DERMATOLOGIC DISEASE
From Clinical Pediatrics, presented March 3-6, 2005, by the American Academy of Pediatrics, California Chapter 2 and the
Los Angeles Pediatric Society
Alfred T. Lane, MD, Professor of Dermatology and Pediatrics, and Chairman, Department of Dermatology, Stanford
University School of Medicine, Stanford, California
| Introduction: atopic dermatitis “the itch that rashes”; child with sensitive itchy skin scratches it; scratching causes inflammation
and lichenification; most common skin condition in children <11 yr of age (incidence increasing); usually develops
by 1 yr of age (90% by 5 yr of age)
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| Clinical presentation by age
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 | Infantile phase (1-18 mo of age): disease usually not seen at <1 mo of age (consider possibility of ichthyosis); infant <5
or 6 mo of age not coordinated enough to scratch skin (areas of dermatitis located where patient rubs face, back, or
arms against something); generalized dermatitis; signs and symptoms—lichenification; crusting; facial involvement
classic; lichenification on extensor surfaces instead of popliteal or antecubital fossa; generalized diffuse dermatitis; at
<1 yr of age, diaper area usually spared
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| Childhood phase (18 mo to puberty): chronic dermatitis; flexor surface involvement; possible involvement of feet and hands;
callus formation; scratching induces cycle of pruritus; lichenification of dorsum of hands marker for difficult atopic
dermatitis; foot dermatitis (90% atopic dermatitis; occasionally, contact dermatitis; rarely, fungal infection); diffuse
dermatitis
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| Adolescent and adult phases: chronic hand dermatitis; involvement of antecubital and popliteal fossa; occasionally, generalized
dermatitis
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| Scratching at night: frequent awakening after sleep onset often disturbs whole family; child with mild-to-moderate atopic
dermatitis may scratch 1.5 hr/night; some children scratch while sound asleep
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| Triggers: dry skin; sudden change in temperature (heat or cold); occlusive dressings or greasy ointments; friction sensed as pruritus;
soaps and detergents remove lipids from skin; food; infection
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| Dry skin: primary defect inability to maintain water in skin; patients with atopic dermatitis lose more water through normal
skin and areas of dermatitis; measurable insufficiency of water held in stratum corneum
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| Staphylococcus aureus (eg, methicillin-resistant S aureus [MRSA]): makes treatment of atopic dermatitis difficult; as
dermatitis worsens, S aureus numbers increase; often, patients have IgE antibodies to S aureus (those patients more likely to
have IgE antibodies to certain foods); so, S aureus can be infectious agent and allergen; complications—sepsis; lymphadenopathy
(may resolve with treatment of dermatitis); case—patient on long-term dicloxacillin (with discontinuation, recolonization)
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| Pathogenesis: immune defects—TH 2 cells and allergens involved; IgE elevated; knowledge about immune defect weak;
diet—radioallergosorbent test (RAST) often positive (if negative, value ≈95%; if positive, 5%-25%); dogs and cats
(study)—if raised in home that has ≥2 dogs or cats, incidence of atopy lower
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| Atopy and hepatitis A virus (HAV) infection: incidence of atopy increasing (HAV infection decreasing); exposure to HAV
associated with poor hygiene, large families, and attendance in day care center; incidence of atopic dermatitis associated
with good hygiene, small families, and avoiding day care centers; HAV less common than 50 yr ago (as HAV decreased,
atopic dermatitis increased); study—HAV may protect against atopy in individuals who carry variant of gene that encodes
TIM-1, cell-surface receptor used by HAV to infect human cells
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| Antimicrobial peptides: human skin contains antimicrobial peptides known as cathelicidins and β-defensins; S aureus infection
rarely seen in psoriasis (patients with psoriasis make more β-defensins and cathelicidins; patients with atopic dermatitis
do not); probably, topical steroids decrease inflammation, allowing body to produce natural defense mechanisms
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Therapy
| Hydration of skin: in hot humid environment, consider lotion; in dry environment (eg, desert), consider ointment; or, ointments
in winter and lotions in summer; bathe child at least once daily (wet skin 3-5 min; avoid soap); while skin still
moist, apply topical steroid, then apply moisturizing cream or ointment over topical steroids; apply steroids just to areas
of dermatitis (moisturizer over whole body); continue moisturizing throughout day; if problem severe, bath and hydration
twice daily may be better; bathing too long (eg, 10 min) removes skin’s natural moisturizers
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| Topical steroids: relieve pruritus and inflammation and decrease density of S aureus; use lowest effective strength; at <6 mo
of age, hydrocortisone 2.5% inexpensive option; desonide another choice; in older child, fluocinolone or triamcinolone
(speaker uses 0.1% concentration); consider mometasone furoate; low risk for adrenal suppression; as dermatitis decreases,
use less steroid; avoid fluorinated steroids on face (use hydrocortisone or desonide on face and genital area);
speaker prefers steroid cream (some patients incorrectly use steroid ointment as moisturizer)
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| Moisturizers: generic petrolatum fine; Cetaphil (skin moisturizer) less greasy; in humid environment, consider lotion (lotions
contain more water and less oil than creams and ointments
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| Applying topical steroids: families less phobic about steroids if they can control amount; use finger tip unit (FTU; squeeze
out ointment or cream from distal interphalangeal joint to end of finger); 1 FTU should be enough to cover 2 palms (the
smaller the finger, the smaller the palms); daily regimen—goal 2 FTUs/day (when child worse, 10 FTUs may be needed);
initially, hydration and topical steroids bid; as patient improves, hydration bid or more; then, steroids less frequently and
in decreased dose
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| Immunomodulators-macrolactams: potent drugs; approved down to 2 yr of age; no data that this causes lymphoma or cancers
in humans, but data in animals (levels used higher than maximum absorbed through human skin); in patients on tacrolimus
(FK506), increased risk for lymphoma and pseudolymphoma syndrome; increased absorption in children with
Netherton syndrome; second-line drugs (topical steroids first choice); drugs do not work well for lichenified skin; immunomodulators
block calcineurin; alternative to glucocorticosteroids; more expensive than topical steroids; tacrolimus
(Protopic)—slightly more burning and stinging; approved for more severe atopic dermatitis; used around eyelids on face
or on unlichenified areas of dermatitis; speaker may have patient on immunomodulator as well as topical steroid
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| Systemic antibiotics: overgrowth of S aureus common; cephalexin (Keflex) often helpful, even in MRSA; speaker prefers
systemic antibiotics over prednisone (fewer side effects)
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| Oral antipruritics: hydroxyzine (Atarax)—if used too frequently, risk for tachyphylaxis; antihistamines work well with
change in weather to hot and humid; use at night (1-2 mg/kg); diphenhydramine (Benadryl)—not as effective; side effect
of sleepiness helpful
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| Chronic disease: keep skin hydrated; avoid triggers; keep fingernails short; treat secondary infections early; severe
disease—avoid systemic steroids
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| Introduction: acne vulgaris occurs mainly on face, chest, and shoulders (area with most pilosebaceous glands); affects 85%
of patients 15 to 17 yr of age; begins before puberty; 30% of adolescents seek medical attention (75%-80% buy over-the-
counter [OTC] preparations, eg, benzoyl peroxide [Oxy 10; Proactiv solution]); cystic scarring acne occurs in about 1%
of boys (0.2% of girls)
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| Pathogenesis: processes involved—1) plugging of pilosebaceous unit; 2) obstruction of sebaceous gland and increased sebum
production; 3) lipase-producing bacteria (Propionibacterium acnes) hydrolyze triglycerides in sebum to free fatty acids;
4) inflammation (bacteria release cytokines, resulting in inflammation); triggers—hygiene and diet have little effect;
however, milk may cause increased incidence of acne (milk from pregnant cow may contain higher amounts of androgens);
oils and greases applied to skin increase acne by obstructing gland; stress (increased testosterone increases sebum
production)
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| Types of acne lesions: tailor therapy based on type of lesion; with obstruction, development of microcomedo; microcomedo
can become closed comedo (whitehead) or open comedo (blackhead); open comedos not attractive, but not major problem
(usually do not get infected or obstructed); squeezing lesion to express sebum sometimes breaks epithelial wall, causing
inflammatory pustule or cyst; treatment of cystic acne with triamcinolone injection—causes area to blanch because of
vasoconstriction; before isotretinoin (Accutane), cyst frequently would return (treat by excision)
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| Exacerbating factors: certain drugs (eg, lithium) make acne worse; excoriation (patient scratches or picks at lesion)
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| Acne in neonate: multiple erythematous papules; Pityrosporum obiculare may be involved; some children have yeast involved
more than P acnes; treatment benzoyl peroxide
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| Infantile acne: often difficult to distinguish from atopic dermatitis, but lichenification absent; case (because of severity, patient
treated with oral erythromycin); if parents have history of severe acne, neonatal or childhood acne more common;
treat to avoid pitted scars later in life
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| Treatment overview: use of scoring system helpful to track progress; often, patients have unrealistic expectations (takes ≥4
to 6 wk to see benefit)
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| Benzoyl peroxide: available OTC (eg, Proactiv solution) or by prescription; works by decreasing number of bacteria and
opening pilosebaceous gland (breaks down comedo; retinoids more effective); use once daily; speaker usually starts with
5.0% gel; more drying with higher concentrations; used alone, 4 to 6 wk or 8 wk to see much benefit; side effects—
dryness and irritation; ≈1% of population allergic to benzoyl peroxide; to test, apply to forearm 3 or 4 days to rule out allergic
contact dermatitis; stains clothing and sheets (use in morning); can be applied to wet or dry skin
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| Retinoids: tretinoin (Retin-A; also available as generic); adapalene (Differin); tazarotene (Tazorac)—developed for psoriasis;
difficult to use for acne; can be very irritating and have many side effects
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| Retin-A: gel more potent than cream (0.025% cream probably weaker than 0.01% gel); Retin-A Micro gel more expensive
than generic; reverses comedo formation by opening pilosebaceous follicle; beneficial effect usually starts at 4-6
wk (can take as long as 6 mo for maximum effect)
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| Differin: cream, gel, or solution (cream less irritating); not much difference between cream and gel (strengths equally effective);
use each evening
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| Side effects: photosensitivity; acne worse before better; start topical antibiotic at same time as Retin-A; needs to go on
dry skin (when skin wet, penetration better, but want drugs in pilosebaceous glands)
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| Combination therapy (retinoid and benzoyl peroxide): usually, drugs not started at same visit because of irritant side effects
(start second medication 6 or 8 wk later); speaker usually starts with benzoyl peroxide (more easily tolerated; seems
to toughen skin for retinoid)
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| Topical antibiotic therapy: tetracycline, erythromycin, or clindamycin; effective in reducing number of P acnes; usually needed
bid; side effects—usually related to vehicle; if lotion, often moisturizing, and some complain too greasy; if solution, more drying;
clindamycin may cause diarrhea; bacterial resistance
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| Systemic antibiotics: eg, erythromycin or tetracycline (both work by decreasing P acnes); anti-inflammatory (decrease cytokines);
dose usually ≥1 g/day; for minocycline or doxycycline, ≈200 mg/day; side effects—caution about minocycline (may
cause drug eruptions or lupus-like syndromes; if used >2 yr, patients often start to develop dark spots in place of inflammatory
papules) doxycycline slightly safer, but photosensitivity seen in ≈40% of patients; gastric irritation; Candida albicans vaginitis;
bacterial resistance; in animal studies, decreases effectiveness of oral contraceptives (no clear data in humans, but warn
sexually active patients)
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| Hormonal therapy: some birth control medications show beneficial effect for acne (triphasic norgestimate and ethinyl estradiol;
ethinyl estradiol and levonorgestrel; ethinyl estradiol and drospirenone)
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| Accutane: systemic acne therapy; used in severe, cystic-scarring acne; reduces sebum secretion and sebaceous gland size;
once drug discontinued, sebaceous gland resumes normal size, but without obstruction; 2 divided doses/day (total dose
usually 120 to 150 mg/kg); duration of therapy based on patient’s weight and dose
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| Prognosis: potential to cure (30% of patients 18-26 yr of age have no acne for 10 yr); if acne returns, may respond to
medications that did not work before; on average, 70% of patients have major improvement (30% need retreatment);
retreatment more likely in patients <18 yr of age; chest and back respond less rapidly (goal 50% improvement on face
by 8 wk (50% improvement on back and chest by 12 wk)
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| Side effects: dry mouth; teratogenicity; aches and pains; photosensitivity; sometimes, granulomatous lesions; acne fulminans
(possible septic hip due to inflammation); start with low dose and proceed slowly
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| Monitor: triglyceride levels (increase, if any, occurs in first 2 mo of therapy); lipids and liver enzymes; pregnancy tests for
girls before starting therapy (initiate during first few days of menstrual cycle); as side effect, depression resolves when
drug discontinued; requires signed consent and preauthorization; most pediatricians not using drug because of complications
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| Specific therapy: tailored for each patient; speaker comfortable recommending OTC benzoyl peroxide; papules—benzoyl
peroxide and retinoids; pustules or inflammatory lesions—may require topical or oral antibiotics; cystic scars—oral antibiotics
and, potentially, Accutane
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Educational Objectives
| The goal of this program is to educate the listener about atopic dermatitis and acne vulgaris. After hearing and assimilating
this program, the clinician will be better able to:
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| 1. Recognize signs and symptoms of atopic dermatitis.
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| 2. Choose appropriate therapy for atopic dermatitis.
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| 3. Describe the clinical presentation of acne vulgaris.
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| 4. Choose appropriate therapy for acne vulgaris.
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| 5. Prevent and manage complications of acne therapy.
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Discussed on This Program
Adapalene [Differin]
Benzoyl peroxide (several formulations and trade names)
Cephalexin [Biocef, Keflex]
Cetaphil (soap-free therapeutic cleanser)
Clindamycin (several formulations and trade names)
Desonide [DesOwen, Tridesilon]
Dicloxacillin sodium [Dycill, Dynapen, Pathocil]
Diphenhydramine HCl (several formulations and trade names)
Doxycycline (several formulations and trade names)
Drospirenone and ethinyl estradiol [Yasmin]
Erythromycin (several formulations and trade names)
Ethinyl estradiol and norgestimate (several trade names)
Fluocinolone acetonide (several formulations and trade names)
Hydrocortisone (cortisol) (several formulations and trade names)
Hydroxyzine [Atarax, Atarax 100, Vistaril, Vistazine 50]
Isotretinoin (13-cis-retinoic acid) [Accutane]
Levonorgestrel and ethinyl estradiol [Preven, Seasonale]
Lithium [Eskalith, Eskalith CR, Lithobid, Lithonate, Lithotabs]
Minocycline HCl (minomycin; several formulations and trade names)
Mometasone furoate [Elocon]
Prednisone (several formulations and trade names)
Specialized infant foods (several formulations and trade names)
Tacrolimus (FK506) [Prograf, Protopic]
Tazarotene [Tazorac]
Tetracycline HCl (several formulations and trade names)
Tretinoin (trans-retinoic acid; vitamin A acid; several formulations and trade names)
Triamcinolone (oral) [Aristocort, Atolone, Kenacort]
Triamcinolone acetonide (several formulations and trade names)
Suggested Reading
Bergfeld WF: The pathophysiology of acne vulgaris in childre.and adolescents, part 2: Tailoring treatment. Cutis 74:189,
2004; Bergfeld WF: The pathophysiology of acne vulgaris in children and adolescents, part 1. Cutis 74:92, 2004; Cork MJ
et al: Comparison of parent knowledge, therapy utilization and severity of atopic eczema before and after explanation and
demonstration of topical therapies by a specialist dermatology nurse. Br J Dermatol 149:582, 2003; Dohil MA, Eichenfield
LF: A treatment approach for atopic dermatitis. Pediatr Ann 34:201, 2005; Foti C et al: Contact allergy to topical steroids in
children with atopic dermatitis. Contact Dermatitis 52:162, 2005; Gibson LE: Atopic dermatitis. Mayo Clin Proc 80:107,
2005; Holten KB, American Academy of Dermatology: How should we care for atopic dermatitis? J Fam Pract 54:426,
2005; James WD: Clinical practice. Acne. N Engl J Med 352:1463, 2005; Kazaks EL, Lane AT: Diaper dermatitis. Pediatr
Clin North Am 47:909, 2005; Korkut C, Piskin S: Benzoyl peroxide, adapalene, and their combination in the treatment of
acne vulgaris. J Dermatol 32:169, 2005; Ozolins M et al: Comparison of five antimicrobial regimens for treatment of mild
to moderate inflammatory facial acne vulgaris in the community: randomized controlled trial. Lancet 364:2188, 2004; Webster
G: Mechanism-based treatment of acne vulgaris: the value of combination therapy. J Drugs Dermatol 4:281, 2005; Williams
HC: Clinical practice. Atopic dermatitis. N Engl J Med 352:2314, 2005;
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. Dr. Lane has participated in
a clinical trial studying Elidel funded by Novartis.
Dr. Lane was recorded at Clinical Pediatrics, presented March 3-6, 2005, in Palm Springs, California, by the American
Academy of Pediatrics, California Chapter 2 and the Los Angeles Pediatric Society. The Audio-Digest Foundation thanks
Dr. Lane and the sponsors for their cooperation in the production of this program.
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