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A 48-year-old man comes to the physician because of a skin rash his girlfriend noticed on his chest and back. He is not sure how long it has been there. He is in good health and routinely takes vitamin supplements. His job is very demanding and he works out in a gym five nights a week to stay fit and alleviate stress. After his girlfriend commented on the rash he did notice that he has lately started feeling slightly itchy after working out, but did not make anything of that. He has no history of allergies to medications and the family history is negative for skin diseases. On physical examination, the patient is a muscular, fit man in no acute distress. On the sides of the neck, anterior chest, shoulders, and upper back, there are many round and oval, discrete and confluent, hypopigmented patches with a barely visible fine scale that is accentuated by rubbing. An image of the lesion is shown. The rest of the physical examination is unremarkable. Which of the following is most likely mechanism of the pigmentary change?

A. Abnormal transfer of melanosomes

B. Autoimmune destruction of melanocytes

C. Competitive inhibition of tyrosinase

D. Lysosomal defect E. Self-inflicted physical trauma

E. Self-inflicted physical trauma

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الحالة هي النخالية المبرقشة

The correct answer is C. The patient has Tinea versicolor, a common skin infection in young adults who perspire freely. Tinea versicolor is caused by a nondermatophyte, dimorphic fungus that is a normal inhabitant of the skin. As the yeast form Pityrosporum orbiculare, it generally does not cause disease (except for folliculitis in certain cases). However, in some individuals it converts to the hyphal form, Malassezia furfur, and causes characteristic lesions. It is typically promoted by heat and humidity, and is commonly encountered in people who engage in strenuous physical activity. It is characterized by oval scaly macules, papules, and patches most commonly on the chest, shoulders, and back. The lesions appear hypopigmented on dark skin and slightly hyperpigmented on light skin. The hypopigmentation results from competitive inhibition of the enzyme tyrosinase by azelaic acid. Azelaic acid is a dicarboxylic acid produced by the hyphal form of the yeast. A potassium hydroxide preparation from scaling lesions will demonstrate short hyphae and round spores (so-called "spaghetti and meatballs"). Solutions containing sulfur, salicylic acid, or selenium sulfide will clear the infection if used daily for a week and then intermittently thereafter. It also responds well to topical antifungal creams such as ketoconazole 2% or terfenadine. Treatment with a single 400-mg dose of ketoconazole is another effective alternative. Hypopigmentation persists for a while after the infection has been eradicated, until melanocytes synthesize the melanin necessary to repigment those areas.

Abnormal transfer of melanosomes (choice A) is seen in oculocutaneous albinism type 2, formerly known as "tyrosinase positive albinos." A defect is present in the membrane transport protein in melanosome membranes and the mature melanosomes are not normally transferred to surrounding keratinocytes. The cutaneous phenotype of these patients is broad, from nearly normal pigmentation to virtually no pigment.

Autoimmune destruction of melanocytes (choice B) is one of the hypothesized pathogenetic mechanisms of vitiligo. A cytotoxic lymphocyte-mediated reaction would be responsible for destruction of melanocytes in well-demarcated areas, producing the typical well-demarcated, depigmented lesions surrounded by normal-appearing skin. The other two hypothesized mechanisms of melanocyte destruction in vitiligo is toxic injury (such as with phenol or catechol compounds) and neurogenic (as in cases that appear after a significant stressful event in the life of a patient).

A lysosomal defect (choice D) is responsible for hypopigmented skin lesions seen in Chediak-Higashi syndrome, an autosomal recessive disorder characterized by oculocutaneous albinism and immunologic deficiency, including defective phagocyte, lymphocyte, and natural killer cell function. Giant intracytoplasmatic inclusion bodies are seen in most granulated cells, as well as in melanocytes. This causes dilution of pigment, with hypopigmentation of skin, hair, and fundi.
Self-inflicted physical trauma (choice E) can result in hypopigmented or hyperpigmented macules and atrophic scars on areas of the body within easy reach of the hands. This disorder, called neurotic excoriations, is most commonly seen in young or middle-aged women and in patients with posttraumatic stress disorder. There are no primary lesions, only monomorphous excoriations and scarring with postinflammatory pigment disorder.

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