Abstract
Androgenetic alopecia (AGA) is a non-scarring hair loss resulting from androgen-induced shortening of the hair follicle growth phase and eventual hair follicle miniaturization. Clinically, AGA manifests as a distinct hair loss pattern characterized as progressive hair thinning and shedding in androgen-dependent regions of the scalp. Given a pathogenesis centered around androgenic activity, any external stimulus that affects the delicate balance of androgens and estrogens has the potential to impact the clinical course of AGA. A number of drugs that promote androgenic activity or inhibit estrogenic activity carry the risk of unmasking AGA in genetically predisposed individuals or exacerbating existing AGA symptoms. A comprehensive understanding of the specific drugs that contribute to AGA progression and severity is essential in the effective clinical evaluation and management.
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