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Celiac Disease

Algorithm: Rash

CODES

ICD10

L13.0 Dermatitis herpetiformis

CLINICALPEARLS

DH is a chronic, relapsing, intensely pruritic rash that often presents with erosions, excoriations, lichenification, and pigmentary changes secondary to scratching and healing of old papulovesicular lesions.

Strong association with GSE

Diagnosis established with perilesional skin biopsy showing DIF demonstrating granular IgAdeposits in the dermal papillae

Serologic levels of IgAtransglutaminase aid in diagnosis and monitoring of deviations from GFD.

Mainstay of treatment is a GFD with dapsone used primarily for short-term symptom relief.

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DERMATITIS, ATOPIC

Dennis E. Hughes, DO, FAAFP, FACEP

BASICS

DESCRIPTION

Achronic, relapsing, pruritic eczematous condition affecting characteristic sites

Early onset cases have coexisting allergen sensitization more often than late onset.

Clinical phenotypical presentation is highly variable, suggesting multifactorial pathophysiology.

May have significant effect on quality of life for patient and family—similar to that of psoriasis

EPIDEMIOLOGY

45% of all cases begin in the first 6 months of life with 95% onset prior to age 5 years.

70% of affected children will have a spontaneous remission before adolescence.

Incidence on the rise for the past 3 decades in industrialized countries; overall, affects ~15% of children at some time (United States)

Also, may have late-onset dermatitis in adults or relapse of childhood condition—primarily hand eczema

Asians and blacks are affected more often than whites.

60% if one parent is affected; rises to 80% if both parents are affected

ETIOLOGYAND PATHOPHYSIOLOGY

Two main hypothesis: immunologic with unbalanced immune response and/or skin barrier dysfunction (1)

Alteration in stratum corneum results in transepidermal water loss and defect in barrier function.

Epidermal adhesion is reduced either as a result of (i) genetic mutation resulting in altered epidermal proteins or (ii) defect in immune regulation causing an altered inflammatory response.

Interleukin-31 (IL-31) upregulation is thought to be a major factor in pruritus

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mediated by cytokines and neuropeptides rather than histamine excess.

Genetics

Recent discovery of association between atopic dermatitis (AD) and mutation in the filaggrin gene (FLG), which codes for a skin barrier protein (2)

Both epidermal and immune coding likely involved

RISK FACTORS

“Itch–scratch cycle” (stimulates histamine release)

Skin infections

Emotional stress

Irritating clothes and chemicals

Excessively hot or cold climate

Food allergy in children (in some cases). Studies of breastfeeding conveying decreased risk versus increased risk are mixed in conclusion (3)[C].

Exposure to tobacco smoke Family history of atopy

–Asthma

–Allergic rhinitis

COMMONLYASSOCIATED CONDITIONS

Food sensitivity/allergy in many cases

Asthma

Allergic rhinitis

Hyper-IgE syndrome (Job syndrome)

–AD

–Elevated IgE

–Recurrent pyodermas

–Decreased chemotaxis of mononuclear cells

DIAGNOSIS

HISTORY

Presence of major symptoms, including relapsing of condition, family history, typical distribution, and morphology necessary to make diagnosis of AD Upward of 33% report associated mood and sleep disruption.

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PHYSICALEXAM

Primarily skin manifestations

Distribution of lesions

–Infants: trunk, face, and flexural surfaces; diaper-sparing

–Children: antecubital and popliteal fossae

–Adults: hands, feet, face, neck, upper chest, and genital areas

Morphology of lesions

–Infants: erythema and papules; may develop oozing, crusting vesicles

–Children and adults: Lichenification and scaling are typical with chronic eczema as a result of persistent scratching and rubbing (lichenification rare in infants).

Associated signs

–Facial erythema, mild to moderate

–Perioral pallor

–Infraorbital fold (Dennie sign/Morgan line)—atopic pleat

–Dry skin progressing to ichthyosis

–Increased palmar linear markings

–Pityriasis alba (hypopigmented asymptomatic areas on face and shoulders)

–Keratosis pilaris

DIFFERENTIALDIAGNOSIS

Photosensitivity rashes

Contact dermatitis (especially if only the face is involved)

Scabies

Seborrheic dermatitis (especially in infants)

Psoriasis or lichen simplex chronicus if only localized disease is present in adults

Rare conditions of infancy

–Histiocytosis X

–Wiskott–Aldrich syndrome

–Ataxia-telangiectasia syndrome

Ichthyosis vulgaris

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

No test is diagnostic.

Serum IgE levels are elevated in as many as 80% of affected individuals, but

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test is not routinely ordered.

Eosinophilia tends to correlate with disease severity.

Scoring atopic dermatitis (SCORAD) is scoring system for AD comprising scores for area, intensity, and subjective symptoms.

TREATMENT

GENERALMEASURES

Minimize flare-ups and control the duration and intensity of flare-up.

Avoid agents that may cause irritation (e.g., wool, perfumes).

Minimize sweating.

Lukewarm (not hot) bathing

Minimize use of soap (superfatted soaps best).

Sun exposure may be helpful.

Humidify the house.

Avoid excessive contact with water.

Avoid lotions that contain alcohol.

If very resistant to treatment, search for a coexisting contact dermatitis.

Pediatric Considerations

Chronic potent fluorinated corticosteroid use may cause striae, hypopigmentation, or atrophy, especially in children.

MEDICATION

First Line

Frequent systemic lubrication with thick emollient creams (e.g., Eucerin, Vaseline) over moist skin is the mainstay of treatment before any other intervention is considered (1)[A].

Infants and children: 0.5–1% topical hydrocortisone creams or ointments (use the “fingertip unit [FTU]” dosing) (1)[C]

Adults: higher potency topical corticosteroids in areas other than face and skin folds

Short-course, higher potency corticosteroids for flares; then, return to the lowest potency (creams preferred) that will control dermatitis. Antihistamines for pruritus (e.g., hydroxyzine 10 to 25 mg at bedtime and as needed)

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Second Line

Topical immunomodulators (tacrolimus or pimecrolimus) for episodic use for children >2 years. There is a black box warning from the FDAregarding potential cancer risk.

Plastic occlusion in combination with topical medication to promote absorption

For severe AD, consider systemic steroids for 1 to 2 weeks (e.g., prednisone 2 mg/kg/day PO [max 80 mg/day] initially, tapered over 7 to 14 days).

Topical tricyclic doxepin, as a 5% cream, may decrease pruritus.

Modified Goeckerman regimen (tar and ultraviolet light)

Low-dose methotrexate was established as effective treatment in adults, and recent review suggests it is safe for children and adolescents (4)[B].

Dupilumab, a biologic that targets mediators of inflammation (IL-22, IL-17, IFN-γ), has completed phase III trials and is awaiting approval (5).

ISSUES FOR REFERRAL

Ophthalmology evaluation for persistent vernal conjunctivitis

If using topical steroids around eyes for extended periods, ophthalmology follow-up for cataract evaluation

ADDITIONALTHERAPIES

Methods to reduce house mite allergens (micropore filters on heating, ventilation, and air-conditioning systems; impermeable mattress covers)

Behavioral relaxation therapy to reduce scratching

Bleach baths may reduce staph colonization, but definitive evidence for benefit in the condition is lacking. Recommend 1/2 cup of standard 6% household bleach for a full tub of water and soak for 5 to 10 minutes, blotting skin dry upon leaving the bath.

COMPLEMENTARY& ALTERNATIVE MEDICINE

Evening primrose oil (includes high content of fatty acids)

–May decrease prostaglandin synthesis

–May promote conversion of linoleic acid to omega-6 fatty acid

Probiotics may reduce the severity of the condition, thus reducing medication use.

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ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Patient Monitoring

Evaluate to ensure that secondary bacterial or fungal infection does not develop as a result of disruption of the skin barrier. Most patients with AD are colonized by Staphylococcus. There is a little evidence for the routine use of antimicrobial interventions to reduce skin bacteria, but treatment of clinical infection with coverage for Staphylococcus is recommended.

DIET

Trials of elimination may find certain “triggers” in some patients.

Breastfeeding in conjunction with maternal hypoallergenic diets may decrease the severity in some infants (varying opinions).

PATIENT EDUCATION

http://www.aad.org/skin-conditions/dermatology-a-to-z/atopic-dermatitis

National Eczema Association: www.nationaleczema.org

PROGNOSIS

Chronic disease

Declines with increasing age

90% of patients have spontaneous resolution by puberty.

Localized eczema (e.g., chronic hand or foot dermatitis, eyelid dermatitis, or lichen simplex chronicus) may continue in some adults.

COMPLICATIONS

Cataracts are more common in patients with AD.

Skin infections (usually Staphylococcus aureus); sometimes subclinical Eczema herpeticum

–Generalized vesiculopustular eruption caused by infection with herpes simplex or vaccinia virus

–Causes acute illness requiring hospitalization

Atrophy and/or striae if fluorinated corticosteroids are used on face or skin folds

Systemic absorption may occur if large areas of skin are treated, particularly if high-potency medications and occlusion are combined.

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REFERENCES

1.Thomsen SF. Atopic dermatitis: natural history, diagnosis, and treatment. ISRN Allergy. 2014;2014:354250.

2.Wollenberg A, Seba A, Antal AS. Immunological and molecular targets of atopic dermatitis treatment. Br J Dermatol. 2014;170(Suppl 1):7–11.

3.Lin HP, Chiang BL, Yu HH, et al. The influence of breastfeeding in breast-fed infants with atopic dermatitis [published online ahead of print June 29, 2017]. J Microbiol Immunol Infect. doi:10.1016/j.jmii.2017.06.004.

4.Deo M, Yung A, Hill S, et al. Methotrexate for treatment of atopic dermatitis in children and adolescents. Int J Dermatol. 2014;53(8):1037–1041.

5.D’Erme AM, Romanelli M, Chiricozzi A. Spotlight on dupilumab in the treatment of atopic dermatitis: design, development, and potential place in therapy. Drug Des Devel Ther. 2017;11:1473–1480.

ADDITIONALREADING

Boguniewicz M, Leung DY. Recent insights into atopic dermatitis and implications for management of infectious complications. J Allergy Clin Immunol. 2010;125(1):4–13.

Lifschitz C. The impact of atopic dermatitis on quality of life. Ann Nutr Metab. 2015;66(Suppl 1):34–40.

SEE ALSO

Algorithm: Rash

CODES

ICD10

L20.9 Atopic dermatitis, unspecified

L20.89 Other atopic dermatitis

L20.83 Infantile (acute) (chronic) eczema

CLINICALPEARLS

Institute early and proactive treatment to reduce inflammation. Use the lowest

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potency topical steroid that controls symptoms.

Monitor for secondary bacterial infection.

Frequent systemic lubrication with thick emollient creams (e.g., Eucerin, Vaseline) over moist skin is the mainstay of treatment before any other intervention is considered.

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DERMATITIS, CONTACT

Anne Walsh, ANP-BC Konstantinos E. Deligiannidis, MD, MPH, FAAFP

BASICS

DESCRIPTION

Acutaneous reaction to contact with an external substance

Different mechanisms result in similar skin manifestation (1)

Primary irritant dermatitis (ID) results from direct damage to the stratum corneum by chemicals or physical agents occurring faster than the skin is able to repair itself, leading to an inflammatory nonimmunologic cutaneous reaction. Prior sensitization is not required (2).

Allergic contact dermatitis (ACD) affects only individuals previously sensitized to a substance. It represents a delayed hypersensitivity reaction, requiring several hours for the cascade of cellular immunity to be completed to manifest itself (2).

System(s) affected: skin/exocrine

Synonym(s): dermatitis venenata

EPIDEMIOLOGY

Common

Incidence

Occupational contact dermatitis: 20.5/100,000 workers/year in one Australian study

Prevalence

Contact dermatitis represents >90% of all occupational skin disorders. Predominant sex: male = female

–Variations due to differences in exposure to offending agents, as well as normal cutaneous variations between males and females (eccrine and sebaceous gland function and hair distribution)

Geriatric Considerations

Increased incidence of ID secondary to skin dryness

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