Updated: Dec 9, 2008
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 the disease 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.
Incidence statistics are not available; the disease is rare.
Incidence statistics are not available; the disease 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.
Chromhidrosis is noted after puberty, when the apocrine glands are activated.
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:
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.5,6,7,8
Hyperbilirubinemia9,10
Pseudomonas infection
Poisoning
Dermatitis simulata
Bleeding diathesis (red sweat, hematohidrosis)
Alkaptonuria (ochronosis)11
Copper exposure (blue sweat)
Contamination from corynebacteria, paint, or clothing dye
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.
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 3 cases with mixed results. BOTOX® is predominantly used to decrease eccrine sweat in persons with hyperhidrosis. However, recent reports demonstrated improvement of facial chromhidrosis with BOTOX® lasting 19 weeks post treatment. The mechanism by which BOTOX® suppresses apocrine chromhidrosis is unclear. BOTOX® may suppress apocrine secretion by blocking cholinergic stimulation and substance P release.13,14
A few reports have described successful treatment with capsaicin cream.15,16 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.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Counterirritants may be used to treat chromhidrosis.
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.
Apply to affected area bid; not to exceed 4 applications/d
Administer as in adults
None reported
Documented hypersensitivity; broken or irritated skin
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Causes significant irritation and a burning sensation during first few days of use; for external use only; avoid contact with eyes; do not use tight bandage; discontinue use if condition worsens or symptoms persist for 14-28 d.
These agents inhibit the transmission of nerve impulses at the neuromuscular junction of skeletal muscle and/or autonomic ganglia.
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.
Facial chromhidrosis: 3-5 U spaced approximately 1 cm apart over affected area; total of 10-15 U into each side of face
Not established
Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy; mild transient weakness and muscle weakness at toxin-treated sites may occur but resolve within 2-5 wk
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Barankin B, Alanen K, Ting PT, Sapijaszko MJ. Bilateral facial apocrine chromhidrosis. J Drugs Dermatol. Mar-Apr 2004;3(2):184-6. [Medline].
Mali-Gerrits MM, van de Kerkhof PC, Mier PD, Happle R. Axillary apocrine chromhidrosis. Arch Dermatol. Apr 1988;124(4):494-6. [Medline].
Griffith JR. Isolated areolar apocrine chromhidrosis. Pediatrics. Feb 2005;115(2):e239-41. [Medline].
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. [Medline].
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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. [Medline].
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. [Medline].
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. [Medline].
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. [Medline].
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. [Medline].
Matarasso SL. Treatment of facial chromhidrosis with botulinum toxin type A. J Am Acad Dermatol. Jan 2005;52(1):89-91. [Medline].
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. [Medline].
Marks JG Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J Am Acad Dermatol. Aug 1989;21(2 Pt 2):418-20. [Medline].
Rumsfield JA, West DP. Topical capsaicin in dermatologic and peripheral pain disorders. DICP. Apr 1991;25(4):381-7. [Medline].
Cilliers J, de Beer C. The case of the red lingerie - chromhidrosis revisited. Dermatology. 1999;199(2):149-52. [Medline].
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.
Shelley WD, Hurley HJ Jr. Localized chromhidrosis: a survey. Arch Dermatol Syphilol. 1954;69:449-71.
chromhidrosis, pseudochromhidrosis, chromidrosis, colored sweat, discolored sweat, pigmented sweat, yellow sweat, green sweat, blue sweat, black sweat, lipofuscin, Corynebacterium bacteria
June Kim, MD, Staff Physician, Department of Dermatology, University of New Mexico
June Kim, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.
Wingfield Rehmus, MD, MPH, Co-Director of Clinical Trials, Clinical Instructor, Department of Dermatology, Stanford University Medical Center
Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology
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.
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.
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, 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
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.