Steroid Atrophy - Findings

Findings

General skin atrophy consists of a reduction in epidermal and dermal thickness, regression of the sebaceous glands, subcutaneous fat loss, and muscle-layer atrophy. These changes are typically observed following 2 to 3 weeks of moderate- to high-potency topical corticosteroid use. A single application of a very potent topical steroid can cause an ultrasonographically detectable decrease in skin thickness that lasts up to 3 days. Even low-potency topical steroids can cause slight skin atrophy that often reverses upon discontinuation of the drugs. Atrophy and striae are of concern on areas of the skin with high permeability, such as the face and intertriginous areas, but these adverse events can occur anywhere, especially after long-term use of moderate- or high-potency topical corticosteroids. While mild atrophy and telangiectasia might be reversible upon discontinuation of corticosteroids, overtly visible changes in skin texture and striae are considered permanent manifestations of corticosteroid-induced atrophy and are resistant to treatment.

The therapeutic effects of topical steroids can be negated by the resulting thinning of the stratum corneum. Such thinning impairs its barrier function and allows transepidermal water loss that can lead to skin irritation. Sometimes, the visible and textural changes to the skin are described as looking like “cigarette paper.” The skin thins because of decreased production of fibroblasts and abnormal deposition of collagen and elastin. Loss of hyaluronic acid leads to decreased retention of dermal moisture.

The structural changes and the signs and symptoms of chronologically aged skin and those of corticosteroid induced chronic atrophy of the skin are partially very similar. Thinning of epidermis and laxity as well as dryness, purpura and echymoses occur in both conditions. However, in chronologically aged skin striae are not observed, while in corticosteroid atrophy premalignant or malignant tumours are seldom observed.