Background
First described by Brocq in 1907, using the term eczema craquelé, asteatotic dermatitis is characterized by pruritic, dry, cracked, and polygonally fissured skin with irregular scaling. It most commonly occurs on the shins of elderly patients, but it may occur on the hands and the trunk.
In 1971, Domonkos described the appearance of this dermatitis as cracked porcelain. The pattern of cracking has been likened to a crazy pavement pattern. In 1999, Fitzpatrick likened asteatotic eczema to a dried-up riverbed. According to Caplan, superficial bleeding and fissures can occur as the epidermis loses water, as it splits, and as it cracks deeply enough to disrupt papillary dermal capillaries. The inflammation can be associated with asymmetric leg edema. Eczema with increased lichenification occasionally supervenes as patients rub and scratch the pruritic areas.
The eruption can be generalized or localized. Generalized asteatosis is a distinct entity and should provoke a search for possible associated diseases. Guillet divides the localized forms into 4 types:
- Asteatotic eczema of the lower extremities in elderly persons secondary to aging, dehydrated skin, and malnutrition
- Cracked erythema secondary to irritant contact dermatitis from soaps or detergents
- Eczema craquelé in areas in which corticosteroid therapy was discontinued
- Asteatotic eczema in neurologic disorders
Pathophysiology
Initially, excess water loss from the epidermis results in dehydration of the stratum corneum with upward curling of corneocytes. The outer keratin layers require 10-20% water concentration to maintain their integrity. A significant decrease in free fatty acids in the stratum corneum is present in people with asteatotic dermatitis. Stratum corneum lipids act as water modulators, and cutaneous loss of these lipids can increase transepidermal water loss to 75 times that of healthy skin.[1] Elderly persons with decreased sebaceous and sweat gland activity, patients on antiandrogen therapy, people using degreasing agents, and people bathing without replacing natural skin emollients lost to bath water are at risk for asteatotic eczema.
When the stratum corneum loses water, the cells shrink. A significantly decreased cellular volume can stress the skin's elasticity, creating fissures. Edema in the dermis leads to additional stretch on the overlying epidermis. Fissures rupture dermal capillaries, causing clinical bleeding. The disruption of cutaneous integrity can result in inflammation with risk of infection. Transepidermal absorption of allergens and irritants is increased as the epidermis is damaged, increasing susceptibility to allergic contact dermatitis and irritant contact dermatitis.[2] Allergic contact dermatitis and irritant contact dermatitis may cause a persistent and possibly more extensive dermatitis despite therapy. Furthermore, low environmental humidity contributes to xerosis, creating a clinical picture of asteatotic dermatitis in some dermatologic conditions, such as atopic dermatitis.
Epidemiology
Frequency
United States
Seasonality is prominent, and most patients present in the winter months, especially in areas where indoor humidity is decreased by heating. The frequency of asteatotic dermatitis is increased in the northern United States, particularly during the winter season.
Mortality/Morbidity
Although most cases resolve without ill effects, asteatotic dermatitis can be chronic with relapses frequent during the winter months and during times of low humidity.
Sex
Men older than 60 years develop asteatotic dermatitis more commonly than women.
Age
The median patient age at presentation is 69 years. Asteatosis can also occur in young people.
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