Pathophysiology of Hyperpigmentation in Tinea Versicolor
The hyperpigmentation in tinea versicolor is not due to increased melanin production or melanocyte activity, but rather represents a direct pigmentation effect from the Malassezia organism itself or its metabolic byproducts. 1
Mechanism of Hyperpigmentation
The pathophysiology of hyperpigmented lesions in tinea versicolor remains incompletely understood and differs fundamentally from the hypopigmented variant:
Hyperpigmentation is NOT melanin-mediated: Light and electron microscopic examination of hyperpigmented tinea versicolor lesions, particularly those involving vitiliginous skin, reveals an absence of melanosomes and melanocytes, definitively proving that the reddish-tan and fawn-colored hyperpigmentation is not due to melanin pigment. 1
The pigment source remains unclear: Currently, there is no definitive scientific explanation for the mechanism of hyperpigmented lesions in tinea versicolor, though the pigmentation appears to originate from the fungus itself or its metabolic products rather than from host melanin. 2
Fungal overgrowth drives pathogenesis: Malassezia species, which are normal commensal yeasts in seborrheic areas, undergo overgrowth in both filamentous and yeast structures when triggered by contributing factors including oily preparations, increased ambient humidity, corticosteroid use, or genetic predisposition. 2
Contrast with Hypopigmentation Mechanism
Understanding the hyperpigmentation mechanism requires contrasting it with the well-established hypopigmentation pathway:
Hypopigmentation has a known mechanism: Exposure to sunlight stimulates Malassezia to produce azelaic acid, which inhibits tyrosinase and causes the characteristic hypopigmented spots seen in tinea versicolor. 2
Hypopigmented lesions show distinct histology: Under light microscopy, hypopigmented lesions on dark skin demonstrate a thicker stratum corneum, more tonofilaments in the stratum granulosum, and more sequestered melanosomes compared to normal skin. 3
Clinical Implications
Mixed presentations are common: Tinea versicolor manifests clinically as asymptomatic hypopigmented macules, hyperpigmented macules, or a combination of both, with most dark-skinned patients presenting predominantly with hypopigmented lesions. 3
Diagnostic confirmation remains straightforward: Despite the unclear mechanism of hyperpigmentation, diagnosis relies on identifying the dimorphic fungus (both hyphal and yeast forms) under light microscopy with KOH preparation. 3, 4
Common Pitfalls
Do not assume melanin excess: Clinicians should not attribute hyperpigmentation in tinea versicolor to increased melanin production or melanocyte hyperactivity, as this is histologically disproven. 1
Recognize differential diagnoses: Hyperpigmented tinea versicolor must be distinguished from confluent and reticulated papillomatosis, seborrheic dermatitis, and post-inflammatory hyperpigmentation, all of which have different pathophysiologic mechanisms. 3