Eczema
Philippine Dermatological Society
Rm. 1015 South Tower, Cathedral Heights Building Complex
St. Luke’s Medical Center
E. Rodriguez Avenue, Quezon City, Philippines 1102
Telephone No.: (632) 723-0101 loc 2015
Telefax No.: 727-7309
E-mail: pds_org@pldtdsl.net, pds_org@yahoo.com
Website: www.pds.org.ph
Officers and Board of Directors (2011-2012)
President
Vice-President
Secretary
Treasurer
Ma. Teresita G. Gabriel, MD
Rosalina E. Nadela, MD
Ma. Angela M. Lavadia, MD
Daisy K. Ismael, MD
Immediate Past President
Georgina C. Pastorfide, MD
Directors
Eileen Liesl A. Cubillan, MD
Lonabel A. Encarnacion, MD
Evelyn R. Gonzaga, MD
Ma. Jasmin J. Jamora, MD
Ma. Juliet E. Macarayo, MD
Noemie S. Ramos, MD
Francisco D. Rivera IV, MD
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131
Eczema
Diagnosis and Treatment of Eczema
CLINICAL FEATURES
Infantile phase
Eczema (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 physician’s clinic.
• 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
Common Features of Eczematous Dermatitis (ED)
Childhood Phase
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.
• 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.
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.
Adult phase
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.
CAUSES
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
• Similar to the childhood phase, although erythroderma
is more common
• 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 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
132
Figure 1. Infantile AD with facial involvement
Eczema
nocturnal 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 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, 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
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
THIRD-LINE TREATMENT
1. Systemic corticosteroids – although oral corticoste­
roids 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 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 condition 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
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133
Eczema
to extend 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)
• 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
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
134
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
Eczema
DIAGNOSIS
COMMON CONTACTANTS:
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
- 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
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
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 super­
infection is suspected
5. Skin Biopsy: Eczematous Dermatitis with mild eosino­
philia
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
Figure 7. Tapioca-like vesicular eruption on lateral surface of
fingers
• 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 8. Vesicular eruption of the soles with superimposed
bacterial infection
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Eczema
V. ASTEATOTIC DERMATITIS
CLINICAL FEATURES
• Acquired dermatitis super imposed 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
• 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
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
136
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.
Eczema
TABLE 1.POTENCY RANKING OF SOME COMMONLY
USED TOPICAL CORTICOSTEROIDS
Adapted from Fitzpatrick’s Dermatology in General Medicine Fifth Edition
CLASS
Very High Potency I
GENERIC NAME
Betamethasone dipropionate - augmented 0.05% - ointment
Clobetasol propionate 0.05% - cream
and ointment
igh Potency Betamethasone dipropionate 0.05% - ointment
H
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 general­ly
have a minimal therapeutic effect on the dermatitis
C. INTRALESIONAL STEROID
•Employed to rapidly thin down thick dry patches
D. IMMUNOMODULATORY DRUGS
•Systemic corticosteroids are known to be effect­
ive 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. 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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137
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, PPD Pocket Version, PPD Text, PPD Tabs).
Cephalosphorins
First Generation
Cefalexin
Airex
Am-Europharma Cefalexin
Bandax
Bloflex
Cefalin Capsule
Cefalin Drops/Suspension
Celoxone
Ceporex
CFA
Difalex
Drugmaker's Biotech Cefalexin
Edexin
Eliphorin
Forexine
Halcepin
Keflex
Lewimycin
Lexibase
Lyceplix
Medilexin
Medoxine
Oneflex
Oranil
Pharex Cefalexin
Ritemed Cefalexin
Xinflex
Zeporin
Cefadroxil
Drolex
Drozid
Drugmaker's Biotech Cefadroxyl
Lexipad
Wincocef-500
Cefradine
Altozef
Drugmaker's Biotech Cefradine
Senadex
Tolzep
Velodyne
Yudinef
Zepdril
Second Generation
Cefuroxime
Aeruginox
Altacef
Ambixime
Axet
C-Tri T
Cefogen
Cefurex
Cefurox
Cefuxime 500
Cevox
Cimex Powder for Inj
Cimex Powder for Susp
Drugmaker's Biotech Cefuroxime
Ecocef
Elixime
Eurimax
Furocem
Ifurax
Infekor
Kefox 250/Kefox 750
Kefstar
Kefsyn
Revacef
Rovix Film Coated Tablet
Roxetil
Roxicef
Roxym
138
Teikeden-500
Xorimax
Zefur
Zegen Capsule
Zinacef
Zinnat
Cefaclor
Ceclobid
CFC
Clorcef
Drugmaker's Biotech Cefaclor
Pharex Cefaclor
Remedlor
Ritemed Cefaclor
Surecef
Verzat/Verzat-ER
Xelent
Xeztron
Ilosone/Ilosone DS
Pharex Erythromycin
Upperzin
Roxithromycin
Macrol/Macrol OD
Pharex Roxithromycin
Plethirox
Roxid
Roxithro
Rulid
Ruthison
Thromyn
Winthrop Roxithromycin
Third Generation
Cefpodoxime
Cebarc
Cefadox (OEP)
Zudem
Penicillins
Amoxicillin
Amoxil/Amoxil Forte
Amusa
Cartrimox
Cilfam
Clearamox
Daisamox
DLI Amoxicillin
Drugmaker's Biotech Amoxicillin
Eleomox
Globamox
Globapen
Himox
Lewixin
Medimoxil
Medvox
Multicare Amoxicillin
Novamox
Pediamox
Pharex Amoxicillin
Ritemed Amoxicillin
Sterimox
Teramoxyl
Valzimox
Xybatron
Yugoxil
Zedroxyn
Zymoxyl
LIncosamides
Clindamycin
Anerocin
Clindal
Cliz
Dalacin C HCl/Dalacin C Palmitate/ Dalacin C Phosphate
Klindex
Pharex Clindamycin
Potecin
Zindal 300
Macrolides
Azithromycin
Aztrocin
Azyth
Geozit
Sitimax
Zenith
Zithromax
Zmax One Dose
Clarithromycin
Baclecin-500
Claranta
Clariget/Clariget OD
Clarilide
Claristad
Clarithrocid
Galemin
Klaret
Klargen
Klaricid/Klaricid OD
Klarmyn
Klaz
Klaz OD
Larizin
Maclar
Maxulid
Onexid
Oracid
Pharex Clarithromycin
RiteMED Clarithromycin
Ritromax
Winthrop Clarithromycin
Erythromycin
Drugmaker's Biotech
Erythromycin
Erasymin
Erythrocin/Erythrocin DS
Monocyclic Beta-Lactam Antibiotic
Aztreonam
Azactam
Amoxicillin/Sulbactam
Ultramox
Ampicillin
Ampimax
Ampicin
Cilisod
DLI Ampicillin
Drugmaker's Biotech Ampicillin
Eurocin
Excillin
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Spectraban Ultra 28
Calamine/Diphenhydramine
Caladryl Lotion
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Light Liquid Paraffin
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