Chromhidrosis

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Background

Chromhidrosis is a rare condition characterized by the secretion of colored sweat. Two glands produce sweat: eccrine and apocrine glands. Eccrine glands secrete a clear, odorless fluid that serves to regulate body temperature. Apocrine glands secrete a thick, milky sweat that, once broken down by bacteria, is the main cause of body odor.

Chromhidrosis is apocrine in origin. Although apocrine glands are found in the genital, axillary, areolar, and facial skin, chromhidrosis is reported only on the face,[1] axillae,[2] and breast areola.[3, 4] Lipofuscin pigment is responsible for the colored sweat. This pigment is produced in the apocrine gland, and its various oxidative states account for the characteristic yellow, green, blue, or black secretions observed in apocrine chromhidrosis.

In contrast, eccrine chromhidrosis is rare and occurs with ingestion of certain dyes or drugs, and pseudochromhidrosis occurs when clear eccrine sweat becomes colored on the surface of the skin as a result of extrinsic dyes, paints, or chromogenic bacteria.

Approximately 10% of people without chromhidrosis have colored sweat that is regarded as acceptable and within the normal range.

Pathophysiology

Lipofuscin is a yellowish brown pigment that is normally found in the cytoplasm of relatively nondividing cells (eg, neurons). In chromhidrosis, lipofuscins are found in a higher-than-normal concentration or a higher-than-normal state of oxidation in apocrine glands. However, why some glands experience these changes is unclear. This increased level of oxidation results in the green, blue, and even black sweat seen in chromhidrosis.

The yellow, green, and blue apocrine secretions produce a yellow fluorescence under a Wood lamp (UV 360 nm), whereas the dark brown and black apocrine secretions seldom autofluoresce. Substance P is also postulated to be an important neurotransmitter in this process.

Pseudochromhidrosis is of an extrinsic etiology in which a chemical on the surface of the skin reacts with eccrine secretions and produces the color transformation.

Epidemiology

Frequency

Incidence statistics are not available; chromhidrosis is rare.

Race

Apocrine chromhidrosis appears to be more common in blacks than in whites, but facial chromhidrosis is described only in whites.

Sex

No sexual predilection is reported for chromhidrosis.

Age

Chromhidrosis is noted after puberty, when the apocrine glands are activated. However, rare cases in infants have been reported.[5, 6]

Prognosis

Chromhidrosis persists throughout life, but slow regression of the disease is noted, as apocrine glands regress with time. The prognosis for chromhidrosis is good if an extrinsic cause can be identified and addressed appropriately.

History

History taking should include a detailed investigation of the patient's environment and lifestyle to exclude exogenous causes.

Quantities of apocrine sweat are less than those of eccrine sweat. Usually, patients report axillary staining of their undershirt, staining of their bra,[7] or, less frequently, staining of the face or areola. Yellow is the most common color of axillary staining. An aura of warmth or a prickly sensation prompted by emotional or physical stimuli may precede the onset of colored sweat. Facial apocrine chromhidrosis is rarely described. It occurs most frequently on the cheeks and malar eminences. The secretion can often be expressed mechanically.[8]

Familial chromhidrosis has been reported.[9]

Physical

On careful inspection, the following signs can often be observed in chromhidrosis:

Causes

The increased numbers of lipofuscin pigments in the secretory apocrine cells are presumed to be the cause of apocrine chromhidrosis.

Several extrinsic causes of eccrine chromhidrosis and pseudochromhidrosis include chromogenic bacteria, especially Corynebacterium species, fungi, dyes, drugs, and chemical contactants.[10, 11, 12, 13, 14]

Laboratory Studies

No significant laboratory abnormalities have been noted with apocrine chromhidrosis. The following test may help to rule out other causes:

Other Tests

Wood lamp examination of colored sweat may be positive. If no sweat is produced at the time of the test, manual expression or pharmacologic stimulation with intradermal epinephrine or oxytocin (Pitocin) can be used to stimulate sweat secretion.

Clothing fibers in contact with the secretions may also fluoresce yellow-green with standard UV microscopy.[20]

Histologic Findings

The apocrine glands appear normal in size and morphology, but the number of glands varies. The increased number of yellow-brown lipofuscin granules is observed in the cytoplasm of secretory cells on routine hematoxylin-eosin staining. The granules are positive on periodic acid-Schiff stains and demonstrate autofluorescence under a UV excitation wavelength of 360-395 nm. Schmorl stains may also be weakly positive.[8]

Medical Care

Apocrine chromhidrosis has no fully satisfactory cure or treatment. Patients can manually or pharmacologically empty the glands to achieve a symptom-free period of about 48-72 hours or until the glands replenish the pigment.

BOTOX® injections have been attempted in 5 cases of chromhidrosis, with mixed results. BOTOX® is predominantly used to decrease eccrine sweat in persons with hyperhidrosis. However, recent reports demonstrated improvement of facial and axillary chromhidrosis with BOTOX®.[21, 22] The mechanism by which BOTOX® suppresses apocrine chromhidrosis is unclear. BOTOX® may suppress apocrine secretion by blocking cholinergic stimulation and substance P release.[23, 24]

A few reports have described successful treatment of chromhidrosis with capsaicin cream.[25, 26] Capsaicin, a crystalline alkaloid found in red peppers, is commonly used for the temporary relief of pain from rheumatoid arthritis, osteoarthritis, and neuralgias. Capsaicin depletes neurons of substance P, a neurotransmitter important in apocrine sweat production. Clinical relapse occurs when therapy is stopped.

Medication Summary

The goals of pharmacotherapy for chromhidrosis are to reduce morbidity and to prevent complications.

Capsaicin (Dolorac, Zostrix)

Clinical Context:  Capsaicin is derived from plants of the Solanaceae family. It may render the skin and joints insensitive to pain by depleting substance P in peripheral sensory neurons. Use 0.025% cream.

Class Summary

Counterirritants may be used to treat chromhidrosis.

OnabotulinumtoxinA (BOTOX®)

Clinical Context:  OnabotulinumtoxinA prevents calcium-dependent release of acetylcholine and produces a state of denervation at the neuromuscular junction and postganglionic sympathetic cholinergic nerves in the sweat glands.

Class Summary

These agents inhibit the transmission of nerve impulses at the neuromuscular junction of skeletal muscle and/or autonomic ganglia.

Author

June Kim, MD, Mohs Surgeon/Dermatologist, Cascade Eye and Skin Center, PC

Disclosure: Nothing to disclose.

Coauthor(s)

Wingfield Rehmus, MD, MPH, Dermatologist, BC Children's Hospital, Vancouver, British Columbia

Disclosure: Received grant/research funds from Abbot t Laboratories for sub-investigator; Received honoraria from Valeant Canada for advisory board; Received honoraria from Pierre Fabre for advisory board.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD, Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Günter Burg, MD Professor and Chairman Emeritus, Department of Dermatology, University of Zürich School of Medicine; Delegate of The Foundation for Modern Teaching and Learning in Medicine Faculty of Medicine, University of Zürich, Switzerland

Günter Burg, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, and Pacific Dermatologic Association

Disclosure: Nothing to disclose.

Nelly Rubeiz, MD Consulting Staff, Department of Dermatology, American University of Beirut Medical Center; Associate Professor, Department of Dermatology, American University of Beirut, Lebanon

Nelly Rubeiz, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Shereen S Timani, MD Resident Physician, Department of Dermatology, American University of Beirut, Lebanon

Disclosure: Nothing to disclose.

References

  1. Barankin B, Alanen K, Ting PT, Sapijaszko MJ. Bilateral facial apocrine chromhidrosis. J Drugs Dermatol. 2004 Mar-Apr. 3(2):184-6. [View Abstract]
  2. Mali-Gerrits MM, van de Kerkhof PC, Mier PD, Happle R. Axillary apocrine chromhidrosis. Arch Dermatol. 1988 Apr. 124(4):494-6. [View Abstract]
  3. Griffith JR. Isolated areolar apocrine chromhidrosis. Pediatrics. 2005 Feb. 115(2):e239-41. [View Abstract]
  4. Saff DM, Owens R, Kahn TA. Apocrine chromhidrosis involving the areolae in a 15-year-old amateur figure skater. Pediatr Dermatol. 1995 Mar. 12(1):48-50. [View Abstract]
  5. Carman KB, Aydogdu SD, Sabuncu I, Yarar C, Yakut A, Oztelcan B. Infant with chromhidrosis. Pediatr Int. 2011 Apr. 53(2):283-4. [View Abstract]
  6. Yöntem A, Kör D, Hızlı Karabacak B, Karakaş M, Önenli Mungan N. Blue-colored sweating: four infants with apocrine chromhidrosis. Turk J Pediatr. 2015 May-Jun. 57 (3):290-3. [View Abstract]
  7. Polat M, Dikilitas M, Gozubuyukogullari A, Alli N. Apocrine chromhidrosis. Clin Exp Dermatol. 2009 Oct. 34(7):e373-4. [View Abstract]
  8. Wang A, Wysong A, Nord KM, Egbert BM, Kosek J. Chromhidrosis: A Rare Diagnosis Requiring Clinicopathologic Correlation. Am J Dermatopathol. 2013 Mar 14. [View Abstract]
  9. Gaffney DC, Cooper HL. Coloured sweat in two brothers: First report of familial chromhidrosis. Australas J Dermatol. 2016 Feb. 57 (1):e23-5. [View Abstract]
  10. Singal A, Thami GP. Red pseudochromhidrosis of the neck. Clin Exp Dermatol. 2004 Sep. 29(5):548-9. [View Abstract]
  11. Thami GP, Kanwar AJ. Red facial pseudochromhidrosis. Br J Dermatol. 2000 Jun. 142(6):1219-20. [View Abstract]
  12. Yoshida R, Kobayashi S, Amagai M, Tanaka M. Brown palm pseudochromhidrosis. Contact Dermatitis. 2002 Apr. 46(4):237-8. [View Abstract]
  13. Hill S, Duffill M, Lamont D, Rademaker M, Yung A. Pseudochromhidrosis: blue discolouration of the head and neck. Australas J Dermatol. 2007 Nov. 48(4):239-41. [View Abstract]
  14. Krishnaram AS, Bharathi S, Krishnan S. An interesting case of bisacodyl (dulcolax)-induced chromhidrosis. Indian J Dermatol Venereol Leprol. 2012 Nov-Dec. 78(6):756-8. [View Abstract]
  15. Allegue F, Hermo JA, Fachal C, Alfonsín N. Localized green pigmentation in a patient with hyperbilirubinemia. J Am Acad Dermatol. 1996 Jul. 35(1):108-9. [View Abstract]
  16. Kanzaki T, Tsuda J. Bile pigment deposition at sweat pores of patients with liver disease. J Am Acad Dermatol. 1992 Apr. 26(4):655-6. [View Abstract]
  17. Keum DI, Hong H, Lee SH, Ahn SK. Eccrine Chromhidrosis Resembling Clinical Features of Pompholyx with Bile-Like Greenish Pigmentation on the Right Palm and Soles. Ann Dermatol. 2015 Aug. 27 (4):482-3. [View Abstract]
  18. So JK, Romero L. Eccrine chromhidrosis secondary to hyperbilirubinemia. Dermatol Online J. 2014 Dec 14. 21 (3):[View Abstract]
  19. Albers SE, Brozena SJ, Glass LF, Fenske NA. Alkaptonuria and ochronosis: case report and review. J Am Acad Dermatol. 1992 Oct. 27(4):609-14. [View Abstract]
  20. Cox NH, Popple AW, Large DM. Autofluorescence of clothing as an adjunct in the diagnosis of apocrine chromhidrosis. Arch Dermatol. 1992 Feb. 128(2):275-6. [View Abstract]
  21. Pérez-Tato B, Zamora-Martínez E, Sánchez-Albisua B, Pérez-González YC, Polimón-Olabarrieta I, Marinero-Escobedo S, et al. Facial and axillary apocrine chromhidrosis. Dermatol Online J. 2012 Mar 15. 18(3):13. [View Abstract]
  22. Beer K, Oakley H. Axillary chromhidrosis: report of a case, review of the literature and treatment considerations. J Cosmet Dermatol. 2010 Dec. 9(4):318-20. [View Abstract]
  23. Matarasso SL. Treatment of facial chromhidrosis with botulinum toxin type A. J Am Acad Dermatol. 2005 Jan. 52(1):89-91. [View Abstract]
  24. Wu JM, Mamelak AJ, Nussbaum R, McElgunn PS. Botulinum toxin a in the treatment of chromhidrosis. Dermatol Surg. 2005 Aug. 31(8 Pt 1):963-5. [View Abstract]
  25. Marks JG Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J Am Acad Dermatol. 1989 Aug. 21(2 Pt 2):418-20. [View Abstract]
  26. Rumsfield JA, West DP. Topical capsaicin in dermatologic and peripheral pain disorders. DICP. 1991 Apr. 25(4):381-7. [View Abstract]
  27. Daoud MS, Dicken CH. Disorders of the apocrine sweat glands. Fitzpatrick's Dermatology in General Medicine. 6th ed. New York, NY: McGraw-Hill; 2003. 708-9.
  28. Shelley WD, Hurley HJ Jr. Localized chromhidrosis: a survey. Arch Dermatol Syphilol. 1954. 69:449-71.