initial diagnosis of HIV infection should have CD4+T cell measurements performed
approximately every 6 months and more frequently if a declining trend is noted. At a
minimum antiretroviral therapy is generally indicated when the CD4+Tcell count falls below
500/ul, and a declining CD4+Tcell count may provide an indication for changing therapy.
Once the CD4+T cell count is 200/l these patients should be place on a regimen for carinii
42
pneumonia (PCP) prophylaxis. All effective forms of antiretroviral therapy to date have been
associated with at least a transient increase in either CD4+T cell count.
Direct measurements of HIV RNA
Facilitated by techniques for the precise quantitation of small amounts of nucleic
acids, the measurement of serum or plasma levels of HIV RNA has become the most
commonly used approach for the direct detection of HIV. Two basic techniques are used the
reverse transcriptase PCR (RT-PCR) assay and the branched DNA (bDNA) assay. The RTPCR assay involves the PCR amplification of cDNA generated from viral RNA. The bDNA
assay involves the use of solid-phase nucleic acid capture system and signal amplification
through successive nucleic acid hybridization to detect small quantities of HIV RNA. Both
assays generate date in the form of number of copies of HIV RNA per milliliter and is
positive in >90% of patients All effective forms of anti retroviral therapy to date have been
associated with a drop in levels of HIV RNA.
B2 Microglobulin levels
B2 microglobulin is an 11Kda protein that is expressed on the surface of most
nucleated cells. Free B2 microglobulin can be measured in the serum and urine. Levels of
B2 microglobulin are elevated in a variety of conditions characterized by lymphocyte
activation and/or lymphocyte destruction among these are lymphoproli ferative syndromes,
auto-immune diseases, and viral infections, including HIV infection.
Clinical manifestations
. HIV disease can be divided empirically on the basis of the degree of
immunodeficiency into an early stage (CD4+T cell count 200 to 500/l), an intermediate
stage (CD4+Tcell count 200 to 500/l) and an advanced stage (CD4+T cell count < 200/l).
Most AIDS defining opportunistic infections and true malignancies occur in the advanced
43
stage of disease, while neurologic disease and Kaposis Sarcoma are not as strictly related
to the degree of immunodeficiency. The two major classification systems for staging HIV
disease are the CDC system and the Walter reed medical center system; these are to be
distinguished from the case definition for AIDS, which is used for surveillance purposes.
The acute HIV syndrome
It is estimated that 50-70% of individuals with HIV infection experiences an acute
clinical syndrome approximately 3 to 6 weeks after primary infection. Varying degrees of
clinical severity have been reported, and it has been suggested that symptomatic
serocoverision leading to the seeking of medical attention indicates an increased risk for an
accelerated course of disease. Clinical findings occur along with a burst of plasma viremia
and p24 antigenemia. The syndrome is typical of an acute viral syndrome and has been
likened to acute infections mononucleosis symptoms usually persist for 1 to several weeks
and gradually subside as an immune response to HIV develops and the levels of plasma
viremia decrease.
Total lymphocyte and T cell subsets (CD4+and CD8+) are initially reduced. An
inversion of the CD4+/CD8+T cell ratio occurs later because of the rise in the number of
CD8+T cell subsets, as determined by T cell receptor analysis. The total circulating CD8+T
cell levels usually remain some what depressed, normal lymphodonopathy
The acute HIV syndrome
It is estimated that 50-70% of individuals with HIV infection experiences an acute
clinical syndrome approximately 3 to 6 weeks after primary infection. Varying degrees of
clinical severity have been reported. Clinical findings occur along with a burst of plasma
viremia and p24 antigenemia. The syndrome is typical of an acute viral syndrome and has
been likened to acute infections mononucleosis symptoms usually persist for 1 to several
44
weeks and gradually subside as an immune response to HIV develops and the levels of
plasma viremia decrease. Opportunistic infections have been reported during this stage of
infection, reflecting the immunodeficiency that results from reduced numbers of CD4+T cells.
Total lymphocyte and T cell subsets (CD4+and CD8+) are initially reduced. An inversion of
the CD4+/CD8+T cell ratio occurs later because of the rise in the number of CD8+T cell
subsets, as determined by T cell receptor analysis. The total circulating CD8+T cell levels
usually remain depressed, although there may be a slight rebound towards normal.
Lymphadonopathy occurs in approximately 70% of individuals with primary HIV infection.
Most patients recover spontaneously from this syndrome and have a mildly depressed
CD4+T cell count that remains stable for a variable period before beginning its progressive
decline. In most patients, primary infection with or without the acute syndrome is followed by
a prolonged period of clinical latency.
The asymptomatic stageClinical latency although the lengths of time form initial infection to the development
of clinical disease varies greatly the median time id approximately 10 years. HIV disease
with active virus replication usually progresses during this asymptomatic period. Some
patients called long term non-progressors, show little decline in CD4+Tcells counts over an
extended period. These patients generally have extremely low levels of HIV RNA. In these
patients, the appearance of an opportunistic disease may be the first manifestation of HIV
infection.
Some
patients
otherwise
asymptomatic
develop
persistent
generalized
lymphadenopathy during this time. With few exceptions, CD4+T cell counts fall progressively
during this asymptomatic period at an average rate of approximately 50 cells /l per year.
When the CD4+cell count falls below about 200/l, the resulting state of immuno deficiency
45
is severe enough to place the patient at high risk for opportunistic infections and neoplasm
and hence are clinically apparent disease.
Early symptomatic disease
At some point, usually after the CD4+T cell count has fallen below 500/l patients
begin to develop signs and symptoms of clinical illness. Many of these problems can be
traced to minor opportunistic infections, not sufficiently indicative of a defect in cell-mediated
immunity to be considered AIDS defining illness, while some of them appear to be direct
effects of long standing HIV infection. This stage of HIV infection has been given a variety of
names in the past, among them pre-AIDS and AIDSrelated complex (ARC). Generalized
lymphadenopathy.
This condition, defined as the presence of enlarged lymph nodes (1cm) in two or
more extrainguinal sites for more than 3 months without an obvious cause its often the
earliest symptom of HIV infection after primary infection. It is due to marked follicular
hyperplasia. The nodes are generally discrete and freely movable. This feature of HIV
46
disease, which may be seen at any point of time, is not associated with an increased
likelihood of developing AIDS. Paradoxically a loss in lymphadenopathy or a decrease in
lymph nodes size may be a prognostic marker of disease progression. In the early and
intermediate stages of HIV infection, the main differential diagnosis is an adenopathic form
of Kaposis sarcoma. Late in the course of disease, differential diagnosis expands to include
lymphoma, mycobacterium infection, toxoplasmosis, systemic fungal infection and bacillary
angiomatosis. Lymph node biopsy is not indicated in-patients with early stage disease
unless there are sings and symptoms of systemic illness such as fever and weight loss, or
unless the nodes begin to enlarge, become fixed or coalesce.
Oral lesions
Oral lesions, including thrush, hairy leukoplakia-and aphthous ulcers, are particularly
common during this phase. Thrush due to candida infection and oral hairy leukoplatia, are
usually indicative of fairly advanced immunologic decline, generally occurring in patients
with fewer than 300 CD4+Tcells per microliter.
Herpes zoster (shingles)
This condition is seen in 10 to 20% of patients. This reactivation syndrome of
Varicella zoster virus indicates a modest decline in immune function and is often the first
clinical indication of immunodeficiency..
Thrombocytopenia
Thrombocytopenia also may be an early consequence of HIV infection.
Approximately 3% of patients with HIV infection and CD4+T counts above 400/l have
platelet count fewer than 150,000/l. This incidence increases to 10%. Thrombocytopenia is
rarely a serious clinical problem in these patients.
47
Neurologic disease
Clinical disease of the nervous system accounts for a significant degree of morbidity
in a high percentage of patients. The Neurologic problems that occur in HIV-infected
individuals may be either primary to the pathogenic processes of HIV infection or secondary
to opportunistic infections or neoplasm.
Clinical findings in the acute HIV syndrome
General
Neurologic
Fever
Encephalitis
Pharyngitis
Peripheral neuropathy
Lymphadenopathy
Myelopathy
Dermatological
Arthralgias / myalgias
Lethargy/malaise
Mucocutaneous ulceration
symptoms
T4 (helper)
Infection
Opportunistic
others
Malignant
Kaposis sarcoma
and fever
tumours
Lymphomas
lymphocytes >
500/mm3
The table shows AIDS associated diseases and sites.
48
Opportunistic infections
Opportunistic infections are late complications of HIV infection, for the most part
occurring in patients with less than 200 CD4+T cells per microliter. While the causative
agents characteristically are opportunistic organisms, such as pneumocystis carimi,
mycobacterium avium complex, CMV, and other organisms that do not ordinarily cause
disease in the absence of a compromised immune system, they also include common
bacterial and mycobacterium pathogens. Opportunistic infections are the leading cause of
morbidity and mortality I patients with HIV infection. Approximately 80% of AIDS patients die
as direct result of an infection other than HIV, with bacterial infections heading the list.
Protozoal infections
Pneumocystis carinii infection is one of the most common causes of infection
patients generally present with fever and cough that is usually nonproductive or productive
of only scant amounts of white sputum. They may complain of a characteristic retro-sternal
chest pain, which is usually course on inspiration and described as either sharp or burning.
In more severe cases, patient usually notes dyspnoea on exertion, fatigue and weight loss.
One may see a chest x-ray pattern with upper lobe cavity disease, reminiscent of
tuberculosis.
Protozoal diarrhea:
Cryptosporidium is a well-known cause of Diarrhoea in animals and may cause a
self-limited Diarrhoeal infection in the immuno competent host. It is spread through fecal-oral
contact. In HIV-infected individuals, cryptosporidial infection may present in a variety of
ways, ranging from a self-limited or intermittent diarrhoeal illness in patients in the early
stages of HIV disease to a severe, life threatening Diarrhoea in severely immuno deficient
individuals. Therapy is purely symptomatic at present. Patients can minimize their risk of
49
developing cryptosporidiosis by avoiding contact with human and animal feces and by not
drinking water from lakes or rivers.
Microsporidia
The main species causing disease in humans is Enterocytozoon bieneusi. In contrast
to cryptosporidia, microsporidia have been noted in a variety of extraintestinal locations,
including the eye, muscle, liver and cause conjunctivitis and hepatitis. As in the case of
cryptosporidia, no effective therapy is known and treatment is purely symptomatic.
Isospora belli
The clinical syndromes caused by these organisms appear to be identical to those
caused by cryptosporidia one important difference is that this infection can be treated with
trimethoprim/seulfamethoxazole. Entamoeba histolytica and Giardia lamblia are also
common with HIV infection.
Bacterial infections
Bacterial infections are the leading cause of death in HIV infected individuals.
Disseminated mycobaterial infection, particularly due to the Mycobacterium avium complex
(MAC) is the most common opportunistic bacterial infection.
Infections with atypical mycobteria:MAC infection is a late complication of HIV infection,
occurring in patients with CD4+T cell counts of < 100/l.
Mycobacterium fartuitum, mycobacterium chelonas, mycobacteruum marinum,
mycobacterium scrofulceum and mycobacterium haeneophilum all causes disseminated
disease and septic arthritis. Mycobacterium gardnae, generally a nonpathogenic in humans,
and mycobacterium zeropi, a colonizer of water storage tanks, may cause disseminated
disease. Therapy of the latter organisms is extremely difficult.
50
Tuberculosis
M. Tuberculosis, once thought to be on its way to extinction in United States,
experienced resurgence. Tuberculosis is a particularly important problem with HIV infection.
HIV disease progresses more rapidly when associated with tuberculosis, the level of plasma
viremia increases during active tuberculosis and successful treatment of tuberculosis causes
plasma viremia to fall back to baseline levels. Given the fact that, in contrast of HIV infection,
with M. tuberculosis can be spread via respiratory droplets and close, non-sexual contact,
this epidemic of tuberculosis probably represents the greatest health risk to the general
public and the health care profession associated with the HIV epidemic. Tuberculosis may
be the earliest clinical sign of HIV infection. Patients present with fever, cough, dyspnoea on
exertion, weight loss, night sweats and a chest X-ray revealing cavity apical disease of the
upper lobes. Disseminated disease is more common with low CD4+T cell counts.
Viral infections:
Herpes virus infection: Human herpes virus infections present substantial problems
throughout the course of HIV infection. Among the members of this group that are
particularly disabling of patients with HIV infection are CMV, Herpes simplex viruses,
Varicella zoster viruses, Epstein barr virus and HIV-8
Cytomegalovirus infections: Retinitis, esophagitis, and colitis are the most common
manifestations of CMV infection in-patients with AIDS.
Treatment: Three drugs-ganciclovir, foscarrnet and cidofavir are currently licensed for
systemic treatment of CMV infection.
Herpes simplex virus infections: Infection with herpes simplex virus (HSV) in HIV
infected individuals is associated with recurrent labial, genital, and peri anal lesions. As HIV
disease progresses and CD4+T cell count declines, these infections become more frequent
51
and severe. Lesions often appear beefy red, are exquisitely painful and have a tendency to
occur high in the gluteal cleft.
Treatment: The treatment for severe or recurrent HSV infection is acyclovir. For most cases,
200mg is given orally five times per day for 10 to 14 days
Varicella-zoster virus infections:
Varicella-zoster virus (VZV), the etiologic agent of chickenpox, assumes a latent form
a dorsal root ganglia following primary infection. Reactivation is associated with shingles the
appearances of shingles in any patient under 50 years of age should be an indication for
work up of an underlying immuno deficiency, particularly HIV.
Treatment
Treatment is with acyclovir and hyperimmune globulin. While treatment of shingles is
not required, it can often result in a reduction in the time to resolution of lesions, and most
physicians choose to treat it with high-dose oval or intravenous acyclovir or oral famciclovir.
Neoplastic diseases:
A variety of neoplastic and pre-malignant diseases occur with increased frequency
in HIV-infected individuals. They are Kaposis sarcoma, lymphoma and intraepithelial
dysplasia of the cervix and anus. These diseases are significant contributors to the morbidity
and mortality of patients with HIV infection.
Kaposis sarcoma
Kaposis sarcoma is a multi centric neoplasm consisting of multiple vascular nodules
appearing in the skin, mucous membranes and viscera. Diagnosis of Kaposis sarcoma is
based on biopsy of a suspicious lesion.
52
53
conformational charges in the enzyme that render it inactive. Two members of this class,
Nevirapine and Delavirdine are currently available for use.
Protease inhibitors
The licensure of four separate HIV-1 protease inhibitors (saquinavir, ritonavir,
indinavir and nelfinavir) heralded a major change in the options available for antiretroviral
therapy of HIV infection. Unlike reverse transcriptase inhibitors, which interfere with cellular
DNA polymerases as well as inhibiting the reverse transcriptase of HIV-1, the HIV protease
inhibitors are exquisitely selective for the protease enzyme of HIV-1.
VACCINES
Given the fact that human sexual behavior is extremely difficult to change, the best
hope for preventing the spread of HIV infection rests with the development of a safe and
effective vaccine. This task is extremely problematic for number of reasons including the
high mutability of virus.
PREVENTION:
Education, counseling and behavior modification are the corner stones of an HIV
prevention strategy. Wide spread voluntary testing of individuals who have practiced or are
practicing high-risk behavior, together with counseling of infected individuals, is
recommended. Information gathered from such an approach should serve as the basis for
behavior-modification programs, both for infected individuals who may be unaware of their
HIV status and who could infect others and for uninfected individuals practicing high-risk
behavior
54
Ojovardhini Yoga
The ingredients of Ojovardhini Yoga were properly identified. The standard
manufacturing guidelines are followed for the preparation. The combination and proportion of
Ojovardhini Yoga is as follows.
1. Amruta (Tinospora cordifolia)
2Parts
1 Part
1 Part
1 Part
1 Part
1 Part
1 Part
8. Mrutunjaya Rasa
1 Part
9. Swarnamakshika Bhasma
1 Part
55
Family
Menispermaceae
Sanskrit synonyms
Amritalata,
Amritavalli,
Bhishakpriya,
Dhira,
Madhuparni,
Pittaghni,
Guduchi,Vatsadani, Chinnaruha
Kula
Guduchyadhi Kula
Vernacular names
Hindi
Kannada
Amrutaballi
English
Tinospora
Varieties
Parts used
Description of Synonyms:
1. Vishaghna that which detoxifies
2. Vayastha helps to maintain youth
3. Jwaranashini that which cures fever
4. Bhutaghni Anti microbial
5. Jeevanthi that which re infuses life
6. AmritaThat which confers longevity, equal to ambrosia
56
The stern has been investigated by several workers and the different
compounds named tinosporin, tinosponic acid and tinosporal have been reported in the stem
(Anon, 19701. The leaves are rich in protein and fairly rich in calcium and phospherus.
Pharmacological
action:
Guduchi
is
Rasayana,
Balya,
Jwarahara,
Mutrajanana,
57
58
sheep erythrocytes by guinea pig serum by inhibiting the C3-convertase of the classical
complement pathway the compounds also gave rise to significant increase in IgG antibodies in
serum. Both humoral and cell mediated immunity were dose dependently enhanced.
Macrophage activation was reported for cordioside (TC-2) cordiofulioside A (TC-5) and cordiol
(TC-7) and this activation was more pronounced with increasing incubation times. (Kapil A et
al, Immuno potentiating compounds from Tinospora cordifolia J. ethnopharmocol, 1997; 58;
89-95)
2) In normal mice, high doses of Tinospora cordifolia significantly increased Apoptosis in bone
marrow cells. The therapeutic doses (100-200mg/kg) were devoid of such effect, however, at
the same therapeutic doses, it induced Apoptosis in malignant cells, but protected the normal
bone marrow from Apoptosis induced by cyclophospamide. This variable effect of Tinospora
cordifolia (of increasing or decreasing Apoptosis) depending on the stressor (either cancer or
cyclophosphamide) as well as the cell type (5-180 or bone marrow cells) suggests its true
potential as an adaptogen. It is of further interest to not that Tinospora cordifolia increases the
bone marrow proliferative fractions at 100 and 200 mg/kg doses thus leading to leucocytosis. If
the dose is increased Apoptosis is observed and the leucocytosis is blunted. This apparent
paradox may be due its effects both proliferations as well as induces Apoptosis depending on
the environment. It is exciting thus to hypothesis that Tinospora cordifolia may be producing
some of its effects via activation, of c-myc and inducing genotype adaptation (Proceedings of
the international workshop, CDRI, Lucknow (Dec 2-5,1997) 143).
59
Solanaceae
Sanskrit synonyms
Varahakarni , Hayagandha
Kula
kantakarikula
Vernacular names
Hindi
Asgandh
Kannada
Hiremaddu
English
Winter cherry
Varieties
Parts used
Taxonomy: Shrub growing to the height of 1-5ft. The branches are rounded in shape and
grow in all the directions. Leaves- alternate, 3-4 in length oval in shape with wide lain on it.
Inflorescence yellowish green in colored flowers will be in-group
Fruit: 2.5 to 3 diameter, round in shape when unripe green in colour on ripen become red.
Seeds:- small, yellow, kidney shaped unctuous to touch
Root: - gray externally, whitish internally look like human fingers, firm in consistency 1-11/2 ft
in length. The root smells like horse for which it is named as ashwagandha. By property, the
root stimulates the nerves, which energizes human body and it is also reason for this name.
Habitat: tunajas, maharasta rajastan, madhyapradesh, u.p himalayan mountains above 5000ft hight Distribution: Found all over India
Pharmacological Properties: shothahara, vedanastapaka, rakta shodhaka, swasahara,
vajeekara, rasayana, garbhasthapaka, shotahara, kustaghna, switraghna,
Phytochemistry: 3 withanolides Viz, withacoagin, coagulin and withasomidienone have been
isolated from plant. Withanolides and withaferin A.3B- hydroxy 2,3 dihydro withanolide F,
60
isolated from the fruits, Roots have steroidas lactones, withanolids, viz. Withaferin A 5, 2oa (R)
-dihydroxy 6a, 7a-epoxy 1 oxo- 5a-witha 2-, 24- dienolide and 2minor withanolids,
chlorogenic acid is present in leaves.
Pharmacological action:
Rasa
Guna
: Laghu, Snigdha
Veerya
: Ushana
Vipaka
: Madhura
61
62
A. Volubilis Ham;
A. fasiculatus Br;
A. dubius DG;
Family
Liliaceae
Sanskrit synonyms
Shathapadhi,
Shathamuli,
Bahusuta,
Rasona Kula
Vernacular names
Hindi
Shatavar
Kannada
Halavumakkalatai
English
Asparagus
Varieties
Shathavari:
A.
racemosus
willd.,
Description of Synonyms:
Madabhanjani antagonistic to alcohol
Mythology: Works like Rigveda, Atharvaveda etc, have mentioned the manifold action
of the drug, which is indicated by synonyms like shatavirya and dasavirya.
Pharmacological standards
Taxonomy: According to the synonyms given in the texts, the plant has several roots
(satamuli, satapadi) which are intertwined (jatamula) and with which the plant is
anchored (indivari, narayani, and satavari). These terms also indicate that it is an
efficacious tonic, acceptable to hundreds. The plant produces several tillers (bahusuta)
and minute leaves (sukshmapatra);
Habit : Extensively branched, rambling, spiny shrub;
63
64
Preparations:
1) Shatliavaryadhi churna (indicated for the purpose of vajikarana,
Shathavaryadi lehya (indicated in Rajayakshma);
2) Shathavari Gritham (indicated in kamala; amlapittha, mutrakruchra etc.)
3) Shathavaryadhi Gritham (indicated in amlapittha, rakthapitta),
4) Shathavaryadihi Tailam (indicated in vatharogas),
5) Maha Narayana taila and Narayana taila (indicated in vathaja rogas),
(Bharatha Bhaisajya Ratnakara).
Recipes:
1. In urinary bleeding, take two hundred grams of Shatavari roots and one tablespoon of
Jeeraka.
Crush the roots, extract juice and add it to the powdered Jeeraka.
This
mixture is taken early in the morning on an empty stomach for seven days. 2. To cure
heavy bleeding - crush fifty grams of Shatavari roots with ten grams of Jeeraka powder
and put in a vessel with one It. of water. Boil it till the quantity reduces to two glassful.
One cup is taken twice a day for seven days. 3. Extract the juice from quarter kg of
Shatavari root and five grams of jeeraka. Add one cup of milk and take for seven days
in fever. 4. A preparation called peya is prepared by adding sugar and milk to the
extracted juice. This is given in body pain and weakness. 5. Boiled leaves smeared with
ghee are applied to boils, small pox, etc. 6. Fresh root juice given with honey is used as
a demulcent. (B.P.N.).
Dosage:
Churna 1 2 tolas Anupana Milk, Honey.
Research Updates
1) This plant produces leucocytosis with predominant neutrophilia and prevented to
varying degrees, the leucopenia, induced by cyclophosphemide. They were found to
activate the polymorphonuclear and monocyte macrophage systems. Only those
65
66
Azadirikhta indica
Family
Meliaceae
Sanskrit synonyms
Nimba, Vembaka
Kula
Guduchyadi kula
Vernacular names
Hindi
Nim or Nimb
Kannada
Bevu, Kahibevu
English
Varieties
Parts used
Description of Synonyms:
Pichumarda that which cures diseases
Puyari which drains out the pus
Arista which prevent diseases
Taxonomy: a lofty and fascinating tree, bearing small, white scented flowers.
Fruit: small yellowish green fruits.
Distribution: All over India
Pharmacological Properties:
Rasa Katu, Tiktha
Guna Laghu, Rooksha
Veerya Ushna
Vipaka Katu
67
68
Preparations:
Nimbadi churna
Nimbamritadi churna
Katunimba taila
Panchanimbadi vati
Panchatikta ghrita
Recipes:
) The root bark and young fruits are used as an alternative, antiperiodic and as
a tonic.
) Green twigs are used as toothbrushes for cleaning teeth and as a
prophylactic for mouth and teeth complaints.
) The bark is used as a bitter tonic, astringent, antiperiodic, antipyretic and
against nausea and vomiting.
) Gum is demulcent tonic in catarrhal affections.
) Leaves are used as poultice for boils. Decoction of leaves used as an
antiseptic in ulcers and eczema.
) Dry flowers are stomachic. Seed oil is a stimulant, antiseptic, alterative in
rheumatism and skin diseases (Indian pharmacopoeia)
) Berries are purgative, emollient and anthelmintic.
) An extract of leaves is used in toothpastes. Neem oil is effective in the
treatment of leprosy and skin diseases.
Dosage:
Research Updates
1) Oral treatment with leaf extract of Azadirachta indica reversed the inhibitory effect of
restraint stress on formation of anti-sheep RBC antibody titers in rats immunized with
69
sheep RBC and also the increased in foot pad thickness. It reversed the DDT
induced suppression of antibody response and leukocyte migration inhibition in
tetanus toxoid immunized rats. Restrain stress along with administration of DDT in
sub threshold doses resulted in an inhibition of the immune response. A. indica,
attenuated the immunotoxicity of environmental and xenobiotic stressors. Ref; Ray A
et al.
2) Influence of neem leaf extract on the immunotoxicity of stress and xenobiotics in
experimental animals. Indian J. pharmacology, 1997; 18; 82-4,
3) An experimental and clinical evaluation of immuno modulating potential of
Azadirachta indica extract. Indian J. cli. Pharm. Ther. 1997; 18; 82-4,
4) Azadirachta indica also induced cell-mediated response as seen from the
enhancement of macrophage migration inhibition and footpad thickness. Ref; Ray A.
et al modulation of humoral and cell mediated. Immune responses by Azadirachta
indica in mice. Indian J. Exp. Biol. 1996;34;698-701
5) The ethanolic extract of Azadirachta indica leaves demonstrated much more
significant anti dermatophytic activity as compared to the aqueous extract, when
tested in vitro, against 88 clinical isolates of dermatophytes using the agar dilution
technique. The MIC 90 of ethnotic extract was 100ug/ml where as that of aqueous
extract was 500ug / ml Ref; Venugopal P.V; Anti-dermatophytic activity of neem
leaves, in vitro. Indian J. Pharmacology, 1994; 26; 141-3
70
Family
Euphorbiaceae
Sanskrit synonyms
Bhumyamalakika,
bhauphala,
shiva,
bahuveerya,
tamlaki,
ajata,
bahupatra,
bhudatri,
jata
Vernacular names
Hindi
Bhuamia
Kannada
Nelanelli
Varieties
Parts used
whole plant
Description of Synonyms:
Vishaghni that which detoxifies
Pharmacological standards: Water solubility 16.8%; 2. Moisture 1.5%; 3. pH- 5.69
Taxonomy: The synonym indicate, Bahupatra- having many small leaves, bahuphalamany fruits .The term bahuvirya indicates the several potencies of the drug. Habit- herb
flowering season Jan-Jul; Sept-Oct; colour of the flower-greenish yellow. Fruit
capsule. Distribution found wild in all the zones of central and south India.
Pharmacological Properties:
Rasa Kashaya, Amla, Tiktha
Guna Laghu,
Veerya- Sheetha
Vipaka Katu;
Prabhava vishagna and kshayagna
71
72
Preparations:
Bhumyamalaki lepa,
Chyavanaprasha
Recipes:
1. The kwatha of whole plant is given in malaria and jaundice
2. The tender stem's phanta is given in Jaundice.
3. The poultice mode out of Phyllanthus with rice washed water is applied on wounds.
4. A poultice of the leaves mixed with salt cures, itch and other skin affections.
Dosage: Swarasa - 2-3tola, Churiia 3-6 masha with Anupana: Rice water, Honey,
Research Updates
1) Recently, in an in vitro study, the extract of Phyllanthus amarus was incubated with
the Alexander cell line, a human hepato celluler carcinoma derived cell line which has
the property of secreting the hepatitis B surface antigen (HbsAg) in the supernatant. The
results demonstrated that Phyllanthus amarus was effective in inhibiting the secretion of
HbsAg for 48 hours thus proving its anti Heptitis B virus property at the cellular level. Ref
; Jayaram S. et al Inhibition of HbsAg secretion from Alexander cell line by Phyllanthus
amarus. Indian J. Pathal. Microbiol. 1996; 39; 211-5
2) Preparation of the whole plant of Phyllanthus amarus was administered to 9 mild
hyper tensive subjects for 10 days. The results suggest that it is a potential diuretic,
hypotensive and hypoglycaemic drug for human beings. Ref; Srividya N. periwal s.
Diuretic, hypotensive and hypoglycaemic effect Phyllanthus amarus Indian J. Exp. Bio.
1995; 33; 861-4
73
G. glandulifera
Family
Leguminasae (papilionaeeae)
Sanskrit synonyms
Madhuyashti, Kleetaka
Kula
Shimbi Kula
Vernacular names
Hindi
Mulethi
Kannada
Jesthamadhu, athimadhura
English
Licorice
Varieties
Parts used
Root (rhizome)
Description of Synonyms:
Kleethakam - that which removes impotency (Amarakosh)
Taxonomy: G. glabra is an erect perennial shrub, growing to a height of about 4 feet. Its
principal root doesnt generally grow deep but gives of number of tuberous secondary
roots. Which may reach a length of 4 feet or more. The short stem consists of an erect
stem with a limited number of strong herbaceous branches, which bear alternate oddpinnate leaves with five to seven pairs of ovate oblong, pale greenish leaflets. The
flowers are medium sized, sessile, purplish bluish. Fruits and flattened oblong to linear
glandular pools, of to 1-inch length containing several kidneys shaped buds.
The drug sold in Indian bazaar is the cut pieces of rhizomes, which are dry, tough,
woody, fibrous in nature, grayish yellow in colour. These pieces break easily with a
fracture, which is fibrous in the bark, and splintery in the wood, drug has a characteristic
odour and feebly nourishing sweetish taste.
74
Habitat: Southern Europe, Arab, Iran, and Turkistan, Afghanistan, In India it is grown in
Punjab, Sindh and Peshawar and Kashmir.
Pharmacological Properties: It is cooling in nature. Beneficial for improving strength
and complexion improves voice, anti inflammatory in action. Root is also used in
scorpion sting.
Phytochemistry: It has a chemical glycyrrhizin in the form of glycyrrhizic acid. It is
sweeter than sugar. It also has a glycoside isoliquiritin, which gets converted into
liquiritin, on exposure of atmosphere. Starch: 27.4%, ash 6.3%, For total extraction
petrol ether 1.3%, ether 4.3%, alcohol 21.7%, chloroform 4.5% and water 24.2% It has
iron, manganese, calcium potassium and sodium and trace elements. Glycosides
saponins, Feavonoids -iquiritin, Coumari derivative-Herniarin
Pharmacological action:
Rasa
: Madhura
Guna
: guru, Snigdha
Veerya
: Sheeta
Vipaka
: Madhura
75
Research Updates
1) Glycyrrhizin, a triterpenoid glycoside obtained from Glycyrrhiza glabra (yasti) was
tested against RNA viruses like the Chandripura virus, Measles virus, Polio virus /
type 1 2 &3 polio wild type viruses 1, 2 & 3, as well as DNA viruses like Herpes type
1 & 2 viruses in vitro. It inhibited the DNA virus plaque formation at lower
concentration (0.608mM) while the RNA viruses were inhibited at higher
concentration (1.216mM) Ref; Badam L.
2) In vitro studies on the effect of Glycyrrhizin, from Indian G.glabra in some RNA and
DNA viruses, Indian J. of pharmacology 1994; 26:194-99.
76
Family
Compositae (Asteraceae)
Sanskrit synonyms
Markava,
Bhringa,
Angaraka,
Kesharaja,
Vernacular names
Hindi
Bagara
Kannada
Garaga
Varieties
1. Svetha Bhringharaja,
2. Peetha Bhringharaja
3. Nila Bhringharaja
Parts used
Whole Plant
Description of Synonyms:
Nagamaram which kills snakes / in all forms of Visha it can be used as vishaghna
Pharmacological standards: Moisture content - 17.5%, Water solubility - 17.6%, pH 6.48 %
Taxonomy: This is one of the ten auspicious herbs that constitute the group
Dhashapushpam (ten flowers) which is considered to destroy the causative factors of all
unhealthy and unpleasant diseases. The words Bhringharaia, Kesharanjana, Bhringha,
etc., signify its profound action promoting hair growth and its natural colour. Two words
Angharakha signify its efficacy of stimulating liver and gastric functions.
Habit - Branched Herb; Flowering - July, Sep - Feb.; Colour of the Flower - White; Fruit
- Cypsella.
Distribution: common weed of moist places
77
Pharmacological Properties:
Rasa katu, tikta
Guna laghu, rooksha
Veerya ushna
Vipaka katu
Pharmacological action: Rasayana, krimighna, varnya, kustahara, shotahara, keshya,
yakruthuttejaka, dipana, pachana, sramsana, swasahara, panduhara, danthya, balya,
nethrasirorogahara, medhya. Anthelmentic, gastric stimulant, digestive, tonic, promotes
hair growth, promotes colour and complexion of skin, beneficial to eyesight.
possesses
specific
pharmacological
action
in
liver
disorder,
anemia,
It
cough,
indications:
Kushta,
kasa,
swasa,
pandu,
krimiroga,
netraroga,
78
Mrutunjaya Rasa72
Ingredients
Shudha vatsanabha
1 part
Maricha
1part
Pippali
1part
Shudha gandha
1part
Shudha tankana
1part
Shudha hingula
2parts
Preparation: Vatsanasha is kept in gomootra for 3 days and should be dried under sun
light on 4th day hingula should be given bhavana with jambeena rasa. All the drugs are
made in to sookshma churna and given bhawana with nimbu swarasa and a paste is
prepared. Tablets of one green gram size or of 125mg weight are to are prepared out of
this, are dried in shade and preserved in air tight containers.
Properties: It is told if this drug is used with different anupana, it can cure all types of
diseases i.e. infections diseases. For all types of fevers, if taken with honey it cures the
fever, in sannipata jwara it is taken with ardraka swarasa. In ajeerna jwara it should be
taken with jambeera rasa. In vishama jwara, it should be taken with jeeraka churna and
guda. In a young man with chronic fever, it should be given in full dose i.e. 4 tablets per
dose. In children and weak persons and in old age only 1 tablet should be given. In a
strong person with vata pittaja jwara where in there is no kapha prabhava, and for the
patients with burning sensation ( daha) sugar should be given as anupana, along with
tender coconut water.
79
The globule
remaining after heating is Magnetic. The mineral is dissolved if treated with Nitric acid.
'Pyrite' in some of its forms, resembles gold so closely, that it is often known as
fools' gold. 'Chalcopyrite' is scratched readily with a knife blade or a foil while pyrite
resists both, as pyrite contains no copper.
Physical Properties: Makshika are said to be niskonas as (having no angles), guru
(heavy), Suvarna Varna (bright yellow colour with slight bluish tinge) Snigdha (oily),
when rubbed on nikasa- produce golden lining but if rubbed on hand produce blackish
colour over the hand. On fracture it seems to be golden in colour. Soft, brittle and could
be cut with a knife. On extraction it yields satwa like copper in colour. Colour of Bhasma
is Red which resembles sindoora.
80
- Tikta, Madhura
Guna
- Seeta, laghu
Virya
- Sheeta
Vipaka - Katu
Karma : Balya, Yogavahi, Rasayana, Paramavrishya, Chakshushya,
Sakalamayaghna, Rasendraprana, Gunottara, Durmala,
Doshaprabhava:
Vyadhiprabhava:
Krimi,Visha,
Udara,
Sotha,
Kandu,
Mandgni.
Kamala,
shosa,
81
3. Copper is an essential nutrient for optimal function of the immune system; deficiency
results in impairment of both humoral and cell-mediated components. Copper
deficiency in rodents results in decreased numbers of CD4+ (helper) and total T
cells. This defect has been traced to impaired production of interleukin-2, a cytokine
essential for T-cell division and differentiation. Impairment of quiescent cell
proliferation is reversed by both in vivo and in vitro copper supplementation. O'Dell
BL. Interleukin-2 production is altered by copper deficiency. Nutr Rev 1993
Oct;51(10):307-9 Department of Biochemistry, University of Missouri, Columbia
65211.
4. These data indicate that a decline in copper status decreases IL-2 production by
activated human T-cells due to reduced synthesis and/or stability of IL-2 mRNA.
Hopkins RG, Failla ML. Copper deficiency reduces interleukin-2 (IL-2) production
and IL-2 mRNA in human T-lymphocytes. J Nutr 1997 Feb; 127(2): 257-62
Department of Food, Nutrition & Food Service Management, The University of North
Carolina Greensboro, 27412-5001, USA.
5. The immune system requires copper to perform several functions, of which little is
known about the direct mechanism of action. Animal models and cells in culture have
been used to assess copper's role in the immune response. Some of the recent
research showed that interleukin 2 is reduced in copper deficiency and is likely the
mechanism by which T cell proliferation is reduced. Percival SS. Copper and
immunity. Am J Clin Nutr 1998 May;67(5 Suppl):1064S-1068S Food Science and
Human Nutrition Department, University of Florida, Gainesville 32611, USA.
82
Nimba
(Melia
azadirikhta),
Bhumyamalaki
(Phyllanthus
niruri),
83
Mrithyunjaya Rasa was taken to potentiate these properties and for faster action of
the drug as it is one of the best jwara hara drugs. It was taken for its ama pachaka
property, as there is involvement of Ama in the pathogenesis.
Even though there is no reference of Ojovardhini yoga in classical text a rational
combination was made taking the individual properties of the ingredients into
consideration. Care was taken not to include drugs having antagonist properties.
Criteria for quantity of drugs; the standard therapeutic doses of each drug was taken
into consideration and 500mg capsule was made with two parts of Amrita and one part
each of other drugs. Amrita was taken in 2 parts because it has rasayana, krimigna and
jwarahara properties.
Preparation of Ojovardhini yoga; As HIV infection is a grave condition care was taken
to prepare the drug with good manufacturing practices (GMP). For this purpose the drug
was prepared at M/s Om pharmaceuticals, Bangalore which is an ISO 9001 certified
unit.
Steps followed in the preparation of Ojovardhini yoga
METHOD OF IMM-011 CAPSULE PREPARATION
SR.NO.
1
Mrutyanjay Ras
INGREDIENTS
QTY./CAP
50 mg
Suvrnamakshik Bhasma
50 mg
Ashwagandha
50 mg
Shatavari
50 mg
Nimba
50 mg
Bhuiamalki
50 mg
Yasti madhu
50 mg
Bhringraj
50 mg
Amruta
100 mg
Total
84
500 mg
STEPS :
1. All herbal materials are cleaned. All the inputs including empty Gelatin Capsules and
packing materials are QA approved.
2. Ingredients are weighed as per required batch quantity
3. Herbal material (c ,e & f) are crushed to fine powder and triturated with (a), (b) & (d)
with sufficient quantity of water.
4. Other Herbal materials 3 to 9 also disintegrated to coarse powder and divided in two
lots (a) for Churna (b) for Extraction.
5. Churna, item No: 2 along with material from step 3 are triturated well with aqua
extract 4 (b) to get homogeneous paste.
6. The bulk is dried, pulverized and passed through 80-mesh shifter to get granules and
mixed well.
7. It is sampled for QA check for moisture (Moisture NMT 5%).
8. After QA approval the total quantity of granules are filled equally in empty Gelatin
Capsule (Size 0) as per batch size.
The process of Capsule filling conducted in dehumidified and air-conditioned room.
Weight variation is checked at an interval of hrs (NMT 10 %)
9. After final compliance with QA parameters i.e. weight variation and moisture %, the
Capsules are packed in 60 ml HDPE containers, 60 Capsules per pack and heat
sealed with Aluminum circles.
Analytical test and standardization
This drug was coded as IMM-011 and sent to Sri Dhootapapeshwar Research
Foundation Mumbai for analytical test, acute toxicity test and drug standardization.
Reports of said tests are given below.
85
ANALYTICAL REPORT -1
Report No:
BGL/H-115/01-02
IMM011
Batch No:
IMM011/Lot1
Date:
21/01/2002
Description
Ash Content:
18.52 %
4.81 %
Water-soluble extractive:
21.22 %
6.670 %
Average Weight:
0.5539gm
Disintegration Time:
17 minutes
Elemental Assay
TLC Report:
ANALYTICAL REPORT -2
Report No:
BGL/H-115/01-02
IMM011
Batch No.
IMM011/Lot2
Date:
21/01/2002
Description:
Ash Content:
22.79 %
5.62 %
0.5308gm
Disintegration Time:
19 minutes
Elemental Assay
TLC Report:
86
Report No. 28 B
Date: 21/l/2002
IMM011
RMN
-----
Batch No
Lot No. I
Date of manufacture
30.06.2001
Duration of Study
48 hrs.
Mice
Dose
Route of administration:
Oral
Observation
Mortality
No mortality
observed.
Conclusion
The product IMM - 011 (mfg-. date. 30. 06. 2001 was found
non-toxic in mice when single dose 13 mg / 20 gms (10 X
T.D.) body wt. was administered orally.
Acute toxicity study -2
IMM011
----
30.10.2001
Duration of Study
48 hrs.
Mice
Dose
Route of administration
Oral
Observation
---
Mortality
No mortality
observed.
Conclusion:
2001 was found non-toxic in mice when single dose 13 mg / 20 gms (10 X T.D.) body wt.
was administered orally.
87
Concentration in ppm
Absorbance
Std.1
0
0
Std. 2
100
0.1105
Std . 3
150
0.1707
Std.4
200
0.2276
IMM lot 1
56.8354*
0.063
IMM lot 2
57.1569*
0.0633
* Value of Mercury per capsule is calculated from the above result taking weight
of the sample taken and dilution factor
88
Methods:
Objective of the study;
1. To evaluate the efficacy of Ojovardhini Yoga in improving the clinical status of
Ojokshaya with special reference to HIV infection
2. To assess the role Ojovardhini Yoga on CD4 cell count, which is the marker of
stages of the HIV infection
Research design: As this disease is a grave condition and of high mortality rate and
there is no clinical evidence available for this particular yoga a prospective open clinical
trial was conducted. All the patients received the same medicine. Even though a total of
55 patients were screened during this period, 15 patients were taken for the study. A
detailed Proforma was prepared for case taking.
Inclusion criteria
1. The patients with the HIV infection diagnosed by serological test and Western blot
method will be taken in the study.
2. CD4 count ranging from 200 to 500/cu.mm.
3. Karnofsky Performance score 60 and above.
4. The patients are selected irrespective of Sex and race based on the clinical signs &
symptoms other than that of exclusive criteria,
Exclusion criteria
1. Patients below the age of 20 years and above the age of 50 years, pregnant and
lactating women will be excluded from the study.
2. The patients having diabetes mellitus and other systemic diseases will be excluded
and the patients with concomitant therapy will be excluded.
Criteria for considering for dropouts
1. Inability to attend two successive follow-ups
2. Discontinuation of medication for more than five days
89
90 days
Posology: Two capsules of 500mg each three times daily after food with hot water.
All the patients were asked to attend the OPD for weekly follow-up and medicine
was provided every week. Patients were checked for opportunistic infection, change in
the weight and counseled accordingly.
Laboratory investigation: All the patients were screened for HIV infection by using
ELISA method. For the assessment of HIV status all the patients were investigated, for
CD4 cell count. Other investigations conducted are hemoglobin percent, total count
differential count, erythrocyte sedimentation rate, and random blood sugar, total
lymphocyte count, total platelet count. CD4 cell count assay is inclusive of CD8 cell
count also. All the investigations are repeated after three months of trial medication.
Those patients who had respiratory symptoms were investigated radiologically.
1. The patients are included in the study after obtaining the informed consent.
2. The identity of all the patients are kept confidentially.
3. Special counseling sessions were held for each patients and couples before and
after serological investigations and during the course of treatment.
Special instruction/advice given to patients
1. To stop smoking, alcohol and other habits
2. Not to indulge in strenuous exercise
3. Not to take any other medication except the trial medication.
90
Score range
Best responded
8 to 10
Moderately responded
5 to 7
Mildly improvement
2 to 4
0 and 1
91
S. No
Master chart - 1
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Sex
M
+
+
+
+
+
+
Age
F
+
+
+
+
+
+
+
+
+
11
04
27
50
30
26
40
30
31
26
21
28
26
22
21
30
42
H
+
+
+
Religion
Mu
C
+
+
+
+
+
+
+
+
+
+
+
+
12
03
00
00
Demography chart
Diet
Occupation
V
Mx
1
2
3
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
00
15
Economical status
E1
E2
E3
E4
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
6
00
G. Distribution
G1
G2
G3
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
00
92
S. No
Master chart - 2
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Chief complaints
1
B
+
+
2
A
+
+
+
+
+
+
B
+
+
+
+
+
+
+
+
3
A
+
+
+
+
+
+
10
+
+
+
13
B
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
15
4
A
+
B
+
+
+
5
A
+
+
+
+
+
B
+
+
+
+
+
+
+
6
A
+
B
+
+
+
+
+
+
+
+
+
+
+
+
4
+
+
+
9
+
9
11
1= loss of Appetite; 2 = loss of weight; 3 = fatigue; 4 = Diarrhea; 5 = pruritis / skin eruptions; 6 = Fever
93
S. No
Master chart - 3
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
A1
B
A2
A
+
+
+
+
+
+
+
+
0
0
0
0
0
8
A3
A
B
+
+
A4
A
A5
A
B
+
A6
B A
+
+
Associated complaints
A7
A8
A9
B A B A B A
+
A10
B A
A11
B A
+
A12
B A
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
A15
B A
+
+
+
+
+
+
+
+
+
0
+
+
+
+
+
+
+
+
+
+
+
+
A14
B A
+
+
+
+
+
A13
B A
+
+
A1 = Nausea/Vomiting; A2 = Oral thrust; A3 = Pain Abdomen; A4 = Dyspepsia; A5 = Abdomen Distention; A6 = Giddiness; A7 = Palpitation;
A8 = Bleeding Gums; A9 = Headache, A10 = Cough, A11 = Chest pain,
A12 = Urethral discharge, A13 = Burning micturation; A14 = breathlessness; A15 =drowsiness
94
S. No
Master chart - 4
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
1
B
+
+
+
+
+
+
+
+
+
+
2
A
B
+
+
+
+
+
+
+
3
A
+
+
+
+
+
+
+
B
+
+
+
+
+
+
+
+
+
+
+
+
12
12
11
+
+
+
+
+
9
A
10
A
V1
A
V5
B
+
+
+
+
+
+
+
+
+
+
+
+
+
8
B
+
+
+
+
0
14
+
+
+
1
95
S. No
Master chart - 5
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
1
B
2
A
5
B
6
A
P1
A
B
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
12
+
+
+
+
+
1) Peetamootra 2) Peetanetra 3) Peetavit 4) Peeta twak 5) Atikshudha 6) Atidaha P1) Mandagni P2) Shareera sheetatwam P3) Prabhahani
96
S. No
Master chart - 6
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
1
B
2
A
3
A
4
A
8
B
9
A
10
A
K1
A
B
+
+
1) Agnisadana 2) Praseka 3) Alasya 4) Gowrava 5) Swetangata 6) Sheetangata 7) Shlathangata 8) Swasa 9) Kasa 10)Atinidra
K1) Bhrama K2) Urah shoonyata K3) Shira shoonyata K4) Hriddrava K5) Sandhi saithilya
97
A
+
S. No
Master chart - 7
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
J1
B
+
+
+
+
+
+
+
+
+
+
+
+
+
+
14
A
+
Ojo Vishramsa
J2
J3
B
A
B
A
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
14
J4
B
+
+
+
+
+
+
+
+
+
+
+
1
A
2
A
3
A
Ojo Vyapat
4
5
A
B
A
B
A
+
+
+
+
+
+
+
+
+
+
+
+
+
+
12
+
+
+
+
12
+
+
+
+
6
B
+
+
+
+
+
B
+
+
A
+
+
+
+
+
3
J1) Gatra sadanam J2) Dosha chyavanam J3) Sandhi vislesha J4) Kriya sannirodha
1) Stabdha gatrata 2) Guru gatrata 3) Vata shopha 4) Varna hani 5) Glani 6) Tandra 7) Anidra
98
7
A
S. No
Master chart - 8
OPD
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
1
B
+
+
+
+
+
+
+
+
+
2
A
B
+
+
+
+
+
+
+
+
+
+
3
A
+
+
B
+
+
+
+
+
+
+
+
+
+
+
10
+
+
12
+
+
9
4
A
+
+
+
+
+
12
B
+
+
+
+
+
+
+
Ojo Kshaya
6
7
B
A
B
A
+
+
+
+
+
+
+
+
9
+
+
+
+
+
+
+
+
+
+
+
14
8
B
9
A
10
A
11
A
+
+
+
+
+
+
+
99
B
+
+
+
+
+
+
+
+
+
+
+
+
+
+
14
12
A
+
+
+
+
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Master chart - 9
Master chart - 10
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Hb% Before
10.4
10.8
9.8
14.8
12.4
12.8
10.5
10.8
10.5
11.2
11.5
10.8
14.4
13.8
13.5
178
Hb% After
11.4
11.8
8.0
13.8
12.8
13.2
12.0
11.0
8.9
10.0
16.8
11.0
15.1
11.8
11.6
179.2
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Difference
1.0
1.0
- 1.8
- 1.0
0.4
0.4
1.5
0.2
- 1.6
- 1.2
5.3
0.2
0.7
- 2.0
1.9
100
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
ESR Before
50
64
44
24
20
30
46
64
44
25
24
42
8
30
22
537
ESR After
46
64
50
08
38
46
60
54
48
64
34
52
12
62
42
680
Difference
-4
0
6
- 16
18
16
14
-10
4
39
10
10
4
32
20
Master chart 12
Master chart - 11
Chart depicting the changes in Total Lymphocyte Count
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
TLC Before
5000
2100
1300
1566
2016
1650
1400
1800
2450
1880
3800
1900
2552
2300
1700
33414
TLC After
2100
2100
1800
1900
2300
2100
1100
2500
1800
2300
1400
1200
2150
1200
3400
29350
Difference
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
- 2900
0
500
334
284
450
- 300
700
- 650
420
- 2400
- 700
- 402
- 1100
1700
101
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
WBC Before
7100
8200
6500
5400
6200
5500
5800
5700
6800
13400
8700
5900
8100
7900
6200
107400
WBC After
8100
5600
5400
6900
7200
5600
5100
6800
5800
5900
8400
5400
8800
4700
7900
97600
Difference
1000
- 2600
-1100
1500
1000
100
- 600
1100
- 1000
- 7500
- 300
- 500
700
- 3200
1700
Master chart 13
Master chart - 14
S. No
OPD No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Platelet
count Before
2.85
1.8
1.9
1.7
2.8
2.1
2.1
2.1
2.4
2.1
2.8
1.9
2.3
1.6
1.3
31.75
Platelet
count After
2.1
1.2
1.1
1.8
1.3
2.6
2.0
1.6
1.0
3.3
2.3
1.5
2.95
1.72
2.30
28.77
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Difference
- 0.75
- 0.60
-0.80
0.10
-1.50
0.50
- 0.10
- 0.50
- 1.40
1.20
- 0.50
- 0.40
0.65
0.12
1.0
102
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Before
50
57
51
60
53
50
35
52
36
53
65
47
80
63
58
810
After
54
55
54
62
58
54
38
55
38
55
68
46
80
64
59
840
Difference
4
-2
3
2
5
4
3
3
2
2
3
-1
0
1
1
Master chart 16
Master chart - 15
Chart depicting the changes
in Karnofsky performance score
S. No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Before
70
60
70
80
70
70
60
80
80
60
70
90
90
80
80
1110
After
100
80
100
100
100
90
90
100
90
90
100
90
100
90
100
1420
Difference
30
20
30
20
30
20
30
20
10
30
30
0
10
10
20
103
OPD No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
Before
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
After
3
1
3
3
3
2
2
3
2
3
3
3
2
2
3
38
Master chart 17
530
410
410
520
620
410
350
580
410
430
400
430
418
340
560
6818
- 120
- 100
30
10
70
50
- 25
150
- 60
50
- 60
10
- 220
- 190
180
104
- 2060
100
320
224
- 486
- 250
- 185
- 300
- 395
50
- 1620
- 470
62
570
1000
difference
After
940
1060
850
810
980
1060
420
1170
850
980
580
410
1695
500
1820
14125
3000
960
530
586
1466
1290
605
1470
1245
930
2200
880
1633
1070
820
18685
Difference
After
650
510
380
510
550
360
375
430
470
380
460
420
638
530
380
7043
Before
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
difference
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
OPD
No
Before
S.
No
0.22
0.56
0.71
0.50
0.40
0.30
0.60
0.30
0.40
0.43
0.20
0.51
0.39
0.50
0.48
6.5
0.48
0.38
0.50
0.64
0.63
0.38
0.83
0.47
0.48
0.44
0.68
1.00
0.25
0.68
0.30
8.14
0.26
- 0.18
- 0.21
- 0.14
0.23
0.08
0.23
0.17
0.08
0.01
0.48
0.49
- 0.14
0.18
-0.18
55
47
Excluded
27
Initially included
23
Early dropout
Withdrawals
15
Each and every data pertaining to every patient was recorded in a well-designed case taking
Proforma. The final data is divided into 3 sections for better analysis and convenience of
observation
1. Data related to demography
2. Data related to disease
3. Data related to response to Ojovardhini yoga.
105
Number of
patients
03
08
01
01
01
01
15
Percentage
Sex
20.03
53.33
6.66
6.66
6.66
6.66
100
Male
Female
TOTAL
Number of
patients
11
04
15
Percentage
73.4
26.6
100
4 1 to 4 5
7%
4 6 to 5 0
7%
Female
27%
2 1 to 2 5
20%
3 6 to 4 0
7%
3 1 to 3 5
7%
Male
73%
2 6 to 3 0
52%
106
Religion
Number of
patients
12
03
00
00
15
Hindu
Muslim
Christian
Others
Total
Percentage
Economic status
80
20
00
00
100
Poor
Middle Class
Higher middle class
Higher class
Total
Percentage
40
60
00
00
100
to middle class.
Christian
0%
Number of
patients
06
09
00
00
15
Higher middle
Higher class
class
0%
0%
Poor
Middle Class
40%
60%
Others
0%
M uslim
20%
Hindu
80%
107
Number of
patients
07
03
05
15
Occupation
Percentage
Labour
Business
Transport field
Sedentary
Total
46.66
20.0
33.33
100
Number of
patients
11
01
02
01
15
Percentage
73.33
6.67
13.33
6.67
100
(6.67%) is housewife.
Sedentary
6.67%
Rural
33%
Transport
field
13.33%
Urban
47%
Business
6.67%
SubUrban
20%
108
Labour
73.33%
Number of
patients
00
15
15
Vegetarian
Mixed diet
Total
Source
Homosexuality
Heterosexuality
Blood transfusion
Intravenous Drug user
Total
Percentage
00
100
100
Number of patients
0
15
0
0
15
Out of 15patients it was interesting to note that all the patients got
the infection from heterosexual contact. All the men (11 Patients)
got the infection extra marital sex and women got it from their
husband. In this study four couple were enrolled.
15
Mixed diet
Vegetarian
10
12
Percentage
0
100
0
0
100
14
Number of Patients
16
Number of Patients
109
Number of patients
10
13
15
09
11
11
08
02
11
07
08
04
02
01
03
Percentage
66.66
86.66
100
60
73.33
73.33
53.33
13.33
73.33
46.66
53.33
26.66
13.33
6.66
20
16
Fatigue
14
Skin eruptions
12
Loss of
appetite
Fever
Giddiness
10
Nausea /
Vomiting
8
Headache
Chest pain
Urethral
discharge
Burning
micturation
2
0
Loss of weight
110
Diarrhoea
Oral thrush
Cough
Bleeding gums
Dosha status
Duration
More than 1year
More than 3 years
More than 5 years
Total
Number of patients
4
6
5
15
Percentage
26.66
40.00
33.33
100
Number of
patients
1
Percentage
14
93.33
6.66
In this study all the patients reported after a minimum of one year
patients had the sannipatika lakshana and none of the Dosha was
earlier than 1 year, 6 (40%) got earlier than 3 years and 5 (33.33%)
vriddhi Kapha kshaya and Pitta kshaya lakshanas. Only one had
Vata kshaya Kapha vriddhi and Pitta vriddhi lakshanas.
15
10
5
Number of Patients
111
K K VVPK
K K VVPV
Number of patients
8
2
9
10
3
9
Nidana
Kopa
Shoka
Chinta
Bhaya
Percentage
53.33
13.33
60.0
66.66
20
60.0
Number of patients
10
8
7
6
Percentage
66.66
53.33
46.66
40.0
Bhaya
Kopa
Shoka
Chinta
Bhaya
Ativyayama
Prajagara
Chinta
Vatatapasevana
Alpashana
Ativyavaya
Shoka
Anashana
Nidana
Anashana
Vatatapasevana
Ativyayama
Ativyavaya
Prajagara
10
Alpashana
Kopa
Number of patients
112
10
12
Number of patients
15
12
0
Stage
Percentage
100
80
0
Number of
patients
6
9
0
15
Percentage
16
Advanced
CD4 < 200
0%
14
12
10
8
6
4
Early
symptomatic
CD4 < 500
>200
60%
2
0
Ojovishramsha
Ojovyapat
40
60.0
0
100
Ojojshaya
113
Clinical
latency CD4
> 500
40%
Number of
patients
Before
After
0
0
14
1
1
5
0
9
15
15
Percentage
Before
0
93.33
6.66
0
100
After
0
6.66
33.33
60
100
Before
After
Before
After
3
5
5
2
15
0
0
1
14
15
20
33.33
33.33
13.33
100
0
0
6.66
93.33
100
14
14
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
12
10
8
6
4
2
0
0
Before
0
Before
After
114
After
Table 18
Table depicting impact of Ojovardhini yoga - Dosha status
Dosha status
Number of patients
Percentage
Before
After
Before
After
6.66
14
93.33
6.66
40
Kapha Kshaya
26.66
26.66
Total
15
15
100
100
It was interesting to note that out of 15 patients who had sannipatika Dosha Lakshanas,
4 (26.66%) got relieved of all the symptoms 6(40%) had only Kapha khaya and Vata Vriddhi
and 4 had only Kapha Kshaya Lakshanas, and 1 (6.6%) still had sannipatika Lakshana.
Table 19
Table depicting impact of Ojovardhini yoga - Ojas status
Ojas status
Ojovishramsha
15
Ojovyapat
12
Ojokshaya
115
Table 20
Table depicting impact of Ojovardhini yoga - Body Weight
Grade
Weight
Percentage
Before
After
Before
After
6.66
Grade-0
Grade-1
33.33
13.33
Grade-2
11
53.33
73.33
Grade-4
6.66
13.33
It is interesting to note that maximum patients improved from lower grades to upper grades
following the treatment.
Table 21
Table depicting impact on Investigative parameters
Parameter
Result
Number of patients
Percentage
TLC
RESPONDED
53.33
NOT RESPONDED
46.66
RESPONDED
40.0
NOT RESPONDED
60.0
RESPONDED
53.33
NOT RESPONDED
46.66
RESPONDED
33.33
NOT RESPONDED
10
66.66
RESPONDED
10
66.66
NOT RESPONDED
33.33
RESPONDED
20.0
NOT RESPONDED
12
80.0
TPC
CD4
CD4:CD8
Hb%
E.S.R.
116
Table 22
Table depicting Over all assessment of the response to Ojovardhini yoga
Based on Assessment criteria
S.
No
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
OPD
No
615
908
942
943
954
978
1006
1008
1009
1119
1105
1177
1192
1251
1094
Total
K.P.S
G.H.C
Weight
CD4
CD8
CD4:CD8
T.L.C
T.P.C
T.W.C
E.S.R
Score
Result
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
1
1
1
1
1
1
1
1
1
0
1
1
1
0
0
1
1
1
1
0
1
0
1
0
1
0
0
1
1
0
0
0
1
1
1
1
1
0
1
1
0
0
0
1
0
0
0
1
1
1
1
1
1
1
1
0
1
0
0
0
1
1
1
1
0
1
0
1
0
0
0
0
1
0
0
0
1
0
1
0
0
0
1
0
0
1
1
1
1
0
0
1
1
1
0
0
0
0
0
0
1
0
1
1
0
0
1
0
0
0
1
0
0
0
0
0
0
0
7
2
5
8
8
9
5
8
5
7
5
5
5
5
7
MR
R
MR
BR
BR
BR
MR
BR
MR
MR
MR
MR
MR
MR
MR
15
15
13
10
117
Table 23
Statistical evolution Ojovardhini Yoga on Ojokshaya (HIV +ve)
Parameter
Hb%
E.S.R
T.L.C.
W.B.C
T.P.C
CD4
CD8
CD4: CD8
Weight
K.P. Score
G.H. Condition
Mean
1.347
13.53
856
1593.33
0.675
88.33
538.13
0.204
2.4
20.67
2.533
S.D
1.25
10.74
834.701
1830.87
0.443
68.44
586.04
0.131
1.352
9.612
0.639
S.E
0.323
2.77
215.519
472.73
0.114
17.67
151.31
0.034
0.349
2.482
0.165
t-Value
4.17
4.88
3.97
3.37
5.92
4.99
3.56
6.00
6.87
8.33
15.35
P Value
<0.001
<0.001
<0.001
<0.01
<0.001
<0.001
<0.01
<0.001
<0.001
<0.001
<0.001
Hb% = Hemoglobin
E.S.R = Erythrocyte Sedimentation Rate
T.L.C. = Total Lymphocyte Count
W.B.C = White Blood cell Count
T.P.C = Total Platelet Count
CD4 = Cluster Diffraction 4
CD8 = Cluster Diffraction 8
CD4: CD8 = Ratio of CD4: CD8
Weight = in Kilograms
K.P. Score = Karnofsky performance score
G.H. Condition = General Health Condition
H.S = Highly Significant
118
Remarks
H.S
H.S
H.S
H.S
H.S
H.S
H.S
H.S
H.S
H.S
H.S
The multiple correlation co-efficient of CD4 (X1) on TLC (X2) and WBC (X3) after the
treatment is given by R1.23 is 0.7289. The regression line of CD4 on TLC and WBC is
given by -
0, against R1.23
0. The test
statistic is given by
correlation co-efficient between CD4 and WBC is 0.5189 and the correlation coefficient between TLC and WBC is 0.477.
Similarly the correlation co-efficient of CD8 (X1) on TLC (X2) and WBC (X3) after the
treatment is given by R1.23 is 0.9044. The regression line of CD8 on TLC and WBC is
given by
119
Table 24
Number of patients
4
10
1
0
15
Percentage
26.66
66.66
6.66
0
100
Mildly
Responded
7%
Not
Responded
0%
Moderately
Responded
66%
120
Best
Responded
27%
The aim of this study is to understand the explanations, scientific background of the
traditional Ayurvedic literature and practices, to give practical guidelines for the Ayurvedic
modalities of treatment and approach to the HIV infected patient. Ayurveda has both
preventive and palliative methods of HIV management, as understood by the general study
of the literature. There are many facts yet to be unearthed. This is possible by profound
knowledge of Ayurveda with channeled efforts to explain the same in the light of modern
scientific knowledge by the way if scientific research on literature, drug efficacy and other
methods of Ayurvedic management.
The staggering worldwide growth of HIV pandemic is matched by the explosion of
information in the area of HIV virology, pathogenesis, and treatment of HIV disease
including the opportunistic infectious associated with it. The information related to HIV
disease is much greater than that for any other infectious disease or immunologic disorder.
It becomes almost impossible for health care personnel, to stay abreast of this literature.
This study deals with the present and most current available information regarding
prevalence of the disease, its pathogenesis, treatment and prevention.
The existence of microorganisms is well documented from the time of Atharva Veda
(5000BC) and Ayurvedic texts too have vivid description of pathogens. On the contrary the
scientific community believes that the knowledge of microbiology evolved after 18th century.
The gap between these two periods is a vast one and it is difficult to know why such
knowledge did not grow further from the ancient times. One of the reasons may be because
Ayurveda gave more importance to host factor (kshetra and Ambu) rather than the
pathogens (Beeja) factor.
The second factor may be due to fewer incidences of infectious diseases in those
days. But with the changing times, these are sudden changes in environment due to
121
122
123
gives us an idea about the prevalence of sexually transmitted diseases in ancient period
also. But we do not find the reference of transmission of infection from mother to child, even
though there are references about the congenital disorders and role of genetics in
occurrence of diseases. But there is a reference in Ayurveda about transfer of maternal Ojas
to the foetus in intra-uterine life75. This is significant observation with regard to vertical
transmission.
It is estimated that over 6 million Indians are HIV carriers. WHO and UNAIDS are the
internationally operating organizations, who do research on epidemiology of infection. In
India NACO (National AIDS Control Organization) is working on same guidelines since
1987. In 1992 government of India HIV control project along with many N.G.Os.
But all the activities of government and non-governmental organizations involve only
modern medical professionals. No where Ayurvedic doctor is involved in the AIDS control
program. On the contrary, Ayurveda is a popular medical science in India and the
unqualified quacks started exploiting people in the name of Ayurveda. WHO recognized the
importance of Ayurveda 3 decades ago and since then many modern medical professionals
and scientists are doing research on Ayurvedic drugs. But these are scattered ones, and run
by private people. But in most of these researches, these is no involvement of Ayurvedic
scholars. To succeed in developing a framework of Ayurvedic treatment modality, there
should be profound knowledge of Ayurveda along with scientific research methods.
Ojokshaya is not a disease dealt with in Nidanastana or Chikitsa stana of any samhita. It is
not discussed as a Aristalakshana also. Rather it is a terminal condition of all debilitating
diseases, which cause death. Acharya Charaka and Sushrutha dealt in chapters where
general Vriddhi Kshaya Lakshanas of Dosha Dhatu and Mala are discussed. Ojokshaya is
pathological condition associated with kshataja kasa, grahani, raja yaksma, sannipathaja
124
jwara, raktarsha, pandu, grahani, raktaatisara, shosha, kshayaja kasa, many of which are
infectious diseases.
According to Ayurveda, the Ahara (food) Vihara (activities) and Manasika vaikalya
(psychological disorder) are also causes Ojokshaya. Alpashana (malnutrition), Anasnana
(starvation) are said to be nutritional factors, which directly effect the bodys, defense
mechanism, against infection. In the modern parlance, it is an well-understood fact that
malnutrition is a common cause of immuno deficiency, because protein takes part in the
formation of antibodies. In Vihara (physical activities) Vatatapa sevana (exposing to wind
blow and hot sun) associated with Ativyayama (excessive work) lead to Ojokshaya. Extreme
heat and blows of wind cause severe exhaustion, which leads to immuno deficiency in long
run. This also speaks about the socioeconomic conditions of said population, which is
susceptible to this kind of Ojokshaya. The next cause, Ativyavaya or excessive indulgence
in sex is also a cause for Ojokshaya. Here modern medical understanding differs.
According to Ayurveda, Kshaya (emaciation) can result by two ways. The first type is
anulomakshaya second one pratiloma kshaya. Anulomakshaya is caused due to
malnutrition in which bodily tissues from Rasa, Rakta, Mamsa progressively undergo
depletion. This is caused due to anashana, alpasana, vatatapa sevana type of causes.
Pratiloma kshaya is caused due to shukra kshaya (depletion of shukra dhatu) due to over
indulgence in sex. This is a reverse or opposite type of depletion of bodily tissues. According
to this principle loss of Shukra causes immuno deficiency and modern science doesnt relate
sex and immuno deficiency. Rather there are studies, which revel that sex does immuno
modulation. For this reason, Ayurveda explains seasonal sexual schedule where as modern
science does not believe in this. This Ayurveda has recognized brahmacharya (celibacy) as
125
one of the sub-pillars of the life where as modern science does not attach any importance to
celibacy in sustaining life.
Prajagara (sleeplessness) has been considered as a cause of Ojokshaya. Modern
science also believes in this and a good sleep increases ones immunity.
The next set of causes is manasika karanas (Psychological reason). They are kopa
(anger), shoka (grief), chinta (worry) and bhaya (phobia). In modern parlance the new
branch of medicine, i.e. psycho-neuro- immunology speaks about the role of psychological
causes like stress etc, as causative factors for immunodeficiency. It is also proved that CD4
count depletes under stressful conditions and increases by meditation, chanting mantras.
Sushrutha added dhyana or meditation as a psychological factor responsible for
Ojokshaya. But it is intense intellectual exercise, which was referred as dhayana rather
than meditation.
Sushrutha explains about abhighata or injury as a cause of Ojokshaya. If we look it
in modern angle, apart from the tissue loss in injury, there is a scope or increased
susceptibility for infection after an injury. Very specifically an injury in sexual organs or anus
is a high risk factor for transmission of HIV infection.
When we observe the signs and symptoms of Ojokshaya we lot of similarities in both
systems of medicine. Charaka does not explain the signs and symptoms of Ojokshaya,
whereas Sushrutha then explained different stages of Ojokshaya. The descriptions of
Sushrutha are more elaborate in this regard. He has classified the Ojovikruthi is in three
stages as vishramsha as a direct loss, Vyapat as a vitiation, and Kshaya as depletion. But
Charaka has summarized them in one condition Ojokshaya and we dont get the
advancing stages of diseases. The symptomatologies given here are not in order, but
marana or death comes at the end.
126
When we see the modern classification of HIV disease there are 4 stages of HIV
infection, which results in death at the end. The first stage is primary infection or acute seroconversion stage. This happens after the primary infection followed by an incubation period
of 2-6 weeks in which 50% of individuals feel acute viral syndrome characterized by high
fever, lymph adenopathy, myalgia etc. This lasts for 1-2 weeks, not responding to any line of
treatment. This is usually the uninvestigated phase of HIV infection. In many individuals this
stage may go unnoticed. During this phase there will be sever CD4 lymphopaenia. This
particular stage of HIV infection can not be correlated to the stages of Ojokshaya. This can
be correlated to sannipatika type of Jwara, in which there will be a sudden depletion in Ojas,
which is limited to Ojo-visramsa. At this stage body repairs on its own with the help of Kapha
(Bala), and this results in to the temporary reduction in Ojo-visramsa Lakshanas. But
because virus survives and camouflages, it enters in to chronic phase of infection and the
slow damage of Ojas continues.
In the II stage of HIV infection there will be occasional symptoms of fever, loss of
appetite, loss of body weight, aesthenia, diarrhoea, cough etc. This stage can be compared
to Ojovishramsha stage with special reference to the sequence of symptomatology
explained in sannipataja Jwara where there will be inertness of limbs, chills, looseness of
limbs, low grade fever, body pain etc.
sannipathaja Jwara.
In the stage III of HIV infection along with the above mentioned symptoms there will
be further immuno deficiency due to which many opportunistic infections like herpes
simplex, herpes zooster, oral Candidiasis, tuberculosis, hairy leukoplakia.
In second stage of Ojovikriti natural properties of Ojas under the influence of vitiated
Doshas goes for vyapath phase which gives rise to stabdha gurugatrata, vatasopha,
127
varnabedha, glani, tandra and nidra76. Even though there is no mention of opportunistic
infection in Ojovyapat the symptomatology resembles a infectious conditions leading to
coma.
In the last stage of HIV infection there are, many neurological symptoms like
dementia and altered personality, convulsion, ataxia, visual impairment, neurological
deficits, hemiplegia followed by death. In Ojokshaya (3rd stage) there will be moorcha (loss
of consciousness) mamsakshaya (wasting of muscles) moha (stupor). Pralapa (delirium)
and vyathithendriyata (loss of motor and sensory perception) followed by marana (death).
This is in the strict sense of Susrutas classification of Ojokshaya stages.
None of the classics described the exact Samprapti of Ojokshaya. Regarding the
samprapthi of Ojokshaya, there are two different methodologies explained in different
contexts. The Ojokshaya occurred due to general causes apart from infection and that
caused due to infection are of two different Samprapti. The description about general
Samprapti can be summarized as sited by Charaka in madhumeha77 and panduroga78.
Vitiated Doshas (either Vata or Pitta) vitiate Dhatus, which later loose integrity and get
depleted and subsequently results in depletion of Ojas. This is also called as
Anulomakshaya. The autoimmune mechanism resembles this type of Ojovikriti. The
Samprapti of Ojokshaya caused by infection can be summarized with the available
references in the context of Rajayakshma79 and Sannipata Jwara80. Here in the individuals
who have basic susceptibility for infection, when get infected due to already discussed
causes, get Bhootopaghata a damage of cells (carrying CD4 markers) followed by
abhishanga (penetration) and entry of viral materiel into the cell. This foreign toxic meterial
works like jangama visha (poison of animal origin)81. But as virus is a live matter with RNA
genome instead of causing immediate death it replicates here getting sustenance from
128
bodily cells. Those cells where virus replicates become reservoirs of virus. This virus is
capable of causing srothorodha, raktadi Dhatu Kshaya. Due to the lowered functioning of
dhatwagni resulting in Ama and apachaya (catabolic activity) due to the deficiency of
nutrition which further leads to Ojokshaya82.
The Ama so formed causes further Vata Vriddhi, associated with vikrita Pitta leads to
sannipathika Jwara. Vitiated Vata and Pitta cause damage to Dhatu vaha srotamsi and this
leads to Ojo-visramsa, vyapth and Kshaya in due course of time. So in this way pathological
events following bhootopaghata correlate with modern understanding of HIV infection.
Sadhya sadhata
Sushrutha has clearly said that Ojovishramsha and vyapath can be managed by
rasayana and vajeekarana Chikitsa along with appropriate diet, which increases Bala and
antagonistic to the causative factors of Ojokshaya83. Further it is said, as Ojokshaya will not
be reversed with rasayana or Vajikarana Chikitsa. The prognosis of disease as explained in
Ayurveda and modern science are similar as the early stages of HIV infection can be
managed with antiviral and immuno modulators and advanced stage will not improve with
any available treatment.
Chikitsa sutra
General management of Ojokshaya is by rasayana and Vajikarana, which are
Ojoskara in nature84. But the management of Ojokshaya caused by infection needs an
additional line of treatment, which can be developed on the basis of Krimi Chikitsa as
explained in Charaka Vimana 7th chapter. Among 3 major principles of Krimi Chikitsa, the
prakriti vighata type suits the present context of HIV infection. This can be achieved by
usage of drugs having Krimi prakriti vighata property.
129
130
131
signal for developing countries because they have high-density labour population (Table6/diagram-6).
In the study incidence among people of two different food habits, it was interesting to
note that all the patients (100%) consume mixed diet. This may be because the local
population having maximum people of mixed diet habit. But it is also interesting to note that
not even a single vegetarian subject was seen in this study. As Ayurvedic concept talks
about the role of predisposing factors, there must be a physiological or psychological impact
of non-vegetarian food that may be having a role to play in high incidence of HIV among
non-vegetarians population (Table-7/diagram-7).
Coming to the study related to disease, maximum number of patients (100%) got the
infection from heterosexual contact. This data coincides with the international data.
(Harrison int. medicine)
Even though the incidence changes are more among the patients who got it from
blood transmission and intra-venous drug intake, but more patients got it from heterosexual
contact only. This clearly shows the high rate of unsafe heterosexual practices in our society
population (Table-8/diagram-8).
It was interesting to note that among the couples attended the general screening of
the study one female patient had HIV infection since 8 years. She gave birth to 2 female
issues who also had the HIV infection. This lady got infected due to blood transfusion in
Rajastan in 1992. But her husband is not infected till now even after the normal sex life till
2000 March. Incidentally the family consumes vegetarian diet.
This study correlates with modern medical description as well as Ayurvedic
description of respective conditions. Most of the patients belonged to early symptomatic
132
(Ojovishramsha and Vyapat) group. Among there symptoms, all (100%) had fatigue, 11
(73.33%) had fever 60% had diarrhoea (Table-9/diagram-9).
It was found that maximum number of patients had the infection for more than 3
years (100%). It varied from 1 year to 7 years. This data recognized that the entire patient
attended. This study with known HIV status, this may be because, of the fear of social
stigma and fear of diagnosis associated with lack of awareness regarding the disease
(Table-10/diagram-10).
Tridosha status
The main three bodily humors, which cause diseases, were studied carefully. A
maximum of 14 (93.33%) had Kapha Kshaya, Vata Vriddhi and Pitta Kshaya Lakshanas and
one had Kapha Kshaya, Pitta Vriddhi and Vata Vriddhi Lakshanas. This reflects the events
of pathogenesis ruled by Vata and Pitta vitiation leading to Kapha Kshaya. It is also in line
with the Samprapti (pathogenesis) of Ojokshaya were Vata and Pitta vitiate Kapha and that
leads to Ojovishramsha and Vyapat (Table-11/diagram-11).
It is interesting to note that among the Nidana of Ojokshaya, nutrition causes (53%)
like alpashana, behavioral causes like prajagara (60%) (Table-12/diagram-12) and
psychological causes like kopa (66%) (Table-13/diagram-13) are also found in the subjects
attended the study. This aspect has not been considered in modern science and study
through light on these points.
Status of Ojas
The overall assessment of status of Ojas was done among the subjects attended
study and maximum patients had (100% ) Ojovishramsha and 80% had Ojovyapat and none
had Ojokshaya in strict sense of the stages as explained by Sushrutha. This explains the
133
Ojas status of HIV patients and Susrutas classification of phenomenon Ojokshaya (Table14/diagram-14).
Stages of HIV infection are well understood. It is a proven fact that HIV causes AIDS
and AIDS related complex. The mathematical and statistical evaluation is often used to
explain the biological phenomena, through the years of studying the HIV disease. The
investigation of CD4 and CD8 cells along with lymphocyte count is very much helpful in the
prediction of stages of HIV infection. CD4 count cell is a surrogate marker of
immunodeficiency because lower HIV RNA level and higher CD4 cell counts correlates with
long time survivors in both adult and children85. In this study maximum patients were in early
symptomatic stage (60%) followed by 40% in clinical latency. This also correlates with the
stage wise incidence of Ojokshaya (Table-15/diagram-15).
For the general analysis of overall condition of the subjects, all the subjects were
investigated for hemoglobin percentage, Erythrocyte Sedimentation Rate, Total counts
(WBC). Even though P32 and PCR are recent advances in knowing the exact HIV status, it
was carried out because of financial constraints. Instead CD4 and CD8 along with peripheral
lymphocyte and platelet counts are taken as surrogate markers of the immuno status. This is
in tune with internationally practiced research parameters.
All the patients have undergone these investigations before starting Ojovardhini
yoga, and soon after the completion of three months schedule.
The effect of Ojovardhini yoga on each of the parameters was assessed with base
line data. The Ayurvedic assessment was done with detailed clinical analysis of Dosha
status and Ojas status on the basis presenting symptoms using darshana sparshana and
prasna methodology. This was done before and soon after completion of Ojovardhini yoga.
134
135
136
Investigative parameters
As already discussed as a surrogate marker of immune status vis-a-vis viral load,
CD4 count was done before and after the treatment. 8 patients showed an increase in CD4
cell count, 7 of them showed a fall in their CD4 count. This study is quite similar with
Deshpande but varies from the study of Rajgopal. In the latters study, all patients showed
rise in CD4 level. This variation may be due to the investigatory procedures followed or
because of a potent Ojovardhaka in the said formula. The internationally published data
shows the in consistency in the level of CD4 cell level as compared to the clinical
improvement88.
CD4 CD8 ratio
This ratio is evaluated to know the level of cell mediated immunity. It also predicts
the prognosis, clinical stage of HIV infection and virulence of virus. An increase in ratio is a
good prognosis, as found in 5 cases, in this study. The mean change in CD4, CD8 ratio is
0.204. Which is similar with Rajgopal study. But in his study all patients showed an increase
of 0.2 in ratio, after 6 months of study. In this study this level was achieved with in 3 months.
This may be due to fast acting drugs, having better bioavailability and perhaps due to its
potent viral action.
Haemoglobin percentage (HB%)
Is a general marker of health and 10 patients had increased their HB% after the 3
months medication. The mean change of haemoglobin is 1.34. This result is better than that
of earlier study which is only 0.2%.
Erythrocyte sedimentation rate (ESR)
It is considered as a prognostic parameter in this study. But almost all patients i.e. 12
(80%) had raise in the ESR after the treatment. The mean raise in ESR is 13.53, which
137
denotes a bad prognostic value, although all of the patients got increased body weight,
general health conditions and other objective parameters. As other researches are silent
about the role of ESR in HIV medication, it is felt that but for the present therapy there would
have been further raise of ESR due to opportunistic infections.
Considerations in overall efficacy of therapy
Among 15 patients 4 patients are best responded and 10 patients are moderately
responded none of the patients, went non-responded to the therapy. This variation of
response may be due to different levels of viral loads and immune levels of patients. All sub
groups of HIV(if involved) would not have respond similarly to the drug. Apart from the
pharmacodynamics, the nutritional status, psychological conditions of these patients are
also equally important for better response for the same drug.
Side effects
No side effects or adverse drug reactions are met with during the study. Even after
the completion of the study, no side effects reported. The post medication renal,
hematological and hepatic profiles are also normal. Therefore this drug is safe for human
medication.
Probable mechanisms of action
The efficacy of Ojovardhini yoga is found to be highly significant in all parameters (Pvalue<0.001) (Table no-22). The probable mechanisms of action are discussed here. The
main principle of treatment of Ojokshaya is re-institution of Ojas by Rasayana and
Vajeekarana therapy89. Almost all the drugs in Ojovardhini Yoga directly or indirectly help to
increase Bala or vitality. Amrita, Ashwvagandha, Shatavari, Yastimadhu and Swarna
makshika bhasma are one of the best rasayana drugs. All of them are immuno stimulants,
revitalize bone marrow and thymus axis. Individual phyto-chemicals induce a cytokine profile
138
that favors the host (kshetra) and oppose the viral replication (prakrithi vighata) by the above
actions, Ojovardhini yoga impedes the HIV disease progression.
Guduchi (tenospora cardefolia) by its rasayana, balya, rakta shodhaka vishagna,
jwarahara, properties helps for the over all improvement of the condition. As evidenced by
current researches it is a potent immuno modulator. It increases bone marrow proliferation in
high dose, helps to increase apoptosis in bone marrow cells90.
Ashwagandha by its rasayana and Vajikarana property increase Ojas. It has
madhura vipaka and it is one of the best Ojovardhaka. The current research up dates
supports this observation. It contains steroidal lactones called Withanolides, which have
hepato protective anti-inflammatory activity91. Ashwagandha shows tumour inhibitory activity
arrests mitotic division of carcinoma, (ref) it alters the concentration of neurotransmitters,
which play important role in brain processes92. These activities of ashwagandha are very
useful in preventing and managing different AIDS related complexes, carcinomas and
neurological events.
Satavari by its rasayana and balya properties increases Ojas. Recent researches
also attribute immunomodulatory activity to this drug. It attenuates the OTA induced
suppression of chemotaxis activity as well as 1L-1 production by macrophages. It induces
excessive production of TNF-sigma93.
Nimba - is Krimighna, kusta hara, Jwarahara. It kills Krimi (pathogen) by prakrithi
vighta property. It is an excellent remedy for prevention and control of dermatological
condition associated with HIV infection. Research updates also prove this right. Neem
increases cell mediated immunity and total lymphocyte count and T-cell count94.
Bhumyamalaki - has yakrit roga hara property. It is indicted in kamala and many other
infective conditions. It is a beneficial drug to protect liver from long time usage of drugs.
139
140
141
There are three types of Ojas vitiation mentioned by Susruta i.e. Ojo-visramsa,
Ojovyapat and Ojokshaya.
Cellular immunity is mediated by T8, cells. The cytotoxic T cells attack and destroy
cells that have the antigen, which activated them. Suppressor T cells, which develop more
slowly than cytotoxic T cells, help terminate the immune response by dampening the
immune responses of T and B cells.
HIV, the cause for Acquired Immuno Deficiency Syndrome, is transmitted by
heterosexual and homosexual contact, through blood and blood products and from mother
to child in vertical transmission. The diagnosis of HIV infection depends on the
demonstration of antibodies to HIV and or the direct detection of HIV or one of its
components.
The close relationship between clinical manifestations of HIV infection and
CD4+Tcell count has made measurement of the latter quantity a routine part of the
evaluation of HIV infected.
Immuno deficiency is refereed to as Ojokshaya in Ayurveda. Any depletion of Ojas
can lead to infection disease and death. Sushrutha then explained different stages of
Ojokshaya. When we see the modern classification of HIV disease there are 4 stages of
HIV infection, which results in death at the end. The first stage is primary infection or acute
sero-conversion stage. This particular stage of HIV infection can not be correlated to the
stages of Ojokshaya.
In the II stage of HIV infection there will be occasional symptoms of fever, loss of
appetite, loss of body weight, aesthenia diarrhoea, cough etc. Pathological events following
bhutopaghata correlate with modern understanding of HIV infection.
142
The prognoses of disease as explained in Ayurveda and modern science are similar
because the early stages of HIV infection can be managed with antiviral and immuno
modulators and advanced stage will not improve with any treatment. Among 3 major
principles of Krimi Chikitsa, the prakriti vighata type suits the present context of HIV
infection.
The main three bodily humors, which cause diseases, were studied carefully.
Maximum had Kapha Kshaya, Vata Vriddhi and Pitta Kshaya Lakshanas and one had
Kapha Kshaya, Pitta Vriddhi and Vata Vriddhi Lakshanas.
The overall assessment of status of Ojas was done among the subjects attended
study and maximum patients had Ojovishramsha had Ojovyapat and none had Ojokshaya in
strict sense of the stages as explained by Sushrutha. Stages of HIV infection are well
understood. This also correlates with the stage wise development of Ojokshaya.
This is a prospective clinical trial for the evaluation of Ojovardhini yoga, conducted
in 15 cases of Ojokshaya, due to HIV infection. In this study all the 15 subjects responded to
the trial drug. There was a significant improvement in all-subjective parameters. Eight
patients showed an increase in CD4 cell count, 7 of them showed a fall in their CD4 count. In
the latters study, all patients showed rise in CD4 level.
The main principle of treatment of Ojokshaya due to bhutopaghata is Krimi Prakriti
vighata, re-institution of Ojas by Rasayana and Vajikarana therapy. An ideal drug should
also involve drugs having faster action and better cell penetration capacity. Amrita
increases bone marrow proliferation in high dose, helps to increase apoptosis in bone
marrow cells. Ashwagandha by its rasayana and Vajikarana property increase Ojas.
Satavari by its rasayana and balya properties increases Ojas. Recent researches also
attribute immunomodulatory activity to this drug. Nimba is an excellent remedy for
143
prevention and control of dermatological condition associated with HIV infection. Neem
increases cell mediated immunity and total lymphocyte count and T-cell count.
Bhoomyamalaki is useful in this condition as hepatitis B is also sexually transmitted
disease, co-incidence of HIV infection with hepatitis B is more. Yastimadhu by its rasayana
and Krimighna properties increases Ojas and may bring down the viral load. It is a proven
anti HIV drug. Mrityunjaya Rasa by its Jwara hara and anti microbial action, it prevents and
controls opportunistic infections very specifically respiratory and viral infections. Swarna
makshika bhasma by its rasayana, yoga vahi, tridoshaghna property enhances all the
properties of above drugs, and increases the bioavailability.
Ojovardhini yoga has shown immuno protective, immuno stimulant, antiviral like
activity, which is the probable reason for its efficacy in improving the clinical conditions
encountered in Ojokshaya due to HIV infection.
In the evaluation of efficacy of Ojovardhini yoga in Ojokshaya with special reference
to HIV infection, the final results emerged are as follows. Out of 15 patients 4 patients
(26.66%) are Best Responded, 10 patients (66.66%) are moderately responded and 1
patient (6.66%) is mildly responded for the above said trail. No patients are there under the
Not Responded Group.
144
BIBLIOGRAPHY
Basavaraajeeyam
Varanasi.
Bibliography
Grays Anatomy
by Henry Gray, 1973
Human Physiology
Vol 1 - 2
Introduction to Kayachiktsa,
By C. Dwarkanath,
Published by Chowkamba offest press, Varanasi.
Kashyapa Samhita,
by Vridha Jeevaka,
1953
Bibliography
Trends in AIDS diagnosis and reporting by Centers For Disease Control and
Prevention USA
Bibliography
References
References
85
Phillips AN, Lee CA, Elford J, et al. Serial CD4 lymphocyte counts and
development of AIDS. Lancet. 1991;337:389-392.
86
Rajgopal.K , Clinical evaluation of the efficacy of an Ayurvedic drug
formulation against HIV and AIDS in the proceedings of seminar on
Ayurvedic management of AIDS and Cancer, Jamnagar, 1999
87
Evaluation of immuno potentiating activity of a herbo mineral
formulation PV-150986 in HIV infection 1998
88
Choi S, Lagakos SW, Schooley RT, Volberding PA. CD4+ lymphocytes
are an incomplete surrogate marker for clinical progression in persons
with asymptomatic HIV infection taking zidovudine. Ann Intern Med.
1993;118:674-680.
Volberding PA, Lagakos SW, Grimes JM, et al. A comparison of
immediate with deferred zidovudine therapy for asymptomatic HIVinfected adults with CD4 cell counts of 500 or more per cubic millimeter.
N Engl J Med. 1995;333:401-407
Stein DS, Korvick JA, Vermund SH. CD4+ lymphocyte cell enumeration
for prediction of clinical course of human immunodeficiency virus disease:
a review. J Infect Dis. 1992;165:352-363
89
Susruta samhita sutra 15/28
90
Proceedings of the international workshop, CDRI, Lucknow (Dec 25,1997) 143)
91
Chem Abstr, 1989, 110, 132185; Atta-ur-Rahman et al, J Nat Prod,
1993, 56, 1000; De et al, Indian Drugs, 1993, 30, 355; Rietschoten, Brit J.
Phytother, 1990, 1(3/4), 11
92
Kupchan et al., J. Amer. chem. Soc., 1965, 87, 5805; Shohat et al.,Ioc.
cit.; Chem. Abstr., 1973, 79, 139; 1970, 72, 130740; Lavie et al., J. chem.
Soc., 1965,75171)
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; Dhuley J.N effect of some Indian herbs on macrophage functions in
ocharatoxin treated mice J. of Ethnopharmacol, 1997; 58;15-20
94
Premanathan et al. A survey of some indian medicinal plants for anti
HIV activity, IJMR,112, September 2000, pp73-77
95
Jayaram S. et al Inhibition of HbsAg secretion from Alexander cell line
by Phyllanthus amarus. Indian J. Pathal. Microbiol. 1996; 39; 211-5
96
Premanathan et al. A survey of some indian medicinal plants for anti
HIV activity, IJMR,112, September 2000, pp73-77
Hattoiri.T, Ikematsu.S. et.al. Preliminary evidence for inhibitory effect of
glycerrhizin on HIV replication in patients with AIDS, antiviral Res.,
1989,11,255-262
97
Ibid
98
O'Dell BL. Interleukin-2 production is altered by copper deficiency. Nutr
Rev 1993 Oct;51(10):307-9 Department of Biochemistry, University of
Missouri, Columbia 65211
J Nutr 1997 Feb; 127(2): 257-62 Department of Food, Nutrition & Food
Service Management, The University of North Carolina Greensboro,
27412-5001, USA.
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Human Nutrition Department, University of Florida, Gainesville 32611,
USA
References
Schola r:
D . See tha ra m Pras ad
Sl.No.
2. Sex - M
OPD No
3. Age -
Years
IPD No
Birth data:
Place of Birth
Date
District
Month
State
Year
4. Religion
Hindu
5. Occupation -
Sedentary
Muslim
AM
Time
Hours
Minutes
PM
Christian Other
Active
Middle class
Labor
Higher middle
Higher class
7. Address
Pin
Schedule initiation
8. Selection
9. Result
Included
Responded
Excluded
Schedule completion
Not responded
Discontinued
INFORMED CONSENT
I
Son/Daughter/Wife of
am
Patient's Signature
Sl.
Duration
Complaints
No
Less than 1 yr
Loss of appetite
Loss of weight
Diarrhoea
Fever
1 to 2 years
Above 2 years
7
8
9
2. ASSOCIATED COMPLAINTS
Gastro-Intestinal
Central Nervous
Respiratory
Nausea/ Vomiting
Headache
Cough
Oral thrush
Drowsiness
Pain Abdomen
Incontinence
Breathlessness
Dysphagia
Limb weakness
Chest pain
Abd. distention
Convulsions
Cardiovascular
I r r e l e van t Behavior
Skin eruptions
Genitourinary
Molluscum
Warts
Cutaneous
Giddiness
Palpitation
Burning micturition
Buccal cavity
Urethral discharge
Bleeding gums
Genital ulcers
Hairy leucoplakia
Genital warts
Oro-pharyngeal
Vaginal
candidiasis
candidiasis
Others if any
Intentional / accidental
Blood transfusion
Injections
other
2) Early symptoms
3) Later symptoms
(c) Mode of progress
Typical
Rapid
Diabetes Mellitus
Hypertension
Cancer
Venereal
diseases
Cardiac disease
5. TREATMENT HISTORY
6. FAMILY HISTORY
7. PERSONAL HISTORY
a) Food habits
Vegetarian
Taste
preferred
Mixed diet
Sweet
Pungent
b) Sleep
Day
Sour
Bitter
Night
Salty
Astringent
Sound
Disturbed
c) Hygiene
d) Addictions
Tobacco
Alcohol
Drugs
e) Sexual behaviors
Marital
Heterosexual
Extra marital
Homosexual
multiple
Single
Recipient
Frequency
g) Bowel habits
Loose
Constipating
Normal
Irregular
Amenorrhea
Menopause
8. EXAMINATION
(a) Vitals
Temperature
Pulse
Blood pressure
(b) General
Built & Nutrition
well
Moderate
Poor
Pallor
Mild
Moderate
Severe
Jaundice
Mild
Moderate
Severe
Tongue
Ulcers
Hairy Leucoplakia
Coated
Cervical
Supra clavicular
Axillary
Inguinal
Any other
Resp. rate
(c) Systemic
1) Gastrointestinal tract
Tenderness
Organomegaly
Fluid
Mild
Moderate
Severe
Liver
Mild
Moderate
Severe
Spleen
Mild
Moderate
Severe
Thrill
Present
Absent
Shifting dullness
Present
Absent
Present
Absent
Abdominal Lump
(Advise U.S.G if required)
Report: -
2) Respiratory system
Shape of chest
Normal
Deformed
Trachea
Normal
Right Shift
Movements
Normal
Restricted
Left Shift
Auscultatory findings
Breath Sounds
Added sounds
Vesicular
Ronchi
Bronchial
Crepitation
3) Cardiovascular system
S1
S2
Murmur
Rub
5) Genito-Urinary system
Advise V.D.R.L. if required
Report:9. LABORATORY INVESTIGATIONS
HAEMATOLOGICAL
Hb%
Total Count Lymphocytes
Total Count Platelets
Total Count Leucocyte
E.S.R
gm/dl
/l
/l
/l
mm/1
st
Hour
DIFFERENTIAL COUNT
Lymphocytes
Neutrophils
Eosinophils
Basophils
Monocytes
mg/dl
SPECIAL INVESTIGATIONS
Elisa
HIV- I & II
Rapid (Tridot)
Western Blot
CD4 cell count
CD8 cell count
CD4 : CD8 Ratio
10. DIAGNOSIS
/mm 3
/mm 3
STAGE
Before
SUBJECTIVE
After
Parameter
Karnofsky
performance score
OBJECTIVE
Total Count
Platelets
Total Count
Lymphocytes
E.S.R.
Body weight
NOTES
Side effects
Investigators note
Before
After
Ayurvedic assessment
1. Hetu
Ahara
Vihara
B
Anashana
Alpashana
2. Dosha
Vata Vriddhi
B
Karshya
Karshnya
Ushnakamitwa
Kampa
Anaha
Shakritgraha
Balabhramsha
Nidrabhramsha
Pralapa
Bhrama
Anya
B
Vatatapa sevana
Ati Vyayama
Ati Vyavaya
Sonita a t i v a r t a n a
Prajagara
Koapam - Anger
Soka
Chinta
Bhaya
Bhootopaghgta
Pitta Vriddhi
B
Peetamootra
Peetanetra
Peetavit
Peeta twak
Atikshudha
Atidaha
Kapha Vriddhi
B
Agnisadana
Praseka
Alasya
Gowrava
Swetangata
Sheetangata
Shlathangata
Swasa
Kasa
Atinidra
Vata Kshaya
Pitta Kshaya
Kapha Kshaya
B
A
B
A
B
Angasada
Mandagni
Bhrama
Urah shoonyata
Alpabhshite
Shareera
sh ee ta tw am
Ahitam
Chesta heenata
Prabhahani
Shira shoonyata
Vyamoha
Hriddrava
Sleshma vriddhi
Sandhi saithilya
3. Lakshana
Ojo Vishramsha
Ojo Vyapat
B
A
B
Gatra sadanam
Stabdha gatrata
Dosha chyavanam
Guru gatrata
Sandhi vislesha
Vata shopha
Kriya sannirodha
Varna hani
Glani
Tandra
Nidra
Ojo Kshaya
Bhaya
Dowrbalya
Chinta
Vyathitendriya
Duschaaya
Durmana
Rooksha
Kshama
Moorcha
Mamsa kshaya
Moha
Pralapa
Signature of Guide
Signature of Scholar
Score
100
90
80
70
60
50
40
30
20
10
00
D. SEETHARAM PRASAD
309, 6TH A MAIN, 3RD BLOCK, H.B.R. LAYOUT,
3.
M. D. (Ayurveda) KAYACHIKITSA
4.
Date of admission
September1999
5.
in HIV infection. A number of herbal drugs have been individually evaluated in the treatment
of HIV and AIDS related complex (ARC)3.
By the end of 2000 according to an estimation from UNAIDS and WHO, the number
of people infected by HIV would have crossed 50 million. In India since the detection of HIV
infection in 1986, the epidemic has been frankly out of control. As of now an estimated 4 to 6
million HIV infected cases are present in India. Till now there were 12 million deaths due to
AIDS in entire world.
In-spite of the intense efforts and massive funding for research the world over, antiretroviral therapy has not yet met with modest success. In the Indian scenario the restricted
availability of these anti-retrovirals coupled with the high costs which make them
unaffordable, virtually puts these drugs beyond the reach of most of the HIV infected
population in India. The present study is designed to assess the therapeutic effect of
Ojovardhini yoga in HIV infected patients, which could be a safe, effective and economical
drug.
6.2. Review of literature
Ojas is the essence of all dhatus and also called as Bala4, which is responsible for
Vyadhikshamatva or immunity against infections5. The condition in which Ojas gets depleted
is called Ojokshaya. Susruta explained the stages of the depletion of Ojas as Ojovisramsa,
Ojovyapath and Ojokshaya6. Ojokshaya can be defined as qualitative and quantitative
reduction of Ojas. Ojas, the essence of all dhatus, controls the vital functions and immuno
regulation. It is classified in to two types i.e. Para and Apara, out of which Astabindu (Para)
Ojas is depleted by the infection7.
The symptomatology of the HIV infection resembles that of Ojokshaya. Clinical
stages of HIV infection is classified in to five stages on the basis of CD4 count. The anti
retro-viral drugs available now, act at different levels of the stages of the life cycle of HIV and
the combination therapy of them has shown to prolong the life span and to decrease
opportunistic infections and to increase CD4 cells count.
So, any drug which can prolong the life span, improve the quality of life, decrease the
infections and increase CD4 cell count can be taken as a drug useful in the management of
Ojokshaya with the special reference to HIV infection.
Ojovardhini yoga is an herbo-mineral compound rationally formulated on the basis
of individual properties of 9 ingredients described in classical texts.
6.3. Objectives of the study
1. To evaluate the efficacy of Ojovardhini Yoga in improving the clinical status of
Ojokshaya with special reference to HIV infection
2. To assess the role Ojovardhini Yoga on CD4 cell count, which is the marker of
stages of the HIV infection
7. Material and methods
7.1. Source of data
a) Literary: Literary aspects of the study will be collected from standard Ayurvedic
texts, magazines and journals. The information regarding the disease will be
updated from Internet search along with authentic textbooks.
b) Drug: Ojovardhini Yoga
The ingredients of Ojovardhini Yoga will properly identified. The standard
manufacturing guidelines will be followed for the preparation. The combination and
proportion of Ojovardhini Yoga is as follows.
1. Amruta8 (Tinospora cordifolia)
2 Parts
1 Part
1 Part
11
1 Part
12
1 Part
1 Part
1 Part
8. Mrutunjaya Rasa
15
1 Part
9. Swarnamakshika Bhasma
16
1 Part
c) Patients: Patients with Ojokshaya (HIV +ve) will be selected from O.P.D. of Post
Graduation and Research center of Sri D.G.M. Ayurvedic medical college & Hospital,
Gadag by preset inclusion and exclusion criteria.
7.2. Method of collection of data
a) Study design: Prospective open clinical trial
b) Sample size: A minimum of 20 patients
c) Exclusion criteria:
1. Patients below the age of 20 years and above the age of 50 years, pregnant and
lactating women will be excluded from the study.
2. The patients having diabetes mellitus and other systemic diseases will be excluded
and the patients with concomitant therapy will be excluded.
d) Inclusion criteria
1. The patients with the HIV infection diagnosed by serological test and
Western blot method will be taken in the study.
2. CD4 count ranging from 200 to 500/cu.mm.
3. Karnofsky Performance score 60 and above.
4. The patients are selected irrespective of Sex and race based on the
clinical signs & symptoms other than that of exclusive criteria,
e) Posology:
3 gm/24 hours in divided dose or 50mg/Kg-body weight in divided dose orally
f) Study duration: 90 days
g) Assessment of result
The results will be assessed by subjective as well as objective parameters.
7.3. Investigation
1. Screening tests
: Tri-dot
2. Confirmatory tests
: Western Blot
3. Other tests
: Obtained
8. List of references
1
medicinal plants, Lithium carbonate and glucan. Methods find exp clin pharmacol.
1988 October; 10 (10): 639-44
3
A survey of some Indian medicinal plants for Anti-human immuno-deficiency Virus (HIV)
Astanga Hridaya Sutra 11/37, Astanga Hridaya with commentaries of Arunadatta and
Astanga Hridaya Chikitsa 1/95, Astanga Hridaya with commentaries of Arunadatta and
Susruta Samhita Sutra, 15/23-27, Edited by Vd. Jadavaji Trikamji Acharya, published by
Charaka Samhita Shareera 2/10, Edited by Vd. Jadavaji Trikamji Acharya, published by
Bhava prakasha, Guduchyadi Varga, 9-10, The Kashi Sanskrit series No. 130 published by
Ibid, 189
10
Ibid, 186-187
11
Ibid, 18-19
12
13
Bhavaprakasha, Madhyama khand , The Kashi Sanskrit series No. 130 published by the
Ibid
Bhaishajya Ratnavali, Jwaradhikara,409-411 Kashi Sanskrit grandhamala 152
Yogaratnakara pp113, Edited by Dr. Indradev Tripathi, Krishna dasa Ayurveda series
11.1. Guide
READER IN KAYACHIKITSA
DGMAMC, PGARC, Gadag
11.2. Signature
11.3. Co-Guide
: 1)
2)
11.4. Signature
: 1)
2)
11.6. Signature
1. Remarks
12.2. Signature
Manual of HIV therapeutics, edited by William G. Powderly, M.D. published by Lippincott Raven,
New York, 1997
2
Thatte U.M.; Dahanukar; S.A. Comparative study of immunomodulating activity of Indian medicinal
plants, Lithium carbonate and glucan. Methods find exp clin pharmacol. 1988 October; 10 (10):
639-44
3
A survey of some Indian medicinal plants for Anti-human immuno-deficiency Virus (HIV) activity, by
M. Premanathan et all, The Indian Journal of Medical research Vol.112 September
4
Astanga Hridaya Sutra 11/37, Astanga Hridaya with commentaries of Arunadatta and Hemadri By
Harisastry paradakar Vaidya1939 Published by Nirnaya sagar press Bombay.
5
Astanga Hridaya Chikitsa 1/95, Astanga Hridaya with commentaries of Arunadatta and
Hemadri By Harisastry paradakar Vaidya1939 Published by Nirnaya sagar press Bombay.
6
Susruta Samhita Sutra, 15/23-27, Edited by Vd. Jadavaji Trikamji Acharya, published by
Chaukhambha Orientalia, Varanasi, 1980
7
Charaka Samhita Shareera 2/10, Edited by Vd. Jadavaji Trikamji Acharya, published by
Chaukhambha Sanskrit Samstan, Varanasi, 1984
8
Bhava prakasha, Guduchyadi Varga, 9-10, The Kashi Sanskrit series No. 130 published by the
Chowkamba Sanskrit sansthana, Varanashi. 4th edition 1984.
9
Ibid, 189
10
Ibid, 186-187
11
Ibid, 18-19
12
Kayyadeva Nighantu, pp248-250, published by Chaukhambha Orientalia, Varanasi, 1980
13
Bhavaprakasha, Madhyama khand , The Kashi Sanskrit series No. 130 published by the
15
Ibid
Yogaratnakara pp113, Edited by Dr. Indradev Tripathi, Krishna dasa Ayurveda series 54