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Pruritus since childhood

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Differential Dx includes psoriasis and scabies

The differential diagnosis of chronic atopic dermatitis consists of allergic or irritant contact dermatitis, plaque psoriasis, seborrheic dermatitis, scabies, and drug eruptions. Early diagnosis of atopic dermatitis is imperative to prevent sleep disturbances, chronic secondary skin changes, scarring, and the development of skin infections.

Allergic or irritant contact dermatitis is a cutaneous inflammation occurring after contact with an allergen or irritant. The lesions include erythematous, scaling areas with marked borders that are commonly pruritic. Acute cases often present with vesicles and bullae, while lichenification with cracks and fissures are common among chronic cases. Patch testing may be performed if the diagnosis is suspected.

Plaque psoriasis is characterized by areas of dry, erythematous, and well-demarcated plaques with silver scales that are most commonly found on the knees, elbows, scalp, and lower back. Systemic manifestations can include joint pain and joint swelling. Nail pitting and onycholysis are also common. While our patient had skin thickening, it was from the lichenification that is common in atopic dermatitis.

Psoriasis and atopic dermatitis are often confused. Psoriasis has discrete plaques on extensor surfaces and is often associated with nail changes, while the thickening of the skin that comes with chronic itch and scratching of atopic dermatitis is often less well circumscribed and found on flexor surfaces. Family physicians are frequently the first to encounter patients with atopic dermatitis and psoriasis and must be able to distinguish these conditions, as their treatments differ.

Seborrheic dermatitis is a chronic, relapsing inflammatory condition characterized by pruritic, erythematous, greasy, scaly patches on sebum-rich skin such as the scalp, face, and upper trunk. Seborrheic dermatitis is a clinical diagnosis.

Scabies is a pruritic skin condition caused by Sarcoptes scabiei var hominis. Characteristic linear burrows often appear as serpiginous, gray, threadlike elevations in the webbed spaces of the fingers, scrotum, areolae, elbows, axillae, feet, and wrist flexors. Secondary lesions from scratching or inflammation include excoriations, erythema, and hyperpigmentation. The diagnosis is made clinically and confirmed by dermoscopy, when available. Alternatively, mites or eggs may be observed on skin scrapings using light microscopy.

Drug eruptions should be considered in individuals taking medications who develop acute, symmetric cutaneous eruptions that may be morbilliform, urticarial, papulosquamous, pustular, or bullous in nature.

Treatment depends on severity, area of involvement, and patient’s age

Components of atopic dermatitis treatment include skin hydration, negative stimuli avoidance, pharmacologic modalities, and patient education. Improved skin hydration can be achieved by applying thick emollients containing little to no water at least twice daily and after bathing.

Topical corticosteroids are added when emollient use alone fails. Potency selection is based upon the patient’s age, involved body region, and the severity of skin inflammation.8 In order to reduce cutaneous atrophy, only low-potency corticosteroids should be applied to the face, groin, and axillae. Patients with mild disease may apply desonide 0.05% or hydrocortisone 2.5% cream or ointment once or twice daily for 2 to 4 weeks.8 Patients without improvement or with moderate disease may need medium- to high-potency steroids such as fluocinolone 0.025% or triamcinolone 0.1%.

Exacerbations of atopic dermatitis may be caused by heat exposure, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.

Patients with atopic dermatitis on the face, eyelids, neck, and skin folds or those who do not obtain relief from combined emollients and topical corticosteroids may benefit from topical calcineurin inhibitors such as pimecrolimus or tacrolimus.9 However, these agents should be utilized only for short periods of time and avoided in immunocompromised patients and those younger than 2 years of age.9

Patients with uncontrolled moderate to severe refractory disease may consider a trial of phototherapy or cyclosporine if phototherapy is ineffective or unavailable.10 A meta-analysis has shown that once remission is achieved, intermittent therapy with moderate- to high-potency corticosteroids or tacrolimus may be effective in reducing subsequent flares.11

In all cases, sedating antihistamines such as diphenhydramine or hydroxyzine can be utilized for pruritic relief, particularly at night. Additionally, signs suggestive of infection should prompt antibiotic treatment with agents that provide coverage for Staphylococcus and Streptococcus species. Lastly, patients must be adequately educated on stimuli avoidance (eg, hot water, wool) and counseled on the medical and psychological issues that often accompany atopic dermatitis.

Our patient was placed on triamcinolone 0.1% for 4 weeks and her condition improved.

CORRESPONDENCE
Andrea Richardson, MD, MPH, 7414 Carriage Bay, San Antonio, TX 78249; RichardsonAM@livemail.uthscsa.edu.

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