INTRODUCTION — Sweat-related body odor manifests in essentially all individuals at some point during life. Excessively foul-smelling sweat is considered pathologic and termed bromhidrosis, a term derived from the Greek "bromos" (stench) and "hidros" (sweat). Synonyms of bromhidrosis include "bromidrosis," "osmidrosis," and "ozochrotia."
The degree of odor considered "excessive" and sufficient for a diagnosis of bromhidrosis is not definitive. Bromhidrosis is generally diagnosed when noticeable body odor has a negative effect on an individual's self-view, social interactions, or quality of life.
Bromhidrosis is divided into apocrine bromhidrosis and eccrine bromhidrosis. The most common site for apocrine bromhidrosis is the axilla. Eccrine bromhidrosis most often affects the feet.
The clinical features, diagnosis, and management of bromhidrosis will be reviewed here. Hyperhidrosis (excessive sweating) is reviewed separately. (See "Primary focal hyperhidrosis".)
SUBTYPES — Bromhidrosis is subdivided into apocrine and eccrine variants based upon the type of sweat gland involved. Apocrine glands develop after puberty and are most densely distributed in the axillae, anogenital areas, and breasts. The primary role of apocrine glands appears to be the secretion of pheromones. Eccrine glands are widely distributed all over the body, with the exception of the external auditory canal, lips, clitoris, labia minora, and glans penis. Eccrine glands are primarily responsible for thermoregulation.
Apoeccrine glands are an additional type of sweat gland that are smaller than apocrine glands and exhibit features of both apocrine and eccrine glands. Apoeccrine glands localize to the axillae and genital skin and likely also contribute to bromhidrosis.
PATHOGENESIS — All sweat glands are controlled by the sympathetic nervous system. Primary stimuli include heat, exercise, and emotion; other stimuli include certain foods, medications, and disease states.
Sweat is usually odorless when secreted from the sweat gland. Bacterial degradation of secreted sweat or keratin is the primary mechanism leading to bromhidrosis. Occasionally, other factors are responsible for malodor.
Apocrine bromhidrosis — Degradation of apocrine secretions by bacteria is the major cause of apocrine bromhidrosis. Examples of odiferous fatty acids found in axillary secretions include E-3-methyl-2-hexenoic acid (E-3M2H), 3-hydroxy-3-methyl-hexanoic acid, sulfanylalkanols, and 3-methyl-3-sulfanylhexan-1-ol. In the case of E-3M2H, apocrine secretion odor-binding proteins (ASOB1 and ASOB2) bind E-3M2H before it reaches the skin surface . After reaching the skin surface, E-3M2H is released by enzymes in bacterial flora, resulting in malodor.
A variety of bacteria can degrade apocrine sweat. Corynebacterium species are frequent colonizers in the axillae and contain a zinc-dependent N-alpha-acyl-glutamine aminoacylase implicated in axillary odor . In addition, other bacteria, including Staphylococcus and Cutibacterium (formerly Propionibacterium) species, can break down fatty acids into thioalcohols and other odiferous compounds . Treatment of Sphingomonas paucimobilis colonization in the axilla has led to resolution of odor in a patient with bromhidrosis .
Secretion of pheromones from apocrine glands also contributes to axillary odor. The pheromones androstenone (5alpha-androst-16-en-3-one) and androstenol (5alpha-androst-16-en-3alpha-ol) are malodorous even before bacterial degradation .
Certain characteristics may influence risk for bromhidrosis. Findings among patients with bromhidrosis have included larger and more numerous apocrine glands compared with patients without bromhidrosis  and higher levels of dihydrotestosterone than testosterone in the nuclear fraction of axillary skin compared with uninvolved skin, suggesting a role for 5-alpha-reductase [7,8]. Higher sweat volume (ie, hyperhidrosis) may also be associated with odor . In addition, familial bromhidrosis with an apparent autosomal dominant inheritance pattern has occurred .
Poor hygiene that promotes bacterial overgrowth may be associated with bromhidrosis, particularly in patients with diabetes, obesity, or concomitant intertriginous skin diseases, such as intertrigo, erythrasma, and trichomycosis axillaris. Bromhidrosis also has occurred after laser depilation of the axilla . (See "Intertrigo" and "Erythrasma" and "Trichomycosis (trichobacteriosis)".)
Eccrine bromhidrosis — Eccrine bromhidrosis can be localized or generalized. Localized eccrine bromhidrosis occurs as a result of sweating leading to skin maceration, which results in bacterial overgrowth and degradation of keratin.
Generalized eccrine bromhidrosis usually occurs as a result of ingestion of odor-promoting compounds or systemic illness. Examples of associated factors include:
●Diet (eg, garlic, onion, curry, alcohol ingestion)
●Medications (eg, penicillin, bromides)
●Toxins (eg, heavy metals)
●Metabolic disorders (eg, phenylketonuria, trimethylaminuria, isovaleric acidemia, hypermethioninemia)
●Systemic disease (eg, liver or renal failure, gout, scurvy, typhoid)
In addition, occurrences of generalized bromhidrosis following whole-body laser hair removal in a young adult and in association with an intranasal foreign body in a child are documented in case reports [12,13].
EPIDEMIOLOGY — The incidence of bromhidrosis is unknown. Pathologic body odor appears to be a more common complaint in Asian societies, where body odor is considered particularly offensive. Males are more often affected than females. Apocrine bromhidrosis occurs after puberty, and it appears to be rare in older adults. Eccrine bromhidrosis can occur at any age.
CLINICAL PRESENTATION — The sites responsible for malodor associated with apocrine bromhidrosis are restricted to areas of apocrine glands (axilla, anogenital area, breasts). Axillary involvement is most common. Eccrine bromhidrosis may be localized or generalized. Localized eccrine bromhidrosis often involves the feet.
The odor of bromhidrosis may be described as "rancid," "pungent," or "sour." It may be exacerbated by heat or exercise and briefly alleviated by bathing.
Skin in the affected area may appear normal. In sites with associated hyperhidrosis, skin may appear macerated with whitish, moist scale.
ASSOCIATED DISORDERS — Localized bromhidrosis may occur in association with cutaneous disorders that occur with increased frequency in the setting of chronic skin moisture, such as intertrigo, erythrasma (picture 1A-B), and pitted keratolysis (picture 2), particularly in patients with concomitant hyperhidrosis. Generalized eccrine bromhidrosis can occur in association with a wide variety of systemic disorders. (See 'Eccrine bromhidrosis' above.)
HISTOPATHOLOGY — Apocrine and eccrine glands and ducts do not show specific abnormalities in bromhidrosis. There may be a relative increase in the size and number of sweat glands .
History and physical examination — Clinicians are usually able to diagnose bromhidrosis through smelling the affected area and obtaining a history of offensive odor noted by the patient and others. Exacerbation of odor in scenarios where sweating is stimulated, such as hot environments or during exercise, is characteristic.
Odor may be subtle at the time of examination if the patient has recently bathed. If odor is not obvious, the patient should be asked if the odor has been noticed by others to aid in identifying patients who do not have bromhidrosis. Activity to induce sweating (exercise, exposure to heat) may also be helpful in making the diagnosis when odor is not immediately apparent. (See 'Differential diagnosis' below.)
For patients with generalized bromhidrosis, the history and physical examination can be helpful for eliciting underlying causes. The clinician should inquire about diet, current medications, risk for heavy metal toxin exposure, metabolic diseases, and systemic diseases. Generalized bromhidrosis in children should also prompt questioning about the possibility of an intranasal foreign body . A review of systems and physical examination should be performed to detect signs and symptoms of internal disease. (See 'Eccrine bromhidrosis' above.)
The type of odor noted can aid in narrowing the list of potential causes of generalized bromhidrosis. The odor of food-related bromhidrosis often resembles the type of food ingested (eg, garlic, onion, curry). Bromhidrosis related to liver or renal failure may yield an ammonia-like smell. Odors associated with specific metabolic disorders are reviewed separately. (See "Inborn errors of metabolism: Epidemiology, pathogenesis, and clinical features", section on 'Abnormal odors'.)
Laboratory testing — Blood work is usually unremarkable, and therefore unnecessary, in patients with localized bromhidrosis. However, for generalized bromhidrosis, additional evaluation is warranted and directed based upon the patient history and physical examination. When the cause of generalized bromhidrosis is not obvious, we obtain liver and renal function tests to evaluate for liver and renal disease as part of the initial evaluation. The need for testing for toxin exposure and other disorders is based upon the findings of the history and physical examination (see 'Eccrine bromhidrosis' above). Skin biopsies are not helpful. (See 'Histopathology' above.)
DIFFERENTIAL DIAGNOSIS — Bromhidrosis should be distinguished from neurologic or psychiatric conditions that cause the patient to believe offensive body odor is present though odor is not apparent to others. Examples include:
●Olfactory hallucinations induced by schizophrenia, epilepsy, or central nervous system tumors (see "Nonepileptic paroxysmal disorders in adolescents and adults", section on 'Olfactory hallucinations')
●Body dysmorphic disorder (see "Body dysmorphic disorder: Clinical features" and "Body dysmorphic disorder: Assessment, diagnosis, and differential diagnosis")
●Olfactory reference syndrome (fear of exuding offensive body odor) 
A lack of noticeable odor on examination, an absent history of odor noticeable to others, and/or a history of psychiatric disease or symptoms suggest the possibility of these disorders.
TREATMENT — Individuals with bromhidrosis may experience severe impairment in social interactions and quality of life and often seek methods to resolve the condition. The approach to treatment differs for the localized and generalized variants. Data on treatment options for bromhidrosis are limited.
Localized bromhidrosis — Localized bromidrosis usually results from bacterial degradation of secreted sweat or keratin. Therefore, treatment primarily consists of interventions to reduce bacteria and/or sweating in the affected areas.
General approach — Clinical experience suggests the following actions are helpful:
●Improve hygiene and reduce bacteria – Affected areas should be washed daily. Excessive washing should be discouraged to avoid skin irritation. Concomitant skin disorders, such as intertrigo, erythrasma, and pitted keratolysis, may contribute to odor and should be promptly treated. (See "Erythrasma" and "Pitted keratolysis".)
Products that reduce bacterial colonization in the affected area can be expected to help with odor. Antibacterial washes and bar soaps are widely available. Other formulations that affect the pH of the affected area claim to improve bromhidrosis; both acids, such as alpha- and beta-hydroxy acids, and bases, such as baking soda, may be helpful, though skin irritation may develop. There are various herbal deodorants and other products that may have antibacterial or other properties that decrease odor. Charcoal-based topicals may also help absorb odor-causing chemicals.
Wearing of absorbent clothing, particularly cotton or materials that wick moisture away from the skin, may be helpful, particularly in the case of socks for foot odor. Perspiration-soaked clothing should be promptly removed, and clothing should be changed at least daily. Exfoliation to remove excess stratum corneum may reduce odor secondary to bacterial degradation of keratin and may be particularly helpful for foot bromhidrosis.
In the absence of concomitant skin infection, antibiotic therapy is usually reserved for patients for whom these measures are insufficient. Topical erythromycin or topical clindamycin applied twice daily are common initial treatment choices. Repeated or continuous treatment may be necessary to maintain improvement. Patients who do not respond to topical treatment may benefit from systemic antibiotic therapy selected based upon culture results from the affected region.
●Reduce sweating – Reducing the amount of sweating in the affected area may lead to improvement, particularly in patients with eccrine bromhidrosis or with apocrine bromhidrosis associated with hyperhidrosis. Topical antiperspirants, which reduce sweating by creating a temporary plug in the sweat duct, are the initial treatment of choice for reducing localized sweating. Aluminum salts are the most common active ingredients in antiperspirants. Use of antiperspirants is reviewed in detail separately. (See "Primary focal hyperhidrosis", section on 'Treatment'.)
Patients for whom antiperspirants are insufficiently effective and for whom hyperhidrosis appears to contribute significantly to malodor may benefit from other methods to reduce sweat production. Botulinum toxin injections have appeared to be a useful, though temporary, treatment in an uncontrolled study and case reports [15-17]. Iontophoreses, microwave technology , and surgical removal of sweat glands  also decrease sweat production and may improve bromhidrosis, although definitive data are lacking for these treatment modalities. (See "Primary focal hyperhidrosis", section on 'Treatment'.)
●Hair removal – Hair may contribute to bromhidrosis through trapping bacteria and odor. Removal of hair in the affected areas through means such as shaving, chemical epilation, or electrolysis may reduce odor, especially in apocrine bromhidrosis. Laser hair removal may be helpful; however, bromhidrosis has occurred as an adverse effect of laser hair removal .
Refractory localized bromhidrosis — Destruction or removal of apocrine glands is an option for refractory axillary apocrine bromhidrosis. Techniques utilized have included surgical excision [20-23], liposuction [24-27], microwave destruction of sweat glands , and neodymium-doped yttrium aluminum garnet (Nd:YAG) or carbon dioxide laser therapy [28-31]. Data on these therapies are primarily limited to case reports, case series, and uncontrolled studies.
Surgical excision appears to be highly effective but may result in complications and scarring. A systematic review and meta-analysis found that surgery with curettage yielded the lowest incidence of recurrence, laser treatment was most likely to result in recurrence, and liposuction had the lowest risk for complications . However, techniques used in the included trials varied and high-quality comparative trials are necessary to confirm relative efficacy and safety.
Thoracic sympathectomy may also be effective for refractory axillary bromhidrosis but may be most beneficial for patients with accompanying hyperhidrosis . The role for microwave thermolysis in the treatment of bromhidrosis remains to be determined .
Generalized bromhidrosis — The treatment of generalized bromhidrosis involves the identification and removal or treatment of the underlying cause. (See 'Eccrine bromhidrosis' above.)
SUMMARY AND RECOMMENDATIONS
●Bromhidrosis describes the occurrence of excessively foul-smelling sweat. The disorder is divided into apocrine and eccrine subtypes based upon the type of sweat gland involved. (See 'Subtypes' above.)
●Apocrine bromhidrosis occurs in sites with apocrine glands (axilla, anogenital region, or breasts). Malodor typically results from bacterial degradation of fatty acids secreted in apocrine sweat. (See 'Pathogenesis' above.)
●Eccrine bromhidrosis may be localized or generalized. Localized eccrine bromhidrosis usually occurs in sites where sweating leads to skin maceration and subsequent bacterial degradation of keratin. The feet are common sites. Generalized eccrine bromhidrosis typically results from ingestion of odor-promoting substances or systemic illness. (See 'Pathogenesis' above.)
●The odor of bromhidrosis is often described as "rancid," "pungent," or "sour." The diagnosis usually can be made by smelling affected skin and obtaining a history of offensive odor noted by the patient and other individuals. The type of odor detected in generalized bromhidrosis can be indicative of the underlying disorder. (See 'Clinical presentation' above and 'Diagnosis' above.)
●The treatment of localized bromhidrosis focuses on improving hygiene and reducing bacteria and sweating in the affected area. For patients with localized bromhidrosis, we suggest skin hygiene, absorbent clothing, and topical antiperspirants and deodorants as initial treatment (Grade 2C). In addition, associated cutaneous diseases such as intertrigo, erythrasma, and pitted keratolysis should be treated. (See 'Treatment' above.)
●Antibiotic therapy may be added for patients with insufficient responses. Removal or destruction of apocrine glands through surgical excision, liposuction, and laser therapy can be effective for refractory localized bromhidrosis. (See 'Treatment' above.)