Age of menarche in Jordanian girls
Age at menarche in Jordanian girls
Fawaz L. Ammari, MD, FRCP(London),
Heitham K. Ajlouni, MD,
Kamel M. Ajlouni, FACP, FACE
T he most important event in the whole process of
female puberty is the onset of cyclic menses
(menarche). The age of the menarche varies in
different part of the world and is known to be
influenced by genetic, socio-economic status, and
environmental conditions, body status and level of
education, 1 age at menarche was first calculated in
mid 19th century in Denmark,2 since then, many
authors have used different methods to calculate age
at menarche in different parts of the world. Since
age of menarche is an important factor in health
planning, we reported here the distribution of age at
menarche among Jordanian students and compare it
to Jordanian women who was born 40 years ago, to
look for secular trend on any difference between
menarche age now and 20 years ago.
Female university students and their female
relatives were haphazardly invited from first of June
until 30th December 2001 to participate in this
study. The student population of the 3 major
universities; University of Jordan, Jordan University
of Science and Technology and Yarmouk
University, Jordan roughly represent the population
in Jordan with the exception of the age. The system
for university admissions provides allocation for
each district according to its population density, and
all socio-economic stratum are represented. Those
who participated in the study, filled in a
self-administered questionnaire that includes date of
birth and date of the first menstrual period. We
chose only girls who were between 18 and 24 years
of age, (born between 1977 - 1983). For
comparison, we also chose women above 40 years
of age born before 1960, to find out if there is any
Table 1 - Cumulative percentage of girls reporting onset of menarche presently aged between 18-24 and above the age of 40.
Age 9 y (%) 10 y (%) 11 y (%) 12 y (%) 13 y (%) 14 y (%) 15 y (%) 16 y (%) 17 y (%) Total (%)
No. of girls with 2 (0.1) 17 (0.9) 48 (2.6) 175 (9.5) 413 (22.6) 727 (39.8) 305 (16.7) 114 (6.2) 22 (1.2) 1823 (100)
menarche age of 18-22
years
No. of girls with 0 (0.0) 7 (0.9) 26 (3.2)
menarche age of 40
years and above
244 Saudi Med J 2004; Vol. 25 (2) www.smj.org.sa
difference at age of menarche between both group.
In this study, 1823 girls aged between 18 - 24 (born
between 1977 - 1983) responded to the
questionnaire. The mean age of menarche for these
girls was 13.79 ± 1.23 years. Minimum age of
menarche was 9 years old and maximum age was 17
years old, only 0.1% having their menarche at age
of 9 years and 1.2% having at age of 17 years,
approximately 60% of this group having their
menarche at the age of 13 and 14 years (Table 1).
Seven hundred eighty-nine women with the age of
40 years and above, has the mean menarche age of
13.64 ± 1.32 years and a menarche age of 10-17
years. Only 0.9% having their menarche age at 10
years and 2% at age of 17 years, and approximately
60% at age of 13 and 14 years (Table 1). These
results was not statistically significant and
indicating that there are no change in menarche age
in Jordanian girls now and 20 years ago. The
calculated age at menarche in this study is
comparable to the age at menarche reported on
countries of similar culture and geographical
location.3-5 However, it is higher than the age at
menarche reported from European and North
American societies. The age at menarche for the 2
groups is not different, indicating that there is a
trend toward a decrease in the age at menarche in
the last few decades. The sampling procedure allow
some bias to occur. The invited haphazard
participation allows bias due to non-responders. In
the second group, a bias due to recall could occur
due to a longer period. The aim of this study was to
determine the average age at menarche in Jordan,
which is an important issue in school health
planning among females. The presence of a
decreasing trend with time is an important
observation that require periodic revision of health
plan. However, this was not demonstrated in this
study.
N of girls having menarche each year
Mean
Age
13.79
99 (12.5) 256 (32.4) 214 (27.1) 116 (14.7) 55 (6.9) 16 (2) 789 (100) 13.64
Y - years
 Age of menarche in Jordanian girls
Acknowledgment. We are grateful to Dr. M.
Ammari in collecting the data.
Received 10th June 2003. Accepted for publication in final form 13th
September 2003.
From the Department of Medicine, Jordan University of Science and
Technology, Irbid, Jordan. Address correspondence and reprint
requests to Dr. Fawaz Ammari, Department of Medicine, Jordan
University of Science and Technology, PO Box 3030, Irbid 22110,
Jordan. Tel/Fax. +962 (2) 7095010. E-mail:
dr_fammari@hotIntroduction
References
1. Saar E, Shalev C, Dalal I, Sod-Moriah UA. Age at
menarche: The influence of environmental condition. Int J
Biometeorol 1988; 32: 33-35.
2. Manniche E. Age at menarche: Nicolai Edvard Ravn’s data
on 3385 women in mid-19th century Denmark. Ann Hum
Biol 1983; 10: 79-82.
3. Attallah NL, Matta WM, El-Mankonshi M. Age at
menarche of schoolgirls in Khartoum. Ann Hum Biol
1983; 10: 185-188.
4. Kak G, Auxiliadora de Sonata Cruz C,
Velazquez-Melendez G. Secular trend in age at menarche
for women born between 1920-1979 in Rio de Janeiro,
Brazil. Ann Hum Biol 2000; 27: 423-428.
5. Floris G, Murgia E, Sancia GM, Sanna E. Age at menarche
in Sardinia (Italy). Ann Hum Biol 1987; 14: 285-286.
-----------------------------------------------------------------------------
Barbexaclone use in pregnancy
Fusun Yaris, MD, PhD, Mine Kadioglu, MD,
Murat Kesim, MD, Cunay Ulku, MD,
Ersin Yaris, MD, PhD, Nuri I. Kalyoncu, MD
rug exposure in pregnancy is a complex problem
D for obstetricians. Epilepsy is the most common
serious chronic neurological condition with a
prevalence of 4-10/1000, and most of epileptic
patients, including women of childbearing years
(25% of total epileptic populations), require
treatment with anti-epileptic drugs. Due to potential
teratogenic side effects of the antiepileptic drugs,
risks and benefits of the drugs must be assessed for
both the mother and fetus.1,2 Barbiturates and
phenytoin are particularly associated with
congenital heart malformations, facial clefts and
some other malformations.1,3 Barbexaclone is a
levopropylhexedryn salt of barbiturate, and no
available data are present in the literature about
pregnant women, who used barbexaclone alone or
in combination with any other drug. We are
reporting on a patient who used barbexaclone for 2
years before pregnancy and during the first 10
weeks of the pregnancy. A physician, was unaware
of the pregnancy, and prescribed the drug.
A 36-year-old caucasian woman, multigravida
case had begun to use barbexaclone 300 mg/day and
oxcarbazepine 600 mg/day, for 2 years before the
pregnancy, due to epilepsy and continued to use
both drugs until the end of week 10 of her
pregnancy. When she became aware of pregnancy,
she decided to quit taking barbexaclone with our
recommendation, as there was no data regarding this
drug regarding human or animal pregnancy.
Oxcarbazepine 1200 mg/day was continued until the
end of pregnancy. She did not use folic acid before
or during the pregnancy. No clinical worsening in
epilepsy was observed after withdrawal of
barbexaclone. She had a history of one therapeutic
abortion due to carbamazepine use and one
spontaneous abortion. All obstetrical and
ultrasonographical findings of the present pregnancy
were found normal. Due to maternal serum
alpha-fetoprotein was low (0.36 MoM; Multiples of
Median) in the sixteenth week, the case underwent
amniocentesis. No chromosomal abnormality was
found by amniocentesis in the eighteenth week. The
patient elected to have sectio delivery at 37 weeks
of gestation and had a female infant (3.2 kg, 49 cm)
with APGAR scores of 9 and 10, by an
uncomplicated delivery. The case continued to use
oxcarbazepine during the breast feeding period. The
baby was followed for 2 years, and no major
congenital abnormalities or minor malformations
were observed based on physical examinations. Her
physical, motor and mental development at 24
months of age was completely normal. Pregnancy
in epileptic women is known to be associated with a
higher risk of congenital malformations than
non-epileptic pregnant women. The offspring of
women with epilepsy are at increased risk for
congenital malformation, but the impact of the
various contributing factors remains unresolved.1,2
Bokhari et al4 reported strong association between
the presence of coned epiphyses in feet and hands,
but could not be considered a distinctive feature of
teratogenicity of phenytoin and phenobarbital. The
frequency of epileptic seizure may be altered by
pregnancy and seizures may cause complications in
pregnancy. Hypoxic conditions caused by epileptic
seizures may affect the fetus in a serious or negative
way.1,2 All these issues must be considered in the
treatment of epileptic pregnant women. The
incidence of malformations due to the use of
oxcarbazepine was found 8% and 5% in the drug
group and control groups in mice, and this
difference was not statistically significant.5
Carbamazepine, phenytoin and valproic acid have
been shown to be associated with teratogenicity, but
a lower risk was observed with oxcarbazepine
www.smj.org.sa Saudi Med J 2004; Vol. 25 (2) 245
 Barbexaclone use in pregnancy
compared to the other agents.1,5 As the first choice
drug, oxcarbazepine can be used as monotherapy at
the lowest effective dose in the treatment of
epileptic syndrome.1 Careful planning and
management of any pregnancy in women with
epilepsy is essential to increase the likelihood of a
healthy outcome for both mother and infant.1,2 In our
case, pregnancy had not been planned; antiepileptic
drugs were used during the first 10 weeks of the
pregnancy. After consultation among physicians
within our departments, we recommended that she
stop taking barbexaclone due to lack of data in the
literature regarding its effects on pregnant women.
In the light of the previous studies, we
recommended oxcarbazepine as a monotherapy that
could be taken throughout the remainder of her
pregnancy. Oxcarbazepine seems to be safer than
other available agents. Diet before conception and
during organogenesis should contain adequate
amounts of folic acid. This is valid also for pregnant
women using antiepileptic drugs, but our patient did
not elect to use folic acid upon our recommendation.
In the literature, this is the first case of an
observation of barbexaclone exposure in a pregnant
woman. We did not find any congenital anomaly in
the baby. This single case is not enough to define
the drug as "safe in pregnancy," but we wish to
share this information with the other physicians.
Received 28th July 2003. Accepted for publication in final form 20th
October 2003.
From the Department of Family Medicine (Yaris), Department of
Pharmacology (Kadioglu, Kesim, Ulku, Yaris, Kalyoncu), School of
Medicine, Karadeniz Technical University, Trabzon, Turkey. Address
correspondence and reprint requests to Dr. Murat Kesim, Department
of Pharmacology, School of Medicine, Karadeniz Technical University,
TR-61187, Tabzon, Turkey. Tel. +90 (462) 3775306. Fax. +90 (462)
3775498. E-mail: mkesim@meds.ktu.edu.tr
References
1. Morrow JI, Craig JJ. Anti-epileptic drugs in pregnancy:
current safety and other issues. Expert Opin Pharmacother
2003; 4: 445-456.
2. Barrett C, Richens A. Epilepsy and pregnancy: Report of an
Epilepsy Research Foundation Workshop. Epilepsy Res
2003; 52: 147-148.
3. Lindhout D, Omtzigt JG. Pregnancy and the risk of
teratogenicity. Epilepsia 1992; 33 Suppl 4: S41-48.
4. Bokhari A, Connolly S, Coull BA, Harvey EA, Holmes LB,
Bokhari A. Effects on toes from prenatal exposure to
anticonvulsants. Teratology 2002; 66: 122-126. (Erratum
in: Teratology 2002; 66: 348-349).
5. Bennett GD, Amore BM, Finnell RH, Wlodarczyk B,
Kalhorn TF, Skiles GL et al. Teratogenicity of
carbamazepine-10, 11-epoxide and oxcarbazepine in the
SWV mouse. Pharmacol Exp Ther 1996; 279: 1237-1242.
246 Saudi Med J 2004; Vol. 25 (2) www.smj.org.sa
No evidence of persistent
helicobacter pylori infection in
peripheral blood of patients with
coronary heart disease
Abdulaziz S. Al-Khattaf, MSc, PhD.
R .
ecently, it was proposed that coronary heart
disease (CHD) may be associated with chronic
helicobacter pylori infection.1 The data, however,
are conflicting since there are reports denying the
link between the 2 conditions. 2 Similarly, there have
been several claims of strong and significant
correlation between chronic H. pylori infection and
various vascular risk factors such as fibrinogen
concentration and white cell count.3 The presence of
high concentration of immunoglobulin G antibodies
to H. pylori has been associated with chronic gastric
infection.4 Association of chronic H. pylori infection
with CHD was established on the bases of the
evidence that antibodies against H. pylori were
detected in sera of 76.6% of patients with CHD.3
Since antibodies against H. pylori are also present in
the sera of other wise normal healthy individuals
and the significance of these antibodies in sera of
patients with CHD and their association with CHD
remains doubtful.5 In order to investigate the
association between persistent H. pylori infection
and CHD this study was performed to detect the
presence of H. pylori DNA in the peripheral blood
of patients with CHD by polymerase chain reaction
(PCR).
Sera from 20 male patients, with mean age of 54
± 5, diagnosed as having CHD according to the
World Health Organization criteria of non-fatal
myocardial infraction, and 12 healthy blood donors
with mean age of 56 ± 5 with no history of any
significant illness in the past were tested. Ten ml of
blood was collected by venipuncture in sterile tube,
and was allowed to clot at 40C for 2-4 hours. Serum
was separated from whole blood by centrifugation at
1200 x g for 20 minutes at room temperature, and
stored at –200C until used. Table 1 illustrates the
structural design of primers and capture probe used
in this study. The selection of primers and capture
probe was based on the sequence ure C, and had
been used in a previously published study.6
Serum sample was lysed using lysis buffer with
Proteinase K and was precipitated in ethanol, which
was followed by vacuum drying. In the first round
 Investigating Helicobacter pylori infection in peripheral blood of patients with CHD

of amplification, DNA was added to a master
mixture containing 0.4 mM of each primer and 0.2
mM of 4-deoxy nucleotide triphosphate (dNTP) in a
PCR reaction buffer (Roche) and denatured at 940C
for 10 minutes. The denatured product was then
cooled on ice, and 2.5 U taq polymerase was added
prior to 40 amplification cycles (940C for 1 minute,
550C for 1 minute and 720C for 1 minute).
Following the same protocol as for the first round,
the second round reaction (nested PCR) was
performed using the previously amplified DNA and
digoxigenin (DIG) labeled dNTPs (Roche).
Helicobacter pylori NCTC 11637 DNA and sterile
distilled water were incorporated in each run as
positive and negative controls. Samples were run in
duplicate and amplification was performed in a
9600 thermal cycler (Perkin Elmer). The cut off
value was assessed as mean value ± 2 standard
deviations as recommended by the manufacturer
(Roche).
The amplified DNA was then hybridized to a
specific capture probe that was complementary to
the inner part of the amplification product. Before
the hybridization this specific capture probe was
labeled with biotin to allow immobilization of the
hybrid (DNA-probe) to a streptavidin-coated
microtiter plate surface. The bound hybrid was
detected by an anti-DIG peroxidase conjugate using
colorimetric substrate 2,2'-Azino-d(3-ethyl-Benz
Thiazoline)-6-sulfonic acid (ABTS). Briefly, as
indicated by the manufacturer, 40 ml of
denaturation DNA solution was added to 20 ml of
amplification product. After 10 minutes of
incubation at room temperature, hybridization
solution containing biotinylated probe at an optimal
concentration was added to a volume of 500 ml.
Two hundred microliters of this mix was added to
the appropriate wells. Hybridization took place at
500C under mild agitation for one hour. After
hybridization, the plates were washed and 200 ml
of anti-DIG-peroxidase solution was added. The
plates were incubated at 370C for 30 minutes and
then washed prior to the addition of 200 ml of
ABTS substrate solution to each well. After 30
minutes of incubation at 370C, the OD405 was read in
Titertek Multiskan Plus (Labsystems, Finland). A
blank (ABTS substrate solution), a negative
detection control (water), a positive labeling control,
a PCR - enzyme-linked immunoabsorbent assay
(ELISA) blank-negative control, and a PCR positive
control (H. pylori DNA) were tested at the same
time. Table 2 shows the results of the PCR-ELISA
of 20 patients with CHD and 12 normal controls. No
evidence for the presence of DNA was found in sera
of either patients with CHD or normal controls.
Since all the OD405 obtained were below the cut off
value OD405 0.2 nm. Despite reports linking H.
pylori infection with CHD, this study failed to
demonstrate the presence of H. pylori DNA in the
peripheral blood of patients with CHD. Detection of
H. pylori DNA was prompted by the fact that the
presence of antibodies against H. pylori in
peripheral blood has been linked with the presence
of H. pylori gastric infection. On the contrary, CHD
association with the antibodies against H. pylori in
peripheral blood is not strong and there is no
deference in serum antibody titers between CHD
patients and normal controls.3 Moreover, reliance
on antibody detection for present infection has
drawbacks. Serum antibody titer elevated long after
successful treatment for H. pylori and their presence
in the peripheral blood may not necessarily indicate
a persistent H. pylori infection.4 Detection of H.
pylori DNA in the peripheral blood would therefore
be more useful approach to obtain a confirmed
evidence of the existence of H. pylori in peripheral
blood. In a similar study using nested PCR, no
evidence of H. pylori infection in the peripheral
blood of patients with CHD was found which was in

Table 1 - Primers and probe used in the identification of ure C (glmM) gene of H. pylori in the nested PCR-ELISA technique.

Primers and probe Sequence of the ure C (glmM) gene Position

Round 1
Primer 1 5’-AAG CTT TTA GGG GTG TTA GGG GTT T-3 F1 784 - 808
Primer 2 5’-AAG CTT ACT TTC TAA CAC TAA CGC-3’ R1 1054 - 1085

Round 2
Primer 1 5’-CTT TCT TCT CAA GCA ATT GTC-3’ F2 829 - 849
Primer 2 5’-CAA GCC ATC GCC GGT TTT AGC-3’ R2 1012 - 1032

Capture probe 5’- AGA ATT GAA GCA TTG CGC GAT TGG GGA TAA GTT TGT GAG CGA AT-3’ 904 - 946

F - forward amplification (original template), R - reverse (complementary) amplification,

PCR-ELISA - polymerase chain reaction - enzyme-linked immunoabsorbent assay, H. pylori - helicobacter pylori

www.smj.org.sa Saudi Med J 2004; Vol. 25 (2) 247

 Investigating Helicobacter pylori infection in peripheral blood of patients with CHD

Table 2 - Polymerase chain reaction - enzyme-linked patients there is no evidence of persistent H. pylori
immunoabsorbent assay screening sera of patient with
CHD and healthy normal controls for the presence of H. infection at least in the peripheral blood.
pylori DNA. Received 7th June 2003. Accepted for publication in final form 27th
September 2003.

From the Department of Pathology, College of Medicine, King Khalid

Patient Age od (nm) Healthy Age od (nm) University Hospital, King Saud University, Riyadh, Kingdom of Saudi
samples controls Arabia. Address correspondence and reprint request to: Dr. Abdulaziz
S. Al-Khattaf, Assistant Professor (Microbiology), Department of
Pathology (32) College of Medicine, King Khalid University Hospital,
PO Box 2925, Riyadh 11461, Kingdom of Saudi Arabia. Tel. +966 (1)
1 61 0.170 1 59 0.152 4679208. Fax. +966 (1) 4672462. E-mail: alkhattaff2@hotmail.com
2 57 0.118 2 54 0.134
3 59 0.136 3 63 0.164
4 64 0.131 4 61 0.169 References
5 56 0.144 5 54 0.146
6 48 0.162 6 49 0.132
7 55 0.157 7 62 0.170 1. Pieniazek P, Karczewska E, Duda A, Tracz W, Pasowicz
8 62 0.163 8 55 0.150 M, Konturek S. Association of Helicobacter pylori infection
9 49 0.148 9 56 0.149 with coronary heart disease. J Physiol Pharmacol 1999;
10 52 0.136 10 51 0.167 50: 742-751.
11 48 0.133 11 48 0.134 2. Ossewaarde J, Feskens E, De Vries A, Vallinga C,
12 53 0.141 12 63 0.165 Kromhout D. Chlamydia pneumoniae is a risk factor for
13 62 0.140 coronary heart disease in symptom-free elderly men, but
14 50 0.133
15 56 0.142 Helicobacter pylori and Cytomegalovirus are not.
16 59 0.153 Epidemiol. Infect 1998; 120: 93-99.
17 48 0.170 3. Patel P, Mendall M, Carrington D, Strachan D, Leatham E,
18 54 0.170 Molineaux N et al. Association of Helicobacter pylori and
19 49 0.129 Chlamydia pneumoniae infections with coronary heart
20 56 0.139 disease and cardiovascular risk factors. BMJ 1995; 311:
Mean ± SD 54 ± 5 0.137± 0.01 56 ± 5 0.153 ± 0.01 711-714.
4. Hirschl A, Rotter M. Serological tests for monitoring
Helicobacter pylori eradication treatment. J Gastroenterol
PCR-ELISA - polymerase chain reaction - enzyme-linked 1996; 31: 33-36.
immunoabsorbent assay, od - optical density 5. Danesh J, Koreth J, Collins R, Ranjit Arnold J, Balarajan Y,
CHD -coronary heart disease, SD - Standard deviation McGee J et al. Fast-track communication: is Helicobacter
pylori a factor in coronary atherosclerosis? J Clin
Microbiol 1999; 37: 1651.
6. Kerr JR, Al-Khattaf A, Barson AJ, Burnie JP. An
association between sudden infant death syndrome (SIDS)
agreement with the findings of this study.5 The and Helicobacter pylori infection. Arch Dis Child 2000; 83:
429-434.
absence of H. pylori DNA in the peripheral
circulation of patients with CHD observed in this -----------------------------------------------------------------------------
study therefore it shows that H. pylori is not present
in peripheral blood of patients with CHD. Markers Suicide after treatment of
have reported suggesting the presence of chlamydia chloroquine-resistant falciparum
pneumoniae in coronary atheroma of patients with
CHD. It would therefore be quite relevant to malaria with quinine
examine the atheromas for the presence of H. pylori
infection to establish the link between H. pylori Ishag Adam, MD, Mustafa I. Elbashir, MD, PhD
infection and CHD.6 This study was performed
Occasionally,
using a simple practical, reliable, and sensitive unusual patterns of clinical
colorimetric hybridization assay for the detection of manifestations of falciparum malaria involving
amplified H. pylori DNA. The assay was a the central nervous system are seen in Sudan.1
combination of a sensitive DNA hybridization Chloroquine is still regarded the first line treatment
reaction and a colorimetric protocol, similar to those for falciparum malaria, although more than 70%
of conventional enzyme immunoassays, widely used resistance on the drug was reported in Khartoum
in routine clinical microbiology laboratories. The and in Eastern Sudan.2
urease gene region ure C (glmM) of H. pylori was A 27-year-old male presented to New Halfa
targeted, which is considered to be a suitable target Teaching Hospital, Sudan complaining of fever,
site for quantitative PCR due to its high level of sweating, headache, vomiting, and backache for 10
expression. Moreover, the ure C (glmM) has also days. He completed the full course of chloroquine 7
been shown to be more sensitive and specific for days before reporting to the hospital. His weight
detection of H. pylori infection.6 Failure to detect H. was 58 kg, fully conscious, with pulse rate of
pylori DNA among CHD patient specimens in this
study by using a highly reliable, sensitive and 95/minute, blood pressure of 110/70 mm HG,
specific technology supports the notion that in CHD temperature of 38.70C, with clear chest and there

248 Saudi Med J 2004; Vol. 25 (2) www.smj.org.sa

 Suicide after treatment of chloroquine-resistant falciparum malaria with quinine
was no palpable spleen or liver. His hemoglobin
was 10.5 g/dl. The blood film confirmed the
diagnosis of falciparum malaria. He started on 600
mg of quinine, as infusions in 5% dextrose, to be
given 3 times daily until vomiting stops. Five hours
later, in the early morning, the patient was found
dead after hanging himself with his turban (Umama)
in the corridor. We dug deep in the family and
social history, and we found that he was a farmer,
living a stable family life with his wife and 2
children and no history of mental illness.
Malaria can lead to acute psychosis, personality
changes, amnesia, ataxia, apathy and depression.3
Acute psychosis with transient encephalopathy was
reported with mefloquine treatment, which is
chemically related to quinine.4 However, quinine
itself was considered among the drugs, which
should be considered in case of suicide or
attempting to do so.5 This patient was found
hanging himself after the first dose of quinine, there
is a remote possibility of hypoglycemia; hence, the
explanation of mental changes. Falciparum malaria
has been reported to cause hypoglycemia, either
directly or as side effect of quinine, thus, this direct
or indirect hypoglycemia can lead to mental changes
and suicide.
Received 29th July 2003. Accepted for publication in final form 19th
September 2003.
From the Department of Obstetrics and Gynecology (Adam), New Halfa
Teaching Hospital, and the Department of Biochemistry (Elbashir),
Faculty of Medicine, University of Khartoum, Sudan. Address
correspondence and reprint requests to Dr. Ishag Adam, Associate
Professor and Consultant Obstetrics and Gynecologist, PO Box 61,
New Halfa, Sudan. Tel. +249 (421) 22101. Fax. +249 (421) 22070.
E-mail: ishagadam@hotmail.com
References
1. Abdalla MN, Sokrab TE, Zaidan ZA, Siddig HE, Ali ME.
Post-malaria cerebellar ataxia in adult Sudanese patients.
East Afr Med J 1997; 74: 570-572.
2. Adam I, Elhadi M, Ahmed G, Elbasheir M. In Sudan.
Chloroquine resistance is worsening and quinine resistance
is emerging. Sudan Med J 2001; 39: 1-5.
3. Dugbartey AT, Dugbartey MT, Apedo MY. Delayed
neuropsychiatric effects of malaria in Chana. J Ner Ment
Dis 1998; 186: 183-186.
4. Phillips-Howard PA, ter Kuile FO. CND adverse events
associated with antimalarial agents. Facts or Fiction? Drug
Saf 1995; 12: 370-383.
5. Goldenberg AM, Wexler LF. Quinine overdose: Review of
toxicity and treatment. Clin Cardiol 1998; 11: 716-718.
www.smj.org.sa Saudi Med J 2004; Vol. 25 (2) 249