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Eczema

Philippine Dermatological SocietyRm. 1015, Front Tower, Cathedral Heights Building St. Lukes Medical Center, E. Rodriguez Avenue Quezon City, Philippines 1102 Telephone No.: 723-0101 loc 2015 Telefax No.: 727-7309 E-mail: [email protected] Website: www.pds.org.ph

Officers and Board of Directors 2009-2010President Vice-President Secretary Treasurer Immediate Past President Board of Directors Georgina C. Pastorfide, MD Ma. Teresita G. Gabriel, MD Rosalina E. Nadela, MD Lonabel A. Encarnacion, MD Arnelfa C. Paliza, MD 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

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EczemaDiagnosis and Treatment of EczemaEczema (or eczematous dermatitis) is a general term that encompasses a set of etiologically heteregenous inflammatory 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 physicians 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 lichenification, 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. 2. 3. 4. 5. 6. Atopic Dermatitis Contact Dermatitis Dyshidrotic Dermatitis Nummular Dermatitis Asteatotic Dermatitis Stasis Dermatitis 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 herpeticum, Figure 4) is suspected. Patch-testing is particularly useful in adults to identify contact allergens responsible for deterioration of atopic dermatitis.

I. ATOPIC DERMATITIS DEFINITION Chronic inflammatory skin disease that usually occurs in persons with a personal or family history of other atopic conditions, such as asthma and allergic rhinitis. Lifetime prevalence is 1020% in children and 13% 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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Eczemanocturnal itching, but can cause drowsiness the next morning. Non-sedating antihistamines have limited effectiveness 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 corticosteroids. 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 unresponsive to topical treatment or so widespread that topical treatment is impractical. Broadband UVA and UVB, narrowband UVB, combination 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 areas

THIRD LINE TREATMENT 1. Systemic corticosteroids although oral corticosteroids are effective for acute exacerbations of dermatitis, 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 46 weeks) and can cause bone marrow suppression. PROGNOSIS Although there is currently no cure for atopic dermatitis, various interventions can control symptoms. The condition can be expected to clear in 6070% 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 restriction 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 preventive measure in AD have not shown a consistent protective effect. Breastfeeding during the first 4 months has a protective effect when compared with cows milk, but on its own does not constitute an effective prevention strategy. The preventive effects of probiotics on AD may appear to

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 detergents 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 corticosteroid 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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Eczemaextend beyond infancy although further studies needed. Preliminary studies of massage therapy, hypnotherapy, and biofeedback have been encouraging. II. CONTACT DERMATITIS CLINICAL FEATURES Altered state of skin reactivity induced by exposure to 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 Airborne CD due to contactants affect exposed areas, spare covered areas; with involvement of eyelids, inner arms creases of the neck. Clothing-related allergens affect covered areas especially 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 STRONG CONTACT IRRITANTS: o ETHYLENE OXIDE o HYDROFLUORIC ACID o WET CEMENT MILD TO MODERATE CONTACT IRRITANTS: o Soaps, solvents, detergents, fiberglass, metalworking 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 production 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 prognosis Topical treatment indicated for mild cases of contact dermatitis Systemic treatment Indicated for control of itching even in cases of limited extent. Also indicated for moderate to severe acute and/or chronic contact dermatitis.

Figure 4. Dermatitic plaque in the peri-umbilical area due to nickel allergy

Figure 5. Erythematous scaly plaque in the neck area due to necklace

III. NUMMULAR DERMATITIS CLINICAL FEATURES 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 extremities, 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

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EczemaDIAGNOSIS 1. Serum immunoglobulin E levels are normal 2. Skin Biopsy a. Acute: spongiosis, with or without spongiotic microvesicles. b. Subacute: parakeratosis, scale-crust, epidermal hyperplasia, 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 pimecrolimus, and tar preparations are also effective Emollients can be added adjunctively if there is accompanying 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-conditioning and contact with water (e.g. water compresses) Oral antihistamines are useful if pruritus is severe 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 background 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 superinfection is suspected 5. Skin Biopsy: Eczematous Dermatitis with mild eosinophilia 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) 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 development 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 contactants)

Figure 7. Tapioca-like vesicular eruption on lateral surface of fingers

Figure 8. Vesicular eruption of the soles with superimposed bacterial infection


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

Figure 9. Hyperpigmented scaly plaque with ulceration.

B. GENERAL GUIDELINES FOR TREATMENT OF ECZEMAS I. TOPICAL A. STEROIDAL PREPARATIONS Anti-inflammatory medications Ointments (oil-based) are more effective than creams, although creams and lotions (waterbased, 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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EczemaTABLE 1. POTENCY RANKING OF SOME COMMONLY USED TOPICAL CORTICOSTEROIDSAdapted from Fitzpatricks Dermatology in General Medicine Fifth Edition

C. INTRALESIONAL STEROID Employed to rapidly thin down thick dry patches D. IMMUNOMODULATORY DRUGS Systemic corticosteroids are known to be effective in the short-term treatment of eczemas, but no evidence exists to support their use, and rebound flaring and long-term side effects are limiting. 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 solution (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 ointment (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. Fitzpatricks 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

CLASS Very High Potency I

GENERIC NAME Betamethasone dipropionate-augmented 0.05% - ointment Clobetasol propionate 0.05% - cream and ointment

High Potency Betamethasone dipropionate 0.05% - ointment 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 Fluocinolone acetonide 0.025% - ointment Mometasone furoate 0.1% - cream Triamcinolone acetonide 0.1% - cream Betamethasone valerate 0.1% - cream Fluocinolone acetonide 0.025% - cream Fluticasone propionate 0.05% - cream

Mid Potency IV V

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 generally have a minimal therapeutic effect on the dermatitis

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EczemaRecommended TherapeuticsThe 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 First Generation Cefalexin Airex Am-Europharma Cefalexin Bandax Bloflex Cefalin Capsule Cefalin Drops/Suspension Celoxone Ceporex CFA Clephin Difalex Drugmaker's Biotech Cefalexin Eliphorin Forexine Halcepin Keflex Lewimycin Lexibase Lyceplix Medilexin Medoxine Oneflex Oranil Pharex Cefalexin Ritemed Cefalexin Selzef Xinflex Zeporin Cefadroxil Drolex Drozid Drugmaker's Biotech Cefadroxyl Lexipad Cefradine Altozef Drugmaker's Biotech Cefradine Senadex Tolzep Velodyne Yudinef Zepdril Second Generation Cefuroxime Aeruginox Altacef Ambixime Axet C-Tri T Cefogen Cevox Cimex Powder for Inj Cimex Powder for Susp Drugmaker's Biotech Cefuroxime Ecocef Educef Elixime Furocem Ifurax Infekor Kefox Kefstar Kefsyn Panaxim Tab Rovix Film Coated Tablet Roxetil Roxicef Roxym Teikeden-500 Xorimax Zefur Zefurox Zegen Capsule Zinacef Zinnat Cefaclor Cecavil Ceclobid Ceclor/Ceclor CD CFC Clorcef Drugmaker's Biotech Cefaclor Pharex Cefaclor Ritemed Cefaclor Surecef Verzat/Verzat-ER Xelent Xeztron Third Generation Cefpodoxime Cefadox Zudem LIncosamides Clindamycin Anerocin Clindal Cliz Dalacin C HCl/Dalacin C Palmitate/ Dalacin C Phosphate Klindex Pharex Clindamycin Zindal 300 Macrolides Azithromycin Aztrocin Azyth Zithromax Zmax One Dose Clarithromycin Claranta Clariget Clarilide Claristad Clarithrocid Galemin Klaret Klargen Klaricid/Klaricid OD Klarika Klarmyn Klaz Klaz OD Larizin Maclar Macrodin Maxulid Onexid Oracid Pharex Clarithromycin Ritromax Erythromycin Am-Europharma Erythromycin Drugmaker's Biotech Erythromycin Erasymin Erythrocin/Erythrocin DS Ilosone/Ilosone DS Pharex Erythromycin Upperzin Roxithromycin Guamil Macrol/Macrol OD Pharex Roxithromycin Plethirox Roxid Roxil Roxithromycin Rulid Thromyn Monocyclic Beta-Lactam Antibiotic Aztreonam Azactam Penicillins Amoxicillin Amoxil/Amoxil Forte Amusa Cartrimox Clavoxin Clearamox Cilfam Daisamox DLI Amoxicillin Drugmaker's Biotech Amoxicillin Eleomox Globamox Globapen Himox Lewixin Littmox Medimoxil Medvox Multicare Amoxicillin Novamox Pediamox Pharex Amoxicillin Promox Ritemed Amoxicillin Sterimox Sumoxil Teramoxyl Trexil Valzimox Yugoxil Zedroxyn Zymoxyl Amoxicillin/Sulbactam Ultramox Ampicillin Ampimax Ampicin Cilisod DLI Ampicillin Drugmaker's Biotech Ampicillin

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EczemaEurocin Excillin Panacta Pentrexyl Polypen Vatacil Ampicillin/Sulbactam Ampimax Unasan Unasyn Zunamyn Benzyl Penicillin Rhea Benzylpenicillin Cloxacillin Avastoph Bandox Cloxil Drugmaker's Biotech Cloxacillin Encloxil Lewinex Medix Oxaclen Pannox Capsule Pharex Cloxacillin Prostaphlin-A Ritemed Cloxacillin Secloxin Co-Amoxiclav Amoclav Amoclav Suspension Augmentin Augmex Bactiv Bactoclav Bioclavid CAX Clavmex Clavoxin Clavoxel Clovimax Co-AX Drugmaker's Biotech Amoxicillin + Clavulanic Acid Enhamox Exten Gloclav Natravox Penhance-DS/Penhance-625 Sullivan Vamox Flucloxacillin Drugmaker's Biotech Flucloxacillin Fluclox Stafloxin Phenoxymethylpenicillin Sumapen Sultamicillin Unasyn-Oral Zunamyn Quinolones Ciprofloxacin Ciclodin Cifloxin Ciloxan Cipfast-500 Ciprobay/Ciprobay XR Ciprofen Cipromax Cipromet Cirok Drugmaker's Biotech Ciprofloxacin Floxacef Hyprocel Iprolan Ipromax Pharex Ciprofloxacin Proseloc Proxazin Proxivex Quinosyn Quiprime Rapiqure Ritemed Ciproloxacin Sigmacip Xenoflox Xipro Zalvos Ziprocap Zunexan Zyflox Levofloxacin Flevoxin Floxel Glevo Lefloxin Levan Levocin Levoquin Levox Loxeva Pneumocal Pravox Teravox Terlev Wilovex Moxifloxacin Avelox Ofloxacin Baciflox Drugmaker's Biotech Ofloxacin Floxastad Fluraxid Gyros Inoflox Iquinol Itex Lofection Mergexin Ofbeat Oflo Onexacin Pharex Ofloxacin Qiflon Qinolon Pefloxacin Peraxin Tetracyclines Doxycycline Biocolyn Doryx Doxin Dyna-Doxycycline Vibramycin Sulfonamide Combinations Sulfamethoxazole/Trimethoprim Am-Europharma Cotrimoxazole Bactille-TS Bactrim Bacxal Forte Chromo-Z Costazole DLI Cotrimoxazole Drugmaker's Biotech Cotrimoxazole Globaxol Katrim Lagatrim Forte Macromed Moxzole Onetrim Pharex Cotrimoxazole Procor Rimezone/Rimezone Forte Ritemed Cotrimoxazole Rotrace Septrin Soxatrisil Syndal Tricomed Trim-S Trimetazole/Trimetazole DS Trizole Suspension Daptomycin Cubicin Sodium fusidate Fucidin Linezolid Zyvox Antifungals Fluconazole Diflucan Dyzolor Flucoral Funzela Griseofulvin Grisovin-FP Itraconazole Sporanox Ketoconazole Konazole Nizoral Tablet Terbinafine Lamisil Antihistamines Cetirizine Aforvir Allerkid Allermed Alnix Cetimin Cetriz Cetyrol Drugmaker's Biotech Cetirizine HCl H-One Histamed Histazine Prixlae Recozin Rhinitrin Texzine Unizef Virlix Welcet Zetrix Zinex Zyrrigin Zyrtec Chlorphenamine Antamin Barominic


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EczemaDrugmaker's Biotech Chlorphenamine Histacort Tablet Chlorphenoxamine Systral Clemastine Marsthine Tavegyl Tavist Desloratadine Aerius Diphenhydramine Allerin AH Am-Europharma Diphenhydramine Benadryl Drugmaker's Biotech Diphenhydramine Hizon Diphenhydramine Injetion Nebrecon Ebastine Aleva Co-Aleva Fexofenadine Fenafex Fexet Fexoral Neofex Sensitin Telfast Hydroxyzine Drugmaker's Biotech Hydroxyzine Iterax Levocetirizine Xyzal Loratadine Allerta Claritin Lergicyl Loradex Lorano Lorat Loratyne Lordam Lorfast Lorid Onemin Toral Zantih Zylohist Mequitazine Primalan Emollients, Demulcents & Protectants Benzalkonium chloride/Triclosan/ Light Liquid Paraffin Oilatum Plus Butylmethoxybenzoylmethane/ Padimate O/Oxybenzone Spectraban Ultra 28 Calamine/Diphenhydramine Caladryl Calamine/Zinc Oxide Calmoseptine Ointment Lactoserum/Lactic Acid Lactacyd Baby Bath Light Liquid Paraffin Oilatum Shower Gel N-palmitoyl-ethanolamine/ Physiological lipids Physiogel Al Cream Physiogel AI Sun Cream Petroleum Jelly Apollo Petroleum Jelly Saccharide isomerate/Dipalmitoyl hydroxyproline Ellgy H2O Hydro-Replenishing Cream and Lotion Urea Nutraplus Immunosupressants Azathioprine Imuran Ciclosporin Arpimune Sandimmun Neoral Topical Analgesics Menthol/Camphor/Phenol Sarna Methyl salicylate/ Menthol/Camphor Efficascent Oil Omega Pain Killer Topical Corticosteroid Betamethasone Beprosone Ointment/Cream Betnelan Betnovate Celestone Diprolene Diprospan Diprosone Drugmaker's Biotech Betamethasone Betamethasone/Chlorpheniramine maleate Beprosone Ointment/Cream Betneton Betamethasone/Clioquinol Diproform Betamethasone/Clotrimazole Clotrasone Betamethasone/Clotrimazole/ Gentamicin sulfate Triderm Betamethasone/Dexchlorphenamine maleate Celestamine Betamethasone/Ebastine Co-Aleva Betamethasone/Fusidic acid Fucicort Hoebedic Betamethasone/Gentamicin sulfate Diprogenta Garasone Betamethasone/Gentamicin sulfate/ Tolnaftate/Clioquinol Quadriderm Betamethasone/Loratadine Claricort Betamethasone/Mupirocin Foskina-B Betamethasone/Neomycin sulfate Betnovate-N Betamethasone/Salicylic Acid Beprosalic Diprosalic Betamethasone/Sodium Fusidate Hoebenate Clobetasol propionate Clobison Clonate Dermovate Dermovate Scalp Glevate Desonide Desowen Cream/Lotion Fluocinonide Lidemol Lidex Fluocinonide/Neomycin sulfate/ Gramicidin/Nystatin Lidex NGN Fluticasone Cutivate Mometasone Elica Elocon Momate Triamcinolone Kenacort Kenacort-A 0.1% Tricin Cream Triamcinolone/Neomycin sulfate/ Gramicidin/Nystatin Kenacomb Hydrocotisone Cortizan Drugmaker's Biotech Hydrocortisone Lacticare-HC Pharex Hydrocortisone Solu-Cortef Syntesor Hydrocortisone/Bacitracin/ Polymyxin B/Neomycin sulfate Trimycin-H Hydrocotisone/Clotrimazole Candacort Hydrocortisone/Fusidic acid Fucidin H Hydrocortisone/Miconazole nitrate Daktacort Topical Calcineurin Inhibitors Tacrolimus Protopic Pimecrolimus Elidel 1% Cream

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