Drug-induced pigmentation (DIP) denotes abnormal cutaneous pigmentation resulting from exposure to specific medications through distinct pathophysiologic mechanisms. Hyperpigmentation comprises darkening of the skin relative to its baseline color. Numerous pharmacologic classes have been associated with pigmentation, including cytotoxic agents, analgesics, anticoagulants, antimicrobials, antivirals, antiarrhythmics, and heavy metals. Mechanisms implicated in DIP include chronic or acute inflammation leading to postinflammatory pigmentary alteration, stimulation of melanocytes with increased melanin synthesis, and, most frequently, direct deposition of the drug or its metabolites within the dermis or epidermis. Histopathologic findings are typically nonspecific and vary according to the mechanism involved.

Diagnosis of DIP requires a high index of clinical suspicion, detailed knowledge of commonly implicated medications, and evaluation of pigment distribution, anatomic localization, and hue, which may suggest a drug-related etiology. Further diagnostic and therapeutic advances are required to manage refractory or generalized cases, as well as dermal pigment deposition mimicking tattoo-like discoloration.