Chromhidrosis

Abstract

A young woman presented to the office with a history of bluish discoloration involving the superior malar region bilaterally. When the bluish discoloration became darker, she would press on her cheeks resulting in excretion of "black sweat" that temporarily lightened her skin color. Examination revealed ill-defined slightly swollen soft plaques involving both superior cheeks. Upon pressure on the cheeks, a dark brown fluid was expressed. Histologic examination revealed collections of ectopic apocrine glands within midreticular dermis. The diagnosis of apocrine chromhidrosis was made, an uncommon cause of chromhidrosis and one in which bilateral facial presentation is rare.

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Case Report

A 28-year-old woman was referred to our department with a 5-year history of progressive swelling and darkening of the malar eminences. Physical examination revealed mild upper cheek swelling associated with a dark blue hue. Localized pressure over several gland openings produced a black fluid (Figure 1) and manual expression appeared to lighten the color of the malar eminences. Her medical history was unremarkable and she denied taking any medications. Botulinum toxin type A (Botox[R], Allergan Inc., Irvine, CA) injection was attempted with no success. She decided to wait until after her wedding for other treatment options. A 3 mm punch biopsy was performed for histological examination, revealing collections of ectopic apocrine glands in the mid-reticular dermis (Figure 2). Occasional apocrine glands with brown lipofuscin-laden cytoplasm (Figure 3) were observed.

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Apocrine chromhidrosis was first described by Yonge in 1709 (1) and later attributed to lipofuscin pigments by Shelley & Hurley in 1954 (2). Several etiologies of pigmented perspiration include: 1) true eccrine chromhidrosis, which are water-soluble pigments excreted by eccrine glands (3): 2) pseudo-eccrine chromhidrosis, which is caused by compounds on the skin surface mixing with colorless sweat (4,5): and 3) apocrine chromhidrosis, which is caused by lipofuscin granules with shades of yellow, green, blue, blue-black or brown-black (1). The differential diagnosis of colored sweat includes exposure to dyes and chemical contactants, microorganisms, and systemic disease. Excessive ingestion of food coloring agents, dyes in clothing, and contact with colored metals may produce pigmented perspiration (3).

Apocrine chromhidrosis usually manifests in puberty when these glands become functionally active and is unrelated to dietary, systemic, or metabolic alterations, gender, occupation, or geographical predisposition (1,2). The condition can affect the axilla, face, or areolae (4,6,7). Colored sweat is usually discharged in response to emotional stimuli, epinephrine, and mechanical stimulation, and excretion is often preceded by warmth or a prickling sensation (1). The secretions tend to be insoluble to lipid solvents and can stain clothing (3). The morbidity of apocrine chromhidrosis stems from embarrassment and psychological distress.

The diagnosis of apocrine chromhidrosis may require local expression or injection of intradermal epinephrine or pitocin to induce sweat excretion. A positive Wood's lamp and/or autofluorescence of clothing fibers in contact with sweat secretions may also be used (1,6). Histopathology showing increased lipofuscin granules within apocrine glands may also confirm the diagnosis. Under the microscope, the number of apocrine glands is variable and yellow-brown lipofuscin granules may be observed in the apical area of secretory cells with H & E stain.

Treatment is unsatisfactory, but includes manual emptying or surgical excision of the glands (1). More recently, topical capsaicin has been found to be effective (8,9). Although apocrine chromhidrosis persists indefinitely, the symptoms may decrease with age.

References

1. Hurley HJ. Apocrine chromhidrosis. In: Freedberg MI, Eizen ZA, Wolf K et al, eds. Dermatology in General Medicine. 5th ed. New York, NY: McGraw-Hill Co; 1999:811-812.

2. Shelley WB, Hurley HJ. Localized chromhidrosis: a survey. Arch Dermatol 1954; 69:449-471.

3. Cilliers J. de Beer C. The case of the red lingerie: chromhidrosis revisited. Dermatology 1999; 199:149-152.

4. Mali-Gerrits MM, van de Kerkhof PC. Mier PD. Happle R. Axillary apocrine chromhidrosis. Arch Dermatol 1988; 124:494-496.

5. Thami GP. Kanwar AJ. Red facial pseudochromhidrosis. Br J Dermatol 2000; 142:1219-1220.

6. Cox NH, Popple AW. Large DM. Autofluorescence of clothing as an adjunct in the diagnosis of apocrine chromhidrosis. Arch Dermatol 1992; 128:275-276.

7. Saff DM. Owens R. Kahn TA. Apocrine chromhidrosis involving the areolae in a 15-year-old amateur figure skater. Pediatr Dermatol 1995; 12:48-50.

8. Rumsfield JA. West DP. Topical capsaicin in dermatologic and peripheral pain disorders. DICP 1991; 25:381-387.

9. Marks JG. Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J Am Acad Dermatol 1989; 21:418-420.

BENJAMIN BARANKIN MD, KEN ALANEN MD, PATRICIA T TING BSC, MARIUSZ J A SAPIJASZKO MD FRCPC

DIVISION OF DERMATOLOGY, UNIVERSITY OF ALBERTA, EDMONTON, ALBERTA, CANADA

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