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.


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.



United States

Incidence statistics are not available; chromhidrosis is rare.


Incidence statistics are not available; chromhidrosis is rare.


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


No sexual predilection is reported for chromhidrosis.


Chromhidrosis is noted after puberty, when the apocrine glands are activated. However, one case of an infant with chromhidrosis has been reported.[5]


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.


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


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.[8, 9, 10, 11, 12]

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.[16]

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.[7]

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®.[17, 18] The mechanism by which BOTOX® suppresses apocrine chromhidrosis is unclear. BOTOX® may suppress apocrine secretion by blocking cholinergic stimulation and substance P release.[19, 20]

A few reports have described successful treatment of chromhidrosis with capsaicin cream.[21, 22] 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:  Derived from plants of Solanaceae family. May render 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:  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.


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.


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

Disclosure: Nothing to disclose.


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

Disclosure: Abbot t Laboratories Grant/research funds Sub-investigator; Pierre Fabre Dermo Cosmétique Honoraria Speaking and teaching

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.

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Disclosure: Abvie Honoraria Speaking and teaching

Chief Editor

Dirk M Elston, MD, Director, Ackerman Academy of Dermatopathology, New York

Disclosure: Nothing to disclose.

Additional Contributors

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.


  1. Barankin B, Alanen K, Ting PT, Sapijaszko MJ. Bilateral facial apocrine chromhidrosis. J Drugs Dermatol. Mar-Apr 2004;3(2):184-6. [View Abstract]
  2. Mali-Gerrits MM, van de Kerkhof PC, Mier PD, Happle R. Axillary apocrine chromhidrosis. Arch Dermatol. Apr 1988;124(4):494-6. [View Abstract]
  3. Griffith JR. Isolated areolar apocrine chromhidrosis. Pediatrics. Feb 2005;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. Mar 1995;12(1):48-50. [View Abstract]
  5. Carman KB, Aydogdu SD, Sabuncu I, Yarar C, Yakut A, Oztelcan B. Infant with chromhidrosis. Pediatr Int. Apr 2011;53(2):283-4. [View Abstract]
  6. Polat M, Dikilitas M, Gozubuyukogullari A, Alli N. Apocrine chromhidrosis. Clin Exp Dermatol. Oct 2009;34(7):e373-4. [View Abstract]
  7. Wang A, Wysong A, Nord KM, Egbert BM, Kosek J. Chromhidrosis: A Rare Diagnosis Requiring Clinicopathologic Correlation. Am J Dermatopathol. Mar 14 2013;[View Abstract]
  8. Singal A, Thami GP. Red pseudochromhidrosis of the neck. Clin Exp Dermatol. Sep 2004;29(5):548-9. [View Abstract]
  9. Thami GP, Kanwar AJ. Red facial pseudochromhidrosis. Br J Dermatol. Jun 2000;142(6):1219-20. [View Abstract]
  10. Yoshida R, Kobayashi S, Amagai M, Tanaka M. Brown palm pseudochromhidrosis. Contact Dermatitis. Apr 2002;46(4):237-8. [View Abstract]
  11. Hill S, Duffill M, Lamont D, Rademaker M, Yung A. Pseudochromhidrosis: blue discolouration of the head and neck. Australas J Dermatol. Nov 2007;48(4):239-41. [View Abstract]
  12. Krishnaram AS, Bharathi S, Krishnan S. An interesting case of bisacodyl (dulcolax)-induced chromhidrosis. Indian J Dermatol Venereol Leprol. Nov-Dec 2012;78(6):756-8. [View Abstract]
  13. Allegue F, Hermo JA, Fachal C, Alfonsín N. Localized green pigmentation in a patient with hyperbilirubinemia. J Am Acad Dermatol. Jul 1996;35(1):108-9. [View Abstract]
  14. Kanzaki T, Tsuda J. Bile pigment deposition at sweat pores of patients with liver disease. J Am Acad Dermatol. Apr 1992;26(4):655-6. [View Abstract]
  15. Albers SE, Brozena SJ, Glass LF, Fenske NA. Alkaptonuria and ochronosis: case report and review. J Am Acad Dermatol. Oct 1992;27(4):609-14. [View Abstract]
  16. Cox NH, Popple AW, Large DM. Autofluorescence of clothing as an adjunct in the diagnosis of apocrine chromhidrosis. Arch Dermatol. Feb 1992;128(2):275-6. [View Abstract]
  17. 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. Mar 15 2012;18(3):13. [View Abstract]
  18. Beer K, Oakley H. Axillary chromhidrosis: report of a case, review of the literature and treatment considerations. J Cosmet Dermatol. Dec 2010;9(4):318-20. [View Abstract]
  19. Matarasso SL. Treatment of facial chromhidrosis with botulinum toxin type A. J Am Acad Dermatol. Jan 2005;52(1):89-91. [View Abstract]
  20. Wu JM, Mamelak AJ, Nussbaum R, McElgunn PS. Botulinum toxin a in the treatment of chromhidrosis. Dermatol Surg. Aug 2005;31(8 Pt 1):963-5. [View Abstract]
  21. Marks JG Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J Am Acad Dermatol. Aug 1989;21(2 Pt 2):418-20. [View Abstract]
  22. Rumsfield JA, West DP. Topical capsaicin in dermatologic and peripheral pain disorders. DICP. Apr 1991;25(4):381-7. [View Abstract]
  23. Daoud MS, Dicken CH. Disorders of the apocrine sweat glands. In: Fitzpatrick's Dermatology in General Medicine. 6th ed. New York, NY: McGraw-Hill; 2003:708-9.
  24. Shelley WD, Hurley HJ Jr. Localized chromhidrosis: a survey. Arch Dermatol Syphilol. 1954;69:449-71.