DermaDiagnosis

Spreading Lesions on Sun-damaged Skin

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A few years ago, a woman first noticed lesions developing on her legs. The patient sought care from her primary care provider; however, despite a number of treatment regimens, including topical clotrimazole and terbinafine creams, the lesions have not only failed to resolve but have also grown in number and spread to other areas of her body. The woman, now 48, is referred to dermatology for evaluation of her persistent but asymptomatic condition. The patient claims that her health is otherwise excellent, although she has seasonal allergies, was a long-time smoker until two months ago, and has just begun estrogen replacement therapy. She is especially concerned that the lesions have started to appear on the skin of her abdomen. She specifically denies shortness of breath, joint pain, fever, unexplained weight loss, or cough. An examination of her skin reveals a multitude of 2- to 6-mm partially depigmented, roughly round macules uniformly distributed on her legs, arms, and trunk. The lesions, which average about 3 mm, have no palpable component and no observable scale or underlying induration. There is a concentration of them on the anterior tibial areas, as well as on the dorsal forearms; however, none are seen on her face, and the volar surfaces of her forearms are almost completely spared. Significantly, the patient’s exposed skin is tremendously sun-damaged, evidenced by a deep brown color and a weathered, wrinkled look, with many telangiectasias and brown to tan–orange macules on her face.

Given the facts as presented, the most likely diagnostic explanation for these hypopigmented lesions is

a) Vitiligo

b) Tinea versicolor

c) Lupus

d) Idiopathic guttate hypomelanosis

ANSWER

The correct answer is idiopathic guttate hypomelanosis (choice “d”), a common condition primarily seen on sun-damaged patients, but often mistaken for tinea versicolor (choice “b”).

Vitiligo (choice “a”) can present with “confetti” lesions, but would more likely lead to complete loss of pigment in most of the lesions, not the partial loss seen in this patient. Biopsy is indicated in questionable cases.

Tinea versicolor, equally common, is caused by a commensal yeast called Malassezia furfur that feeds on sebum, which is why it favors the oily parts of the body (back and chest, primarily). It is almost never seen on the legs, which have the fewest oil glands on the body. In addition, tinea versicolor is, by its nature, an epidermal process, leading to the formation of a fine KOH-positive scale.

Since lupus (choice “c”) is a form of vasculitis, the associated inflammation can lead to pigment loss, especially in darker-skinned patients. Without a more likely explanation for these lesions, a biopsy might well have been indicated.

DISCUSSION

Biopsy might have suggested any number of other diseases that can also present with hypomelanosis, such as cutaneous T-cell lymphoma or sarcoid. But idiopathic guttate hypomelanosis is far more common, and the patient’s age, gender, and history of chronic UV damage all lend themselves perfectly to this diagnosis.

Idiopathic guttate hypomelanosis, for unknown reasons, tends to appear in women at earlier ages than in men (usually about a decade younger). For either gender, treatment is problematic once the lesions have fully developed. Early in the process, the obvious remedy is better sun protection. Lasers, retinoids, liquid nitrogen, and anti-inflammatory creams have all been tried with little success.

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