Eczema

Philippine Dermatological Society

Rm. 1015, Front Tower, Cathedral Heights Building
St. Luke’s Medical Center, E. Rodriguez Avenue
Quezon City, Philippines 1102
Telephone No.: 723-0101 loc 2015
Telefax No.: 727-7309
E-mail: pds_org@pldtdsl.net
Website: www.pds.org.ph

Officers and Board of Directors

2009-2010
President Georgina C. Pastorfide, MD
Vice-President Ma. Teresita G. Gabriel, MD
Secretary Rosalina E. Nadela, MD
Treasurer Lonabel A. Encarnacion, MD

Immediate Past President Arnelfa C. Paliza, MD

Board of Directors Bernadette B. Arcilla, MD

Marcellano S. Cruz, MD
Evelyn R. Gonzaga, MD
Daisy K. Ismael, MD
Eleanor L. Letran, MD
Ma. Juliet E. Macarayo, MD
Cecilia R. Rosete, MD

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CPM 12TH ED ECZEMA EllenJan7.ind185 185 01/26/2010 10:44:09 AM

 Eczema
Diagnosis and Treatment of Eczema
Eczema (or eczematous dermatitis) is a general term that
encompasses a set of etiologically heteregenous inflam-
matory conditions of the skin characterized as superficial
erythematous, papulovesicular eruptions which often lead
to serous exudation and crusting. These lesions appear
and evolve in a very similar manner. These inflammatory
skin conditions are among the top ten common consults
in a physician’s clinic.
Common Features of Eczematous Dermatitis (ED)
1. ACUTE STAGE: The primary clinical presentation
of acute ED begins with an itchy edematous and red
patch which then develops fluid-filled vesicles which
may later coalesce to become larger bullae. When
these vesicles or bullae erupt and become eroded,
they become more pruritic with occasional pain and
edema.
2. SUBACUTE STAGE: Almost immediately, secondary
changes develop. The fluid filled vesicles or blisters
turn into a wet crust, then into a dry scab, resulting in
a dry, scaly patch.
3. CHRONIC STAGE: The inevitable scratching and
excoriations of the itchy patch lead to varying degrees
of infection which further lead to thickening or licheni-
fication, and post-inflammatory hyperpigmentation or
hypopigmentation of the involved skin. The series of
primary and secondary changes re-occur at the initial
patch, or spread to other areas depending on the
continued activity or presence of the primary cause
in subacute ED.
B. COMMON TYPES OF ECZEMA
Classification of eczema is largely empirical, and in most
circumstances, the diagnosis is based only on clinical
findings. There are many types of eczema recognized
clinically and are discussed below.
1. Atopic Dermatitis
2. Contact Dermatitis
3. Dyshidrotic Dermatitis
4. Nummular Dermatitis
5. Asteatotic Dermatitis
6. Stasis Dermatitis
I. ATOPIC DERMATITIS
DEFINITION
• Chronic inflammatory skin disease that usually oc-
curs in persons with a personal or family history of
other atopic conditions, such as asthma and allergic
rhinitis.
• Lifetime prevalence is 10–20% in children and 1–3%
in adults
• Prevalence has increased two- to three-fold over the
last 30 years in industrialized countries
• A family history of atopic disease remains the strongest
predictor for the development of AD
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CPM 12TH ED ECZEMA EllenJan7.ind186 186
CLINICAL FEATURES
Infantile phase
• Lesions most commonly start on the face (Figure 1);
often spare the ‘napkin area’
• When the child begins to crawl, the extensor surfaces
of the knees can be involved
• Chronic, fluctuating course, varying with factors such
as teething, infections, emotional upset and climate
changes
Childhood Phase
• Lesions commonly involve the elbow (Figure 2) and
knee flexures(Figure 3), the sides of the neck, the wrists
and the ankles
• Hand involvement is sometimes associated with nail
changes (pitting and ridging)
• Acute vesiculation should always suggest the possibility
of bacterial or viral infection.
Adult phase
• Similar to the childhood phase, although erythroderma
is more common
CAUSES
• Multifactorial
• 70% have family history
• Related to mutations in fillagrin (FLG) gene
• Positive food allergy tests are common in children with
AD, but skin prick testing and RASTs poorly predict
actual food reactions in patients.
DIAGNOSIS
• Seldom aided by investigations
• Serum IgE, specific radioallergosorbent tests (RASTs)
and prick tests usually only confirm the atopic diathesis
• 20% of individuals with atopic dermatitis have normal
IgE levels and negative results on RASTs
• Bacteriology to identify bacterial infection and potential
antibiotic resistance
• Viral swab if herpes simplex infection (eczema herpe-
ticum, Figure 4) is suspected.
• Patch-testing is particularly useful in adults to identify
contact allergens responsible for deterioration of atopic
dermatitis.
Figure 1. Infantile AD with facial involvement
01/26/2010 10:44:10 AM

Figures 2 & 3. Childhood AD with involvement of the flexural
areas
SPECIAL CONSIDERATIONS FOR THERAPY OF
ATOPIC DERMATITIS
FIRST-LINE TREATMENT
1. Reduction of trigger factors – atopic dermatitis can be
aggravated by various trigger factors.
• Environmental Control
• Contact allergy: consider this if exacerbation of
previously controlled eczema or patient reacts to
topical treatments.
• Infection: both bacterial (Staphylococcus aureus
and Streptococcus) and viral (herpes simplex) can
worsen eczema.
• House dust mites: reduction of exposure by regular
cleaning of the home by means of vacuuming and
damp dusting may be helpful. Animal dander also
can aggravate atopic dermatitis.
2. Bathing and emollients
• Most patients have dry skin and avoidance of deter-
gents is important.
• Soap substitutes and emollients can improve skin
hydration and barrier function.
3. Topical corticosteroids
• Principal treatment for the inflammation and pruritus
of atopic dermatitis
• Less potent topical corticosteroids should be used
on the eyelids, face and flexural areas
• Shorter periods of medium-potency topical corti-
costeroid use are as effective as a longer course of
low-potency corticosteroids in controlling AD flares.
Maintenance therapy follows once disease has been
stabilized.
4. Antihistamines
• Sedating antihistamines are useful in patients with
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CPM 12TH ED ECZEMA EllenJan7.ind187 187
Eczema
nocturnal itching, but can cause drowsiness the next
morning.
• Non-sedating antihistamines have limited effective-
ness for pruritus in AD.
SECOND-LINE TREATMENT
1. Topical immunomodulators (tacrolimus and pime­
crolimus)
• Approved for intermittent use in mild-to-moderate
disease in patients aged 2 years or above.
• Useful for maintenance therapy after establishing
acute control of disease flares with topical corticoste­
roids.
• Especially helpful in head and neck dermatitis where
steroid use should be limited.
2. Phototherapy (UVB) or photochemotherapy (psoralen
UVA)
• Beneficial in adult atopic dermatitis that is unres­
ponsive to topical treatment or so widespread that
topical treatment is impractical.
• Broadband UVA and UVB, narrowband UVB, combi-
nation UVAB, oral and bath psoralen plus ultraviolet
A (PUVA), and UVA1 have all shown clinical safety
and efficacy in the treatment of AD.
THIRD LINE TREATMENT
1. Systemic corticosteroids – although oral corticoste­
roids are effective for acute exacerbations of derma-
titis, they are seldom used as continuous treatment.
2. Systemic immunosuppressant therapy
• Reserved for severe, recalcitrant cases
• Before starting therapy, the long-term side effects
should be discussed.
• Cyclosporin is most studied; an intermittent, 12-week
course of cyclosporine at dose levels of 5 mg/kg has
been shown to be effective. Side effects include:
hypertension and renal toxicity.
• Azathioprine is effective in severe atopic dermatitis,
but has a slow onset of action (usually 4–6 weeks)
and can cause bone marrow suppression.
PROGNOSIS
• Although there is currently no cure for atopic dermatitis,
various interventions can control symptoms. The condi-
tion can be expected to clear in 60–70% of children by
their early teens, although relapses may occur.
• The mainstay of preventive therapy is avoidance of skin
irritation and dryness. Adults with atopic dermatitis are
advised to avoid occupations such as car mechanic,
hairdresser and nurse.
OTHER SUPPLEMENTAL THERAPIES
• There is no definitive evidence that routine diet restrict­
ion or allergen avoidance has a role in the treatment
of AD except in cases where acute clinically relevant
reactions have occurred.
• Studies regarding breastfeeding as a primary prevent­
ive measure in AD have not shown a consistent protect­
ive effect.
• Breastfeeding during the first 4 months has a protective
effect when compared with cow’s milk, but on its own
does not constitute an effective prevention strategy.
• The preventive effects of probiotics on AD may appear to
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01/26/2010 10:44:11 AM
 Eczema
extend beyond infancy although further studies needed. prognosis
• Preliminary studies of massage therapy, hypnotherapy, • Topical treatment
and biofeedback have been encouraging. • indicated for mild cases of contact dermatitis
• Systemic treatment
II. CONTACT DERMATITIS • Indicated for control of itching even in cases of
limited extent.
CLINICAL FEATURES • Also indicated for moderate to severe acute and/or
• Altered state of skin reactivity induced by exposure to chronic contact dermatitis.
an external agent.
• 2 TYPES:

1. ALLERGIC
- Immunologic: Represents a delayed (type IV)
hyper­sensitivity reaction to the over 3700 allergens
reported
- Exogenous chemicals that have been described
to provoke this reaction

2. IRRITANT
- Non-immunologic: Based on the irritability of the
skin and amount of the contactant
- Direct tissue damage results from contact with
irritants Figure 4. Dermatitic plaque in the peri-umbilical area due to
• Airborne CD due to contactants affect exposed areas, nickel allergy
spare covered areas; with involvement of eyelids, inner
arms creases of the neck.
• Clothing-related allergens affect covered areas es-
pecially posterior aspect of neck, upper back, lateral
thorax, flexor surfaces, axilla (Figures 4 & 5)

CAUSES

• COMMON CONTACT ALLERGENS:

o METALS: chrome, nickel
o PERFUME INGREDIENTS
o RUBBER CHEMICALS
o DYES: formaldehyde
Figure 5. Erythematous scaly plaque in the neck area due to
• STRONG CONTACT IRRITANTS: necklace
o ETHYLENE OXIDE
o HYDROFLUORIC ACID
o WET CEMENT III. NUMMULAR DERMATITIS

• MILD TO MODERATE CONTACT IRRITANTS: CLINICAL FEATURES

o Soaps, solvents, detergents, fiberglass, metalwork-
ing fluids, bleaches, grease removers, insecticides,
fertilizers, rodenticides, waxes, polishers
DIAGNOSIS
1. Patch testing
- standardized diagnostic procedure of choice for
contact dermatitis
2. Skin Biopsy: dermal infiltrate with marked eosinophilia
3. In vitro lymphocyte stimulation tests, migration inhibition
factor, and other laboratory tests of lymphokine pro-
duction remain investigational tools that at present are
insufficiently standardized to allow clinical application.
TREATMENT
• Identify contactant by history or by patch testing
• Observe for prompt improvement when contactant is
discontinued, slow or no improvement when another
cross-reacting product is still used.
• Use barrier creams including petrolatum jelly when
exposure to contact allergen cannot be avoided, or use
cotton gloves under plastic gloves, not rubber gloves
• Irritants: forceful and prolonged irrigation with water
• Complete healing may take 4 weeks, with a good
188
• Also known as discoid eczema; a chronic disorder of
unknown etiology
• Acquired and multifactorial; rare in children
• Some worsen in summer, exacerbated by heat and
humidity
• Single, multiple or episodic, and recurrent at previously
affected sites
• Start out as papules and papulovesicles coalescing
to form well-demarcated, coin-shaped plaques with
pinpoint oozing, crusting, and scale (Figure 6)
• Plaques range from 1 to 3 cm in size
• Pruritus varies from minimal to severe
• Most common sites of involvement are upper extremi-
ties, including the dorsal hands in women, and the lower
extremities in men
CAUSES
The following may cause flare-ups:
• Wool
• Topical medicines: topical steroids
• Drugs: gold, methyldopa, streptomycin, aminosalicylic
acid, INH

CPM 12TH ED ECZEMA EllenJan7.ind188 188 01/26/2010 10:44:13 AM


DIAGNOSIS
1. Serum immunoglobulin E levels are normal
2. Skin Biopsy
a. Acute: spongiosis, with or without spongiotic micro-
vesicles.
b. Subacute: parakeratosis, scale-crust, epidermal hy-
perplasia, and spongiosis with mixed cell infiltrates
c. Chronic: may resemble lichen simplex chronicus
3. Patch testing
• may be useful in chronic recalcitrant cases to rule
out a superimposed contact dermatitis
TREATMENT
• Topical steroids in the mid- to high potency range are
the mainstay of treatment
• Topical calcineurin inhibitors, tacrolimus and pime-
crolimus, and tar preparations are also effective
• Emollients can be added adjunctively if there is ac-
companying xerosis.
• Phototherapy with broad or narrow band ultraviolet B
may be beneficial
• Trial of suspected allergen withdrawal and/or challenge
• Treatment of suspected or identified infection: bacterial
or fungal
• Improve ambient humidity
• Avoid skin-drying conditions like overuse of air-condi-
tioning and contact with water (e.g. water compresses)
• Oral antihistamines are useful if pruritus is severe
Eczema
COMMON CONTACTANTS:
- Nickel, chrome, PPDA, fragrance,balsams
- Neomycin
- Poison oak or ivy related to mango, lacquer tree oil for
furniture, cashew nut shells
- Implanted metals
- Secondary to distant focus of infections which clear
when primary is treated:
• Fungal: dermatophytid
• Bacterial: bacterid
DIAGNOSIS
1. Elevated serum IgE demonstrates atopic back-
ground
2. KOH/fungal culture of skin scrapings to rule out fungal
infection
3. Giemsa staining to rule out viral infection
4. Gram stain and bacterial culture if bacterial superinfec-
tion is suspected
5. Skin Biopsy: Eczematous Dermatitis with mild eosi-
nophilia
TREATMENT
• Does not respond well to treatment
• Intact, large blisters can be drained, but should not be
unroofed
• Avoidance of commonly encountered allergens, such
as foods and plants, and irritants (e.g. soaps, solvents,
acids, and alkalis, can be helpful
• Treatment of suspected or identified infection: bacterial
or fungal
• Use of pure cotton gloves for dry work, plastic or rubber
glove on top of cotton gloves for wet work
• For maintenance, frequent use of emollients helps to
preserve normal skin barrier function

Figure 6. Nummular Eczema. Coin-shaped plaques on the arms

IV. DYSHIDROTIC DERMATITIS (a.k.a. pompholyx) Figure 7. Tapioca-like vesicular eruption on lateral surface of
fingers
CLINICAL FEATURES

• Acute and/or chronic dermatitis clinically characterized

by small vesicles to large blisters on the sides of fingers
with or without palms or soles
• Discomfort and itching usually precede the develop-
ment of the blisters, which have been described as
having a “tapioca” appearance (Figures 7 & 8)
• Blisters may coalesce then desiccate and resolve
without rupture
• Affects adolescents and young adults
• Secondary infections common

CAUSES

Can be endogenous (intrinsic) or exogenous (due to Figure 8. Vesicular eruption of the soles with superimposed
contactants) bacterial infection

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CPM 12TH ED ECZEMA EllenJan7.ind189 189 01/26/2010 10:44:15 AM

 Eczema
V. ASTEATOTIC DERMATITIS • Venous thrombosis from pelvic/lower abdominal op-
erations, prolonged recumbency, leg injuries, varicose
CLINICAL FEATURES veins, thrombophlebitis
• Multiple pregnancies
• Acquired dermatitis superimposed on xerosis usually • Heredity for incompetent valves, causing backflow of
found in the elderly during cold seasons blood
• Manifests as dry, fissured skin with fine scale • Common in wheelchair bound patients
• Primarily on the extensor aspects of the limbs and • All other situations with decreased muscle pump func-
trunk tion for assisting blood return
• May be extremely pruritic
DIAGNOSIS
CAUSES OF XEROSIS
1. Venous Ultrasonography to rule out deep venous
- Aging thrombosis (DVT) in cases with acute onset
- Post-inflammatory change 2. Skin Biopsy shows dilated capillaries with thick walls,
- Post-use of irritants abundant melanin and hemosiderin pigment deposi-
tion
- Low ambient humidity from seasonal change of
weather, prolonged airline flights, air-conditioning TREATMENT
- Frequent bathing using soaps with high or alkaline
pH • Weight reduction
- Diminished use of emollients • Minimize trauma especially from excoriations
- Familial tendency for dry skin • Decrease venous hypertension
Occasionally a presenting sign of hypothyroidism, - Use of support hose for prevention of varicosities in
lymphoma, other systemic diseases those with family history for varicosities
• Avoid irritants and contactants including antibiotic,
DIAGNOSIS stabilizer and steroid ingredients in topical medica-
tions
1. Usually clinical diagnosis
2. Skin Biopsy: Hyperkeratosis with a thin granular layer
similar to Ichtyosis
3. Thyroid function tests
4. Organs check-up as indicated by history and physical
examination

TREATMENT

• Responds to application of medium-potency topical

steroid ointments and/or liberal application of emol-
lients.
• Use emollients liberally, frequently and massage well
into moistened skin
• Correct hyperthyroidism medically
• Correct environment to increase humidity in regards to
use of air conditioning/fans.
• Wrap with flexible plastic overnight to increase moisture Figure 9. Hyperpigmented scaly plaque with ulceration.
content of skin
• Diminish use of soaps
B. GENERAL GUIDELINES FOR TREATMENT OF
ECZEMAS
V. STASIS DERMATITIS

CLINICAL FEATURES I. TOPICAL

• Acquired, due to chronic venous insufficiency A. STEROIDAL PREPARATIONS

• Characterized by erythema, scaling, oozing, crusting
and pigmentary changes
• Often with pruritus and eczematous changes from
scratching and topical medicines used
• Typically occurs in the medial supramalleolar region
where microangiopathy is most intense
• Lesions may lichenify or ulcerate over time (Figure 9)
CAUSES OF POOR VENOUS DRAINAGE
• Obesity
• Trauma
190
• Anti-inflammatory medications
• Ointments (oil-based) are more effective than
creams, although creams and lotions (water-
based, not alcoholic) are useful when the skin is
inflamed.
• Use topical steroids according to strength and
class (See Table 1).
• Cutaneous complications such as striae, atrophy,
and telangiectasia limit the long-term use of these
agents.

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TABLE 1. POTENCY RANKING OF SOME COMMONLY
USED TOPICAL CORTICOSTEROIDS
Adapted from Fitzpatrick’s Dermatology in General Medicine Fifth Edition
CLASS GENERIC NAME
Very High Betamethasone dipropionate-augmented • Systemic corticosteroids are known to be ef-
Potency 0.05% - ointment
I Clobetasol propionate 0.05% - cream
and ointment
igh Potency Betamethasone dipropionate 0.05% - ointment
H limiting.
II Fluocinonide 0.05% - cream and ointment
Mometasone furoate 0.1% - ointment
III Betamethasone dipropionate 0.05% - cream
Betamethasone valerate 0.1% - ointment
Fluticasone propionate 0.005% - ointment
id Potency Fluocinolone acetonide 0.025% - ointment
M
IV Mometasone furoate 0.1% - cream
Triamcinolone acetonide 0.1% - cream
V Betamethasone valerate 0.1% - cream
Fluocinolone acetonide 0.025% - cream
Fluticasone propionate 0.05% - cream
Low Potency Desonide 0.05% - cream and ointment
VI
VII Hydrocortisone or hydrocortisone acetate 1% -
cream and ointment
Hydrocortisone aceponate 0.12% - cream
B. TOPICAL CALCINEURIN INHIBITORS (TCI)
• Tacrolimus 0.1% and 0.03% Ointment (PROTOPIC)
and Pimecrolimus 1% Cream (ELIDEL)
• Can be prescribed for patients of 2 years and
upwards for the treatment of moderate to severe
eczema that is unresponsive to conventional
therapy
• Should not be used under occlusion
• Side effects of usage are:-
• Infection particularly herpes maybe increased
• Burning sensation of the skin, usually temporary
• Occasional inflammatory flare
• Benefits: no atrophy; can be used on the face;
longer time to relapse
II. SYSTEMIC
A. ANTIHISTAMINES
• Bedtime: sedating antihistamines
e.g., Hydroxy­zine or Benadryl
• Daytime: non-sedating antihistamine
e.g., Cetirizine, Loratadine
• Role of antihistamines in controlling itching in
eczema remains to be defined
• For patients with significant sleep disruption
due to itch, allergic dermatographism, or allergic
rhinoconjunctivitis, sedating antihistamines may
be useful.
B. ANTIBIOTICS
• Oral antibacterials or antifungals if infected; or, to
reduce bacterial or fungal population of dermatitic
skin
• Oral anti-viral medications when viral infections
occur
• Without signs of infection, oral antibiotics general­
ly have a minimal therapeutic effect on the
dermatitis
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CPM 12TH ED ECZEMA EllenJan7.ind191 191
Eczema
C. INTRALESIONAL STEROID
• Employed to rapidly thin down thick dry patches
D. IMMUNOMODULATORY DRUGS
fective in the short-term treatment of eczemas,
but no evidence exists to support their use, and
rebound flaring and long-term side effects are
• Cyclosporine is effective in the treatment of
severe AD, but its usefulness may be limited by
side effects.
• Conflicting data exist about the efficacy of azathio­
prine, mycophenolate mofetil, and intravenous
immunoglobulin (IVIg).
III. PHOTOTHERAPY
• To suppress the immune system and decrease skin
hyper-reactivity
• UVA, PUVA, UVB (Broad band or narrow band)
NON-MEDICAL TREATMENT
I. EMOLLIENTS
• Emollients are the first line treatment for atopic
­eczema, having a steroid sparing effect and helping
to restore epidermal barrier function.
II. OTHERS
• Acute Exudative lesions:
i. Oil baths
ii. Soaks with NSS, Burrows Solution (1:20 dilution)
15 – 30 mins twice a day
iii. If infected –
1. potassium permanganate 1:25,000 – 1:50,000
dilution
2. benzalkonium chloride 1:5,000 aqueous solu-
tion (may cause contact dermatitis)
3. 5% acetic acid aqueous solution especially
for Pseudomonas infection
• Subacute: Antipruritic soothing lotions: Calamine
lotion (8% zinc oxide/8% calamine); Witch Hazel
Solution; Camphor 1% - 3%; Coal tar solution 3%
- 10% , Menthol 0.25% - 2.00%; Phenol 0.5% - 1.5%;
Salicylic acid 1.0 – 2.0%
• Chronic dry thickened lesions: Soak affected areas
5 min in water. Immediately apply a hydrophilic oint-
ment (petrolatum) liberally, massage into the skin
thoroughly.
• Occlusion using a thin flexible plastic enhances
penetration of medications.
REFERENCES:
Verallo, VM. Eczema. Compendium of Philippine Medicine. 11th Edition.
2009.
Eichenfield LF, Hanifin JM, Luger TA, Stevens SR, Pride HB. Consensus
Conference on Pediatric Atopic Dermatitis. J Am Acad Dermatol
2003;49:1088-95.
Eric L. Simpson; Jon M. Hanifin. Atopic dermatitis. J Am Acad Dermatol
2005; 53 (1): 115-128
Hanifin JM, Cooper KD, Ho VC, Kang S, Krafchik BR, Margolis DJ, et
al. Guidelines of care for atopic dermatitis. J Am Acad Dermatol
2004;50:391-404.
Shiu Kwan Chan; Nigel P. Burrows. Atopic dermatitis. Medicine. 2009;
37 (5): 242-245
Fitzpatrick TB. Fitzpatrick’s Dermatology in General Medicine Fifth
Edition, Numular Eczema, Chapter 125; Atopic Eczema, Chapter 124;
Vesicular Palmo-plantar Eczema, Chapter 127; Gravitational Eczema
and Asteatotic Eczema, Chapter 146, McGraw-Hill Companies, Inc.,
US 1999
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01/26/2010 10:44:16 AM
 Eczema
Recommended Therapeutics
The following index lists therapeutic classifications as recommended by the treatment guideline. For the prescriber's
reference, available drugs are listed under each therapeutic class. For drug information, please refer to the Philippine
Drug Directory System (PPD, PPDr, PPD Text, PPD Tabs).

Cephalosphorins Rovix Film Coated Tablet Ritromax

First Generation Roxetil
Cefalexin Roxicef Erythromycin
Airex Roxym Am-Europharma Erythromycin
Am-Europharma Cefalexin Teikeden-500 Drugmaker's Biotech Erythromycin
Bandax Xorimax Erasymin
Bloflex Zefur Erythrocin/Erythrocin DS
Cefalin Capsule Zefurox Ilosone/Ilosone DS
Cefalin Drops/Suspension Zegen Capsule Pharex Erythromycin
Celoxone Zinacef Upperzin
Ceporex Zinnat
CFA Cefaclor Roxithromycin
Clephin Cecavil Guamil
Difalex Ceclobid Macrol/Macrol OD
Drugmaker's Biotech Cefalexin Ceclor/Ceclor CD Pharex Roxithromycin
Eliphorin CFC Plethirox
Forexine Clorcef Roxid
Halcepin Drugmaker's Biotech Cefaclor Roxil
Keflex Pharex Cefaclor Roxithromycin
Lewimycin Ritemed Cefaclor Rulid
Lexibase Surecef Thromyn
Lyceplix Verzat/Verzat-ER
Medilexin Xelent Monocyclic Beta-Lactam Antibiotic
Medoxine Xeztron Aztreonam
Oneflex Azactam
Oranil Third Generation
Pharex Cefalexin Cefpodoxime Penicillins
Ritemed Cefalexin Cefadox Amoxicillin
Selzef Zudem Amoxil/Amoxil Forte
Xinflex Amusa
Zeporin LIncosamides Cartrimox
Clindamycin Clavoxin
Cefadroxil Anerocin Clearamox
Drolex Clindal Cilfam
Drozid Cliz Daisamox
Drugmaker's Biotech Cefadroxyl Dalacin C HCl/Dalacin C Palmitate/ DLI Amoxicillin
Lexipad Dalacin C Phosphate Drugmaker's Biotech Amoxicillin
Klindex Eleomox
Cefradine Pharex Clindamycin Globamox
Altozef Zindal 300 Globapen
Drugmaker's Biotech Cefradine Himox
Senadex Macrolides Lewixin
Tolzep Azithromycin Littmox
Velodyne Aztrocin Medimoxil
Yudinef Azyth Medvox
Zepdril Zithromax Multicare Amoxicillin
Zmax One Dose Novamox
Second Generation Pediamox
Cefuroxime Clarithromycin Pharex Amoxicillin
Aeruginox Claranta Promox
Altacef Clariget Ritemed Amoxicillin
Ambixime Clarilide Sterimox
Axet Claristad Sumoxil
C-Tri T Clarithrocid Teramoxyl
Cefogen Galemin Trexil
Cevox Klaret Valzimox
Cimex Powder for Inj Klargen Yugoxil
Cimex Powder for Susp Klaricid/Klaricid OD Zedroxyn
Drugmaker's Biotech Cefuroxime Klarika Zymoxyl
Ecocef Klarmyn
Educef Klaz Amoxicillin/Sulbactam
Elixime Klaz OD Ultramox
Furocem Larizin
Ifurax Maclar Ampicillin
Infekor Macrodin Ampimax
Kefox Maxulid Ampicin
Kefstar Onexid Cilisod
Kefsyn Oracid DLI Ampicillin
Panaxim Tab Pharex Clarithromycin Drugmaker's Biotech Ampicillin
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 Eczema
Eurocin Drugmaker's Biotech Ciprofloxacin Drugmaker's Biotech Cotrimoxazole
Excillin Floxacef Globaxol
Panacta Hyprocel Katrim
Pentrexyl Iprolan Lagatrim Forte
Polypen Ipromax Macromed
Vatacil Pharex Ciprofloxacin Moxzole
Proseloc Onetrim
Ampicillin/Sulbactam Proxazin Pharex Cotrimoxazole
Ampimax Proxivex Procor
Unasan Quinosyn Rimezone/Rimezone Forte
Unasyn Quiprime Ritemed Cotrimoxazole
Zunamyn Rapiqure Rotrace
Ritemed Ciproloxacin Septrin
Benzyl Penicillin Sigmacip Soxatrisil
Rhea Benzylpenicillin Xenoflox Syndal
Xipro Tricomed
Cloxacillin Zalvos Trim-S
Avastoph Ziprocap Trimetazole/Trimetazole DS
Bandox Zunexan Trizole Suspension
Cloxil Zyflox
Drugmaker's Biotech Cloxacillin Daptomycin
Encloxil Levofloxacin Cubicin
Lewinex Flevoxin
Medix Floxel Sodium fusidate
Oxaclen Glevo Fucidin
Pannox Capsule Lefloxin
Pharex Cloxacillin Levan Linezolid
Prostaphlin-A Levocin Zyvox
Ritemed Cloxacillin Levoquin
Secloxin Levox Antifungals
Loxeva Fluconazole
Co-Amoxiclav Pneumocal Diflucan
Amoclav Pravox Dyzolor
Amoclav Suspension Teravox Flucoral
Augmentin Terlev Funzela
Augmex Wilovex
Bactiv Griseofulvin
Bactoclav Moxifloxacin Grisovin-FP
Bioclavid Avelox
CAX Itraconazole
Clavmex Ofloxacin Sporanox
Clavoxin Baciflox
Clavoxel Drugmaker's Biotech Ofloxacin Ketoconazole
Clovimax Floxastad Konazole
Co-AX Fluraxid Nizoral Tablet
Drugmaker's Biotech Amoxicillin + Gyros
Clavulanic Acid Inoflox Terbinafine
Enhamox Iquinol Lamisil
Exten Itex
Gloclav Lofection Antihistamines
Natravox Mergexin
Penhance-DS/Penhance-625 Ofbeat Cetirizine
Sullivan Oflo Aforvir
Vamox Onexacin Allerkid
Pharex Ofloxacin Allermed
Flucloxacillin Qiflon Alnix
Drugmaker's Biotech Flucloxacillin Qinolon Cetimin
Fluclox Cetriz
Stafloxin Pefloxacin Cetyrol
Peraxin Drugmaker's Biotech Cetirizine HCl
Phenoxymethylpenicillin H-One
Sumapen Tetracyclines Histamed
Doxycycline Histazine
Sultamicillin Biocolyn Prixlae
Unasyn-Oral Doryx Recozin
Zunamyn Doxin Rhinitrin
Dyna-Doxycycline Texzine
Quinolones Vibramycin Unizef
Ciprofloxacin Virlix
Ciclodin Sulfonamide Combinations Welcet
Cifloxin Sulfamethoxazole/Trimethoprim Zetrix
Ciloxan Am-Europharma Cotrimoxazole Zinex
Cipfast-500 Bactille-TS Zyrrigin
Ciprobay/Ciprobay XR Bactrim Zyrtec
Ciprofen Bacxal Forte
Cipromax Chromo-Z Chlorphenamine
Cipromet Costazole Antamin
Cirok DLI Cotrimoxazole Barominic

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CPM 12TH ED ECZEMA EllenJan7.ind193 193 01/26/2010 10:44:17 AM

 Eczema
Drugmaker's Biotech Chlorphenamine N-palmitoyl-ethanolamine/ Betamethasone/Loratadine
Histacort Tablet Physiological lipids Claricort
Physiogel Al Cream
Chlorphenoxamine Physiogel AI Sun Cream Betamethasone/Mupirocin
Systral Foskina-B
Petroleum Jelly
Clemastine
Apollo Petroleum Jelly Betamethasone/Neomycin sulfate
Marsthine
Tavegyl Betnovate-N
Saccharide isomerate/Dipalmitoyl
Tavist
hydroxyproline Betamethasone/Salicylic Acid
Desloratadine Ellgy H2O Hydro-Replenishing Beprosalic
Aerius Cream and Lotion Diprosalic

Diphenhydramine Urea Betamethasone/Sodium Fusidate

Allerin AH Nutraplus Hoebenate
Am-Europharma Diphenhydramine
Benadryl Immunosupressants Clobetasol propionate
Drugmaker's Biotech Diphenhydramine Azathioprine Clobison
Hizon Diphenhydramine Injetion Imuran Clonate
Nebrecon Dermovate
Ciclosporin Dermovate Scalp
Ebastine Arpimune Glevate
Aleva Sandimmun Neoral
Co-Aleva Desonide
Topical Analgesics Desowen Cream/Lotion
Fexofenadine
Menthol/Camphor/Phenol
Fenafex
Sarna Fluocinonide
Fexet
Fexoral Lidemol
Methyl salicylate/ Lidex
Neofex
Menthol/Camphor
Sensitin
Efficascent Oil Fluocinonide/Neomycin sulfate/
Telfast
Omega Pain Killer Gramicidin/Nystatin
Hydroxyzine Lidex NGN
Drugmaker's Biotech Hydroxyzine Topical Corticosteroid
Iterax Fluticasone
Betamethasone Cutivate
Levocetirizine Beprosone Ointment/Cream
Xyzal Betnelan Mometasone
Betnovate Elica
Loratadine Celestone Elocon
Allerta Diprolene Momate
Claritin Diprospan
Lergicyl Diprosone Triamcinolone
Loradex Drugmaker's Biotech Betamethasone Kenacort
Lorano Kenacort-A 0.1%
Lorat Betamethasone/Chlorpheniramine Tricin Cream
Loratyne maleate
Lordam Beprosone Ointment/Cream Triamcinolone/Neomycin sulfate/
Lorfast Betneton Gramicidin/Nystatin
Lorid Kenacomb
Onemin Betamethasone/Clioquinol
Toral Diproform Hydrocotisone
Zantih Cortizan
Zylohist Betamethasone/Clotrimazole Drugmaker's Biotech Hydrocortisone
Clotrasone Lacticare-HC
Mequitazine Pharex Hydrocortisone
Primalan Betamethasone/Clotrimazole/ Solu-Cortef
Gentamicin sulfate Syntesor
Emollients, Demulcents & Protectants Triderm
Benzalkonium chloride/Triclosan/ Hydrocortisone/Bacitracin/
Light Liquid Paraffin Betamethasone/Dexchlorphenamine Polymyxin B/Neomycin sulfate
Oilatum Plus maleate Trimycin-H
Celestamine
Butylmethoxybenzoylmethane/ Hydrocotisone/Clotrimazole
Padimate O/Oxybenzone Betamethasone/Ebastine Candacort
Spectraban Ultra 28 Co-Aleva
Hydrocortisone/Fusidic acid
Calamine/Diphenhydramine Betamethasone/Fusidic acid Fucidin H
Caladryl Fucicort
Hoebedic Hydrocortisone/Miconazole nitrate
Calamine/Zinc Oxide Daktacort
Calmoseptine Ointment Betamethasone/Gentamicin sulfate
Diprogenta Topical Calcineurin Inhibitors
Lactoserum/Lactic Acid Garasone Tacrolimus
Lactacyd Baby Bath Protopic
Betamethasone/Gentamicin sulfate/
Light Liquid Paraffin Tolnaftate/Clioquinol Pimecrolimus
Oilatum Shower Gel Quadriderm Elidel 1% Cream
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