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    Subjects/Dermatology/Pityriasis (Tinea) Versicolor — Hypopigmented Macules
    Pityriasis (Tinea) Versicolor — Hypopigmented Macules
    medium
    hand Dermatology

    A 24-year-old male athlete from Mumbai presents with multiple oval hypopigmented and erythematous macules with fine branny scale over his chest and back that have been present for 3 months. Wood's lamp examination shows yellow-green fluorescence. KOH mount of the scale reveals the classic "spaghetti and meatballs" pattern. The condition marked **D** in the diagram is responsible for this presentation. Which of the following best describes the pathogenic mechanism by which this organism causes hypopigmentation in this patient?

    A. Direct destruction of melanocytes through fungal keratinolytic enzymes
    B. Competitive inhibition of DOPA oxidase in the melanin synthesis pathway
    C. Increased production of enlarged melanosomes leading to pigment deposition
    D. Production of azelaic acid that competitively inhibits tyrosinase and suppresses melanocyte function

    Explanation

    ## Why "Production of azelaic acid that competitively inhibits tyrosinase and suppresses melanocyte function" is right The clinical anchor states explicitly that **hypopigmentation in pityriasis versicolor is caused by azelaic acid produced by Malassezia species — a competitive inhibitor of tyrosinase that suppresses melanocyte function**. This is the gold-standard mechanism taught in Bolognia Dermatology and IADVL. The patient's presentation (hypopigmented macules, "spaghetti and meatballs" on KOH, yellow-green Wood's lamp fluorescence) is pathognomonic for Malassezia furfur/globosa infection, and the question tests the student's understanding of WHY hypopigmentation occurs — not just that it does. ## Why each distractor is wrong - **Direct destruction of melanocytes through fungal keratinolytic enzymes**: Malassezia does not destroy melanocytes; it is a superficial stratum corneum infection. The organism does not invade deeper dermis or target melanocytes directly. This is a plausible-sounding mechanism but contradicts the pathophysiology. - **Increased production of enlarged melanosomes leading to pigment deposition**: This mechanism actually causes HYPERPIGMENTATION (not hypopigmentation) in tinea versicolor, as stated in the anchor. This distractor tests whether students confuse the two color variants. - **Competitive inhibition of DOPA oxidase in the melanin synthesis pathway**: While DOPA oxidase is involved in melanin synthesis, the anchor specifically names TYROSINASE as the enzyme inhibited by azelaic acid. DOPA oxidase is a different enzyme in the pathway, and this represents a common confusion point in biochemistry. **High-Yield:** Azelaic acid (Malassezia metabolite) → tyrosinase inhibition → hypopigmentation; enlarged melanosomes + inflammation → hyperpigmentation. Same organism, different pathways = "versicolor" (multiple colors). [cite: Bolognia Dermatology 5e Ch 77; IADVL Textbook 5e]

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