Bromhidrosis 

  • Author: Wingfield Rehmus, MD, MPH; Chief Editor: William D James, MD   more...
 
Updated: Jan 17, 2012
 

Background

Bromhidrosis, also known as bromidrosis or body odor, is a common phenomenon in postpubertal individuals. In rare cases, bromhidrosis may become pathologic if it is particularly overpowering or if the bromhidrosis significantly interferes with the lives of the affected individuals. Bromhidrosis is a chronic condition in which excessive odor, usually an unpleasant one, emanates from the skin. Bromhidrosis, determined largely by apocrine gland secretion, can substantially impair a person's quality of life.

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Pathophysiology

Types of glands and their functions

Human secretory glands are primarily divided into 2 types: apocrine and eccrine.

  • Eccrine glands are distributed over the entire skin surface, where they are involved in thermoregulation by means of sweat production.[1]
  • In contrast, apocrine glands have a limited distribution involving the axilla, genital skin, and breasts. Apocrine elements are also found in the periorbital and periauricular areas. Apocrine glands have no thermoregulatory role but are responsible for characteristic pheromonal odors. They secrete a small amount of oily fluid, which is odorless upon reaching the skin surface. The characteristic odor is due to bacterial decomposition of the oily fluid.[2, 3] Studies have shown that in comparison to controls, individuals with bromhidrosis display more numerous and larger apocrine glands.
  • Lastly, apoeccrine glands are sweat glands that become apparent between the ages of 8 and 14 years. They are functionally and pharmacologically distinct from apocrine glands and contribute heavily to overall axillary sweating. They develop during puberty from eccrinelike precursor glands.
  • Histological findings suggest that eccrine glands are dominant in the dermis, but most apocrine glands are located in the subcutaneous tissue, although the definite location is not yet known.

Control of apocrine glands

Current evidence suggests that the human apocrine gland appears to be under sympathetic nervous control with the peripheral mechanisms regulated by catecholamines. The presence of purinergic receptors within the gland also indicates the use of a secondary sudomotor pathway with nucleotide involvement in the secretory glands.[4]

Apocrine bromhidrosis

Apocrine bromhidrosis is the most prevalent form of bromhidrosis and should be differentiated from the less common eccrine bromhidrosis. Several factors contribute to the pathogenesis of apocrine bromhidrosis. Bacterial decomposition of apocrine secretion yields ammonia and short-chain fatty acids, with their characteristic strong odors. The most abundant of these acids is (E)-3-methyl-2-hexanoic acid (E-3M2H), which is brought to the skin surface bound by 2 apocrine secretion odor-binding proteins, ASOB1 and ASOB2. ASOB2 has been identified as apolipoprotein D (apoD), a known member of the lipocalin family of carrier proteins.[5, 6, 7]

Axillary bacterial florae have been shown to produce the distinctive axillary odor by transforming nonodoriferous precursors in sweat to more odoriferous volatile acids. The most common of these are E-3M2H and (RS)-3-hydroxy-3-methlyhexanoic acid (HMHA), which are released through the action of a specific zinc-dependent N -alpha-acyl-glutamine aminoacylase (N-AGA) from Corynebacterium species. This aminoacylase has been demonstrated to also release other odoriferous acids from glutamine conjugates in sweat, which may be the basis of individual body odor.[8]

Eccrine bromhidrosis

In certain circumstances, eccrine secretion, which is typically odorless, assumes an offensive aroma and causes eccrine bromhidrosis. When eccrine sweat softens keratin, bacterial degradation of the keratin yields a foul smell. Ingestion of some foods, including garlic, onion, curry, alcohol, certain drugs (eg, penicillin, bromides), and toxins may cause eccrine bromhidrosis. Lastly, eccrine bromhidrosis may result from underlying metabolic or endogenous causes.

The role of excessive eccrine secretion, or hyperhidrosis, in the pathogenesis of bromhidrosis is unclear. Hyperhidrosis may promote the spread of apocrine sweat and contribute further to bromhidrosis by creating a moist environment, one ripe for bacterial overgrowth.[9, 10] Conversely, eccrine hyperhidrosis may cause a decrease in odor because the eccrine sweat flushes away the more odoriferous apocrine sweat.

Genetic involvement

Most patients have family members who also have bromhidrosis. An autosomal dominant inheritance pattern has been proposed in one study.

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Epidemiology

Frequency

United States

  • The incidence of bromhidrosis is unclear, but the diagnosis is generally considered rare.

International

  • The diagnosis of bromhidrosis is more common in many Asian countries, where even minimal body odor is associated with personal distress, and can be diagnosed as bromhidrosis, more so than in other regions of the world. Although the incidence of bromhidrosis is not reported, the social stigma of body odor leads more patients to seek treatment in these countries than in other countries.

Mortality/Morbidity

  • No morbid sequelae are known for bromhidrosis.

Race

  • Apocrine bromhidrosis is believed to be more common in patients in dark-skinned ethnic groups than in others.
  • In Asian patients, apocrine bromhidrosis may be associated with a positive family history.
  • Eccrine bromhidrosis occurs in persons of all races.

Sex

  • Bromhidrosis exhibits a male predominance, which may be a reflection of greater apocrine gland activity in men compared with women.

Age

  • Axillary bromhidrosis depends on apocrine function and therefore manifests exclusively after puberty. It occurs only rarely in the elderly population.
  • In contrast, eccrine bromhidrosis is more common than apocrine bromhidrosis during childhood, but it may occur at any age.
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Contributor Information and Disclosures
Author

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

Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Carol E Cheng  Boston University School of Medicine

Disclosure: Nothing to disclose.

Katherine Brown  Stanford University School of Medicine

Katherine Brown, is a member of the following medical societies: American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Timothy McCalmont, MD  Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco; Editor-in-Chief, Journal of Cutaneous Pathology

Timothy McCalmont, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Dermatopathology, California Medical Association, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Apsara Consulting fee Independent contractor

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

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

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology

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.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Shereen Timani, MD, and Nelly Rubeiz, MD, to the development and writing of this article.

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