Asli Bromhidrosis

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BROMHIDROSIS
OVERVIEW
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.
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
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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-dependentN -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.
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.
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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.


PRESENTATION
History
Patients present with particularly offensive body odor that most commonly originates from
the axillary region. However, the condition may also occur as genital or plantar
bromhidrosis. The odor has been described as pungent, rancid, musty, or sour in character.
Physical
Bromhidrosis is a metabolic and functional disease not typically associated with any
anatomic disturbance. Therefore, results of physical examination of patients with axillary
bromhidrosis are usually unremarkable. The skin appears normal, except when
bromhidrosis is associated with concomitant skin conditions such as erythrasma, in which
case a sharply marginated erythematous macular rash is seen, or trichomycosis axillaris, in
which case concretions are visible on the hairs in the affected area.
In contrast, individuals with eccrine bromhidrosis caused by bacterial degradation of
keratin may have maceration and a thick mat of moist keratin on examination. This finding
is most common on the plantar and intertriginous surfaces.
Several case reports in children have described a nasal foreign body as a cause of
generalized bromhidrosis.[11, 12, 13, 14, 15] Therefore, examiners should conduct thorough
visualization and palpation of nasal passages in pediatric patients.
Causes


Excessive secretion from either apocrine or eccrine glands that becomes malodorous
on bacterial breakdown is the predominant cause of bromhidrosis.
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Inadequate hygiene and medical or dermatologic conditions associated with
hyperhidrosis or overgrowth of bacteria may further contribute to its development.
Examples include the following:

Obesity

Diabetes mellitus

Intertrigo

Trichomycosis axillaris

Erythrasma
Nasal foreign body is a reported cause of generalized bromhidrosis in the pediatric
population.[11, 12, 13, 14, 15]
Eccrine bromhidrosis may rarely be caused by metabolic disorders, primarily
disturbances in amino acid metabolism (which include phenylketonuria,
trimethylaminuria [fish odor syndrome]), sweaty feet syndrome, odor of cat syndrome,
isovaleric academia, and hypermethioninemia.
Ingestion of certain foods, drugs, or toxic materials may cause eccrine bromhidrosis.
Older medical textbooks report that offensive smells were characteristic of diseases
like gout, scurvy, or typhoid, secondary to metabolite excretion in sweat.

DIFFERENTIAL DIAGNOSES

Erythrasma

Trichomycosis Axillaris
WORKUP
Laboratory Studies

Typically, the olfactory perception of the diagnostician is the only clinical tool
required for diagnosis.

Chromatography or spectroscopy may help identify odor-producing
chemicals; however, the specific identification of odoriferous molecules is largely of
academic interest and lacks diagnostic or therapeutic importance.

In addition, results of chromatography or spectroscopy do not help in
differentiating normal odor from odor caused by bromhidrosis.

If concomitant erythrasma, a chronic bacterial infection of Corynebacterium
minutissimum is suspected, the skin has a characteristic coral-red fluorescence under
Wood lamp examination, and a potassium hydroxide preparation is negative for hyphae.

Potassium hydroxide preparation shows bacteria within concretions from axillary
hair in cases of trichomycosis axillaris.

If an underlying metabolic disorder is suspected as a cause of odor, specific testing
of urine or sweat may be indicated to detect the aberrant amino acid product.
Imaging Studies

No imaging studies are indicated for the evaluation of bromhidrosis.
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Other Tests

Skin biopsy is rarely indicated in bromhidrosis. However, skin biopsy may be used
to evaluate apocrine glands if surgical treatment options are being considered.
Histologic Findings
Evidence about histologic findings in patients with bromhidrosis is conflicting. Although
some research indicates that no histologic abnormalities are seen in the skin or glands of
patients with apocrine bromhidrosis when compared with control subjects, a few studies
have shown that the number and the size of apocrine glands is increased in bromhidrosis
skin. This finding suggests increased apocrine sweating as a possible cause of this
bothersome condition.
TREATMENT
Medical Care
Several therapeutic modalities are available to treat body odor. When a treatment method is
chosen, it is important to consider the cultural implications and the degree of impairment in
quality of life, as well as the patient's expectations and goals of treatment.
Hygiene and topical antibacterial agents
Conservative measures, which aim to reduce bacterial florae and maintain a dry
environment, include improved hygiene and topical therapy. Hygienic measures, such as
adequate washing of the axillary vault, prompt removal of sweaty clothing, and the use of
topical deodorant (which covers the odor and decreases bacterial counts) are beneficial in
cases of apocrine bromhidrosis. Regular shaving of axillary hair prevents the accumulation
of sweat and bacteria on the hair shafts. Electrolysis might also be considered for hair
removal to minimize bacterial growth.
Use of topical antibiotics such as clindamycin and erythromycin and antiseptic soaps may
yield clinical benefit by limiting the growth of the contributory bacteria that decompose
apocrine secretions, liberating fatty acids that have peculiar smells. Topical antibiotics
should only be used when other antiseptics are ineffective because they are associated with
a greater risk of bacterial resistance. Treatment of coexisting skin conditions, such
as intertrigo, erythrasma, andtrichomycosis axillaris, is important.
Drying agents
Measures to enhance drying and limit maceration, such as the use of antiperspirants
including aluminum chloride, may improve bromhidrosis of either apocrine or eccrine
origin, particularly if hyperhidrosis is a contributing factor. Antiperspirants, unlike
deodorants, contain aluminum salts, which inhibit sweat production.
Iontophoresis, which disrupts sweat production, has a role in the treatment of eccrine
bromhidrosis. With this method, a small electric current is passed through the skin while the
affected area is placed under tap water. Typically used only for volar skin, this treatment is
5

time intensive and should be considered only if excessive eccrine sweating contributes to
the patient's body odor. Amelioration of hyperhidrosis does not reduce apocrine sweat
production.
Conservative methods are ideal for mild cases. However, they do not offer a definitive cure,
and results may be unsatisfactory if odor reduction is short lived and incomplete. Systemic
anticholinergic agents decrease sweating, but they are not commonly used because of their
significant adverse effect profile.
Lasers and botulinum toxin
For patients who desire more long-lasting treatment, a few nonsurgical options have been
developed, although the data on these options are limited. A frequency-doubled, Q-switched
Nd:YAG laser has been effective in axillary bromhidrosis.[17]
The inhibitory action of botulinum toxin A to decrease sweat production by denervating
eccrine sweat glands has also been applied to successfully treat axillary hyperhidrosis. [18,
19]
The effect on axillary apocrine gland secretion is unknown; however, local injections of
botulinum toxin A reduced axillary body odor in a small sample of healthy subjects, and 1
case of improved genital bromhidrosis after botulinum toxin A treatment is reported.
[20]
Although this method has not been widely tested in treating body odor, it may represent
a future therapy for significant bromhidrosis.
Surgical Care
Surgical treatment for axillary bromhidrosis has been used in a limited fashion in the
United States; however, several surgical techniques are used more widely in Asian
countries, where axillary odor causes more social and psychological distress.[21]
Clearly, surgical reduction in the number of apocrine glands diminishes apocrine secretion,
and because some histologic evidence to suggest overactive apocrine sweat glands
contributes to bromhidrosis, surgical techniques may be the most satisfactory methods of
treatment. Surgical treatment improves the long-term management of bromhidrosis, but it is
associated with an increased risk of morbidity, including scarring, surgical complications,
and risk of recurrence. In recent years, new techniques with less morbidity have been
developed, though often at the cost of less effective results.
Surgical removal
A multitude of surgical methods have been reported to date, which can be categorized into
the following 3 classic types[22, 23, 24, 25, 26, 27, 28] :

Removing only subcutaneous cellular tissue without removing skin

Removing skin and subcutaneous cellular tissue en bloc

Removing skin and cellular tissue en bloc, as well as removing the subcutaneous
cellular tissue of the adjacent area: This is often performed by using a shaving technique
on the subcutaneous tissue.[29]

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Depending on the depth of the surgical injury, regeneration of gland function over a period
of years may be observed. Subcutaneous tissue removal has also been combined with
carbon dioxide laser to vaporize the residual apocrine glands.[30]
Superficial liposuction curettage
The superficial liposuction curettage technique is an outpatient procedure that has the
advantage of being less traumatic than open surgery. Small incisions are made in the axilla,
and a suction device is inserted that removes the subcutaneous tissue. This procedure offers
a smaller incision, lower complication rates, and minimal postoperative care. [31, 32, 33,
34]
However, its associated recurrence rate is higher than that of open surgery, leading to
decreased patient satisfaction on long-term follow-up. A similar procedure, ultrasoundassisted suction aspiration, liquefies fat and sweat glands. [35, 36, 37] This treatment has
recurrence rates lower than those of traditional superficial liposuction curettage and results
in similarly small scars.
Upper thoracic sympathectomy has also been performed for axillary bromhidrosis, and one
study in Taiwan reported a satisfaction rate of 70.6%; however, this therapeutic modality
has more frequently been used for axillary and palmar hyperhidrosis.[38]
Diet
Omission of certain foods may be of value if these factors can be isolated or identified as
contributory factors to the bromhidrosis. Common culprits include curry spices, onions,
garlic, and alcohol.
MEDICATION
Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Antibacterial Agents
Class Summary
Bacteria have been implicated in the pathogenesis of bromhidrosis; the organisms
decompose apocrine secretions, liberating fatty acids that have peculiar smells.
Clindamycin topical (Cleocin, Clindagel)
Inhibits bacterial growth by binding to 50S ribosomal subunit and blocking dissociation of
peptidyl t-RNA from ribosomes, arresting RNA-dependent protein synthesis.
Erythromycin topical (Erythro-Statin 2%, Akne-mycin, Theramycin Z)
Macrolide antimicrobial that inhibits bacterial growth by binding reversibly to 50S
ribosomal subunit and blocking dissociation of peptidyl t-RNA from ribosomes, arresting
RNA-dependent protein synthesis. Use 2-4% solution.
Neuromuscular Blocker Agent, Toxin
OnabotulinumtoxinA
Known to be effective in treating hyperhidrosis. Has also been found to decrease axillary
odor in a study of healthy subjects and in one case study in genital bromhidrosis.
7

Antiperspirant
Aluminum chloride topical
Astringent agent used in management of hyperhidrosis. Antiperspirant mechanism of action
is not known, although creation of aluminum-containing casts within the sweat duct has
been postulated.
Solution of 20% aluminum chloride in ethyl alcohol.
FOLLOW-UP
Patient Education
Patients with bromhidrosis should be encouraged to maintain an appropriate level of
hygiene with the use of antibacterial soaps and antiperspirants. Bromhidrosis patients also
should be aware of the odor that may arise from dried sweat on clothes.

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