A specific form of dermal connective tissue degeneration characterized by the accumulation of abnormal, non-functional elastic material in the dermis, directly resulting from chronic, elevated levels of the glucocorticoid hormone cortisol. This pathological process leads to a clinical presentation of thin, fragile skin with increased laxity and a predisposition to bruising and striae formation. It is a recognized dermatological sequela of sustained hypercortisolism, whether endogenous or exogenous in origin.
Origin
The term is a compound of the stress hormone “cortisol,” which is produced by the adrenal cortex, and “elastosis,” a dermatopathology term derived from Greek elastos (ductile) and -osis (abnormal condition). Its clinical context is rooted in endocrinology and dermatopathology, particularly in conditions like Cushing’s syndrome or prolonged systemic corticosteroid use. The descriptor precisely links a hormonal imbalance to a distinct histological and clinical skin finding.
Mechanism
Excess cortisol binds to glucocorticoid receptors on dermal fibroblasts, initiating a cascade that significantly inhibits the synthesis of new collagen and hyaluronic acid. Simultaneously, cortisol promotes the catabolism of existing collagen fibers and disrupts the normal structure and organization of the elastic fiber network. This combined effect of impaired synthesis and accelerated degradation leads to the characteristic structural weakness and pathological accumulation of disorganized elastic tissue within the dermis.
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