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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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Eczema
CLINICAL FEATURES
Diagnosis and Treatment of Eczema
Infantile phase
Eczema (or eczematous dermatitis) is a general term that
encompasses a set of etiologically heteregenous inflam- • Lesions most commonly start on the face (Figure 1);
matory conditions of the skin characterized as superficial often spare the ‘napkin area’
erythematous, papulovesicular eruptions which often lead • When the child begins to crawl, the extensor surfaces
to serous exudation and crusting. These lesions appear of the knees can be involved
and evolve in a very similar manner. These inflammatory • Chronic, fluctuating course, varying with factors such
skin conditions are among the top ten common consults as teething, infections, emotional upset and climate
in a physician’s clinic. changes

Common Features of Eczematous Dermatitis (ED) Childhood Phase

1. ACUTE STAGE: The primary clinical presentation • Lesions commonly involve the elbow (Figure 2) and
of acute ED begins with an itchy edematous and red knee flexures(Figure 3), the sides of the neck, the wrists
patch which then develops fluid-filled vesicles which and the ankles
may later coalesce to become larger bullae. When • Hand involvement is sometimes associated with nail
these vesicles or bullae erupt and become eroded, changes (pitting and ridging)
they become more pruritic with occasional pain and • Acute vesiculation should always suggest the possibility
edema. of bacterial or viral infection.

2. SUBACUTE STAGE: Almost immediately, secondary Adult phase


changes develop. The fluid filled vesicles or blisters
turn into a wet crust, then into a dry scab, resulting in • Similar to the childhood phase, although erythroderma
a dry, scaly patch. is more common

3. CHRONIC STAGE: The inevitable scratching and CAUSES


excoriations of the itchy patch lead to varying degrees
of infection which further lead to thickening or licheni- • Multifactorial
fication, and post-inflammatory hyperpigmentation or • 70% have family history
hypopigmentation of the involved skin. The series of • Related to mutations in fillagrin (FLG) gene
primary and secondary changes re-occur at the initial • Positive food allergy tests are common in children with
patch, or spread to other areas depending on the AD, but skin prick testing and RASTs poorly predict
continued activity or presence of the primary cause actual food reactions in patients.
in subacute ED.
DIAGNOSIS
B. COMMON TYPES OF ECZEMA
• Seldom aided by investigations
Classification of eczema is largely empirical, and in most • Serum IgE, specific radioallergosorbent tests (RASTs)
circumstances, the diagnosis is based only on clinical and prick tests usually only confirm the atopic diathesis
findings. There are many types of eczema recognized • 20% of individuals with atopic dermatitis have normal
clinically and are discussed below. IgE levels and negative results on RASTs
• Bacteriology to identify bacterial infection and potential
antibiotic resistance
1. Atopic Dermatitis
• Viral swab if herpes simplex infection (eczema herpe-
2. Contact Dermatitis ticum, Figure 4) is suspected.
3. Dyshidrotic Dermatitis • Patch-testing is particularly useful in adults to identify
contact allergens responsible for deterioration of atopic
4. Nummular Dermatitis
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 Figure 1. Infantile AD with facial involvement

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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.

Figures 2 & 3. Childhood AD with involvement of the flexural THIRD LINE TREATMENT
areas
1. Systemic corticosteroids – although oral corticoste­
SPECIAL CONSIDERATIONS FOR THERAPY OF roids are effective for acute exacerbations of derma-
ATOPIC DERMATITIS titis, they are seldom used as continuous treatment.

FIRST-LINE TREATMENT 2. Systemic immunosuppressant therapy


• Reserved for severe, recalcitrant cases
1. Reduction of trigger factors – atopic dermatitis can be • Before starting therapy, the long-term side effects
aggravated by various trigger factors. should be discussed.
• Environmental Control • Cyclosporin is most studied; an intermittent, 12-week
• Contact allergy: consider this if exacerbation of course of cyclosporine at dose levels of 5 mg/kg has
previously controlled eczema or patient reacts to been shown to be effective. Side effects include:
topical treatments. hypertension and renal toxicity.
• Infection: both bacterial (Staphylococcus aureus • Azathioprine is effective in severe atopic dermatitis,
and Streptococcus) and viral (herpes simplex) can but has a slow onset of action (usually 4–6 weeks)
worsen eczema. and can cause bone marrow suppression.
• House dust mites: reduction of exposure by regular
cleaning of the home by means of vacuuming and PROGNOSIS
damp dusting may be helpful. Animal dander also • Although there is currently no cure for atopic dermatitis,
can aggravate atopic dermatitis. various interventions can control symptoms. The condi-
tion can be expected to clear in 60–70% of children by
2. Bathing and emollients their early teens, although relapses may occur.
• Most patients have dry skin and avoidance of deter- • The mainstay of preventive therapy is avoidance of skin
gents is important. irritation and dryness. Adults with atopic dermatitis are
• Soap substitutes and emollients can improve skin advised to avoid occupations such as car mechanic,
hydration and barrier function. hairdresser and nurse.

3. Topical corticosteroids OTHER SUPPLEMENTAL THERAPIES


• Principal treatment for the inflammation and pruritus
of atopic dermatitis • There is no definitive evidence that routine diet restrict­
• Less potent topical corticosteroids should be used ion or allergen avoidance has a role in the treatment
on the eyelids, face and flexural areas of AD except in cases where acute clinically relevant
• Shorter periods of medium-potency topical corti- reactions have occurred.
costeroid use are as effective as a longer course of • Studies regarding breastfeeding as a primary prevent­
low-potency corticosteroids in controlling AD flares. ive measure in AD have not shown a consistent protect­
Maintenance therapy follows once disease has been ive effect.
stabilized. • Breastfeeding during the first 4 months has a protective
effect when compared with cow’s milk, but on its own
4. Antihistamines does not constitute an effective prevention strategy.
• Sedating antihistamines are useful in patients with • The preventive effects of probiotics on AD may appear to
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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, • Also known as discoid eczema; a chronic disorder of
fertilizers, rodenticides, waxes, polishers unknown etiology
• Acquired and multifactorial; rare in children
DIAGNOSIS • Some worsen in summer, exacerbated by heat and
1. Patch testing humidity
- standardized diagnostic procedure of choice for • Single, multiple or episodic, and recurrent at previously
contact dermatitis affected sites
2. Skin Biopsy: dermal infiltrate with marked eosinophilia • Start out as papules and papulovesicles coalescing
3. In vitro lymphocyte stimulation tests, migration inhibition to form well-demarcated, coin-shaped plaques with
factor, and other laboratory tests of lymphokine pro- pinpoint oozing, crusting, and scale (Figure 6)
duction remain investigational tools that at present are • Plaques range from 1 to 3 cm in size
insufficiently standardized to allow clinical application. • Pruritus varies from minimal to severe
• Most common sites of involvement are upper extremi-
TREATMENT ties, including the dorsal hands in women, and the lower
• Identify contactant by history or by patch testing extremities in men
• Observe for prompt improvement when contactant is
discontinued, slow or no improvement when another CAUSES
cross-reacting product is still used.
• Use barrier creams including petrolatum jelly when The following may cause flare-ups:
exposure to contact allergen cannot be avoided, or use • Wool
cotton gloves under plastic gloves, not rubber gloves • Topical medicines: topical steroids
• Irritants: forceful and prolonged irrigation with water • Drugs: gold, methyldopa, streptomycin, aminosalicylic
• Complete healing may take 4 weeks, with a good acid, INH
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DIAGNOSIS COMMON CONTACTANTS:
- Nickel, chrome, PPDA, fragrance,balsams
1. Serum immunoglobulin E levels are normal - Neomycin
2. Skin Biopsy - Poison oak or ivy related to mango, lacquer tree oil for
a. Acute: spongiosis, with or without spongiotic micro- furniture, cashew nut shells
vesicles. - Implanted metals
b. Subacute: parakeratosis, scale-crust, epidermal hy- - Secondary to distant focus of infections which clear
perplasia, and spongiosis with mixed cell infiltrates when primary is treated:
c. Chronic: may resemble lichen simplex chronicus • Fungal: dermatophytid
• Bacterial: bacterid
3. Patch testing
• may be useful in chronic recalcitrant cases to rule DIAGNOSIS
out a superimposed contact dermatitis 1. Elevated serum IgE demonstrates atopic back-
ground
TREATMENT 2. KOH/fungal culture of skin scrapings to rule out fungal
infection
• Topical steroids in the mid- to high potency range are 3. Giemsa staining to rule out viral infection
the mainstay of treatment 4. Gram stain and bacterial culture if bacterial superinfec-
• Topical calcineurin inhibitors, tacrolimus and pime- tion is suspected
crolimus, and tar preparations are also effective 5. Skin Biopsy: Eczematous Dermatitis with mild eosi-
• Emollients can be added adjunctively if there is ac- nophilia
companying xerosis.
• Phototherapy with broad or narrow band ultraviolet B TREATMENT
may be beneficial
• Trial of suspected allergen withdrawal and/or challenge • Does not respond well to treatment
• Treatment of suspected or identified infection: bacterial • Intact, large blisters can be drained, but should not be
or fungal unroofed
• Improve ambient humidity • Avoidance of commonly encountered allergens, such
• Avoid skin-drying conditions like overuse of air-condi- as foods and plants, and irritants (e.g. soaps, solvents,
tioning and contact with water (e.g. water compresses) acids, and alkalis, can be helpful
• Oral antihistamines are useful if pruritus is severe • 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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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 • Anti-inflammatory medications
• Often with pruritus and eczematous changes from • Ointments (oil-based) are more effective than
scratching and topical medicines used creams, although creams and lotions (water-
• Typically occurs in the medial supramalleolar region based, not alcoholic) are useful when the skin is
where microangiopathy is most intense inflamed.
• Lesions may lichenify or ulcerate over time (Figure 9) • Use topical steroids according to strength and
class (See Table 1).
CAUSES OF POOR VENOUS DRAINAGE
• Cutaneous complications such as striae, atrophy,
• Obesity and telangiectasia limit the long-term use of these
• Trauma agents.
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C. INTRALESIONAL STEROID
TABLE 1. POTENCY RANKING OF SOME COMMONLY
USED TOPICAL CORTICOSTEROIDS
• Employed to rapidly thin down thick dry patches
Adapted from Fitzpatrick’s Dermatology in General Medicine Fifth Edition

D. IMMUNOMODULATORY DRUGS
CLASS GENERIC NAME

Very High Betamethasone dipropionate-augmented • Systemic corticosteroids are known to be ef-
Potency 0.05% - ointment fective in the short-term treatment of eczemas,
I Clobetasol propionate 0.05% - cream but no evidence exists to support their use, and
and ointment rebound flaring and long-term side effects are
igh Potency Betamethasone dipropionate 0.05% - ointment
H limiting.
II Fluocinonide 0.05% - cream and ointment • Cyclosporine is effective in the treatment of
Mometasone furoate 0.1% - ointment severe AD, but its usefulness may be limited by
III Betamethasone dipropionate 0.05% - cream
side effects.
Betamethasone valerate 0.1% - ointment • Conflicting data exist about the efficacy of azathio­
Fluticasone propionate 0.005% - ointment prine, mycophenolate mofetil, and intravenous
immunoglobulin (IVIg).
id Potency Fluocinolone acetonide 0.025% - ointment
M
IV Mometasone furoate 0.1% - cream
Triamcinolone acetonide 0.1% - cream
III. PHOTOTHERAPY
• To suppress the immune system and decrease skin
V Betamethasone valerate 0.1% - cream hyper-reactivity
Fluocinolone acetonide 0.025% - cream • UVA, PUVA, UVB (Broad band or narrow band)
Fluticasone propionate 0.05% - cream
Low Potency Desonide 0.05% - cream and ointment NON-MEDICAL TREATMENT
VI
VII Hydrocortisone or hydrocortisone acetate 1% -
I. EMOLLIENTS
cream and ointment • Emollients are the first line treatment for atopic
Hydrocortisone aceponate 0.12% - cream ­eczema, having a steroid sparing effect and helping
to restore epidermal barrier function.

B. TOPICAL CALCINEURIN INHIBITORS (TCI) II. OTHERS


• Acute Exudative lesions:
• Tacrolimus 0.1% and 0.03% Ointment (PROTOPIC) i. Oil baths
and Pimecrolimus 1% Cream (ELIDEL) ii. Soaks with NSS, Burrows Solution (1:20 dilution)
• Can be prescribed for patients of 2 years and 15 – 30 mins twice a day
upwards for the treatment of moderate to severe iii. If infected –
eczema that is unresponsive to conventional 1. potassium permanganate 1:25,000 – 1:50,000
therapy dilution
• Should not be used under occlusion 2. benzalkonium chloride 1:5,000 aqueous solu-
• Side effects of usage are:- tion (may cause contact dermatitis)
• Infection particularly herpes maybe increased 3. 5% acetic acid aqueous solution especially
• Burning sensation of the skin, usually temporary for Pseudomonas infection
• Occasional inflammatory flare • Subacute: Antipruritic soothing lotions: Calamine
• Benefits: no atrophy; can be used on the face; lotion (8% zinc oxide/8% calamine); Witch Hazel
longer time to relapse Solution; Camphor 1% - 3%; Coal tar solution 3%
- 10% , Menthol 0.25% - 2.00%; Phenol 0.5% - 1.5%;
II. SYSTEMIC Salicylic acid 1.0 – 2.0%
• Chronic dry thickened lesions: Soak affected areas
A. ANTIHISTAMINES 5 min in water. Immediately apply a hydrophilic oint-
• Bedtime: sedating antihistamines ment (petrolatum) liberally, massage into the skin
e.g., Hydroxy­zine or Benadryl thoroughly.
• Daytime: non-sedating antihistamine • Occlusion using a thin flexible plastic enhances
e.g., Cetirizine, Loratadine penetration of medications.
• Role of antihistamines in controlling itching in
eczema remains to be defined REFERENCES:
• For patients with significant sleep disruption Verallo, VM. Eczema. Compendium of Philippine Medicine. 11th Edition.
due to itch, allergic dermatographism, or allergic 2009.
rhinoconjunctivitis, sedating antihistamines may Eichenfield LF, Hanifin JM, Luger TA, Stevens SR, Pride HB. Consensus
Conference on Pediatric Atopic Dermatitis. J Am Acad Dermatol
be useful. 2003;49:1088-95.
Eric L. Simpson; Jon M. Hanifin. Atopic dermatitis. J Am Acad Dermatol
B. ANTIBIOTICS 2005; 53 (1): 115-128
• Oral antibacterials or antifungals if infected; or, to Hanifin JM, Cooper KD, Ho VC, Kang S, Krafchik BR, Margolis DJ, et
reduce bacterial or fungal population of dermatitic al. Guidelines of care for atopic dermatitis. J Am Acad Dermatol
skin 2004;50:391-404.
Shiu Kwan Chan; Nigel P. Burrows. Atopic dermatitis. Medicine. 2009;
• Oral anti-viral medications when viral infections 37 (5): 242-245
occur Fitzpatrick TB. Fitzpatrick’s Dermatology in General Medicine Fifth
• Without signs of infection, oral antibiotics general­ Edition, Numular Eczema, Chapter 125; Atopic Eczema, Chapter 124;
Vesicular Palmo-plantar Eczema, Chapter 127; Gravitational Eczema
ly have a minimal therapeutic effect on the and Asteatotic Eczema, Chapter 146, McGraw-Hill Companies, Inc.,
dermatitis US 1999

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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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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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