1. Definition and Clinical Relevance
Bromhidrosis (from Greek bromos = odor + hidros = sweat), also known as osmidrosis, is defined as the production of foul and persistent body odor, usually related to the bacterial decomposition of apocrine or eccrine sweat. Although it does not represent a severe organic condition, it carries significant psychosocial impact, potentially leading to social isolation, anxiety, and depression. In dermatological practice, bromhidrosis is considered a diagnosis of exclusion, and systemic or infectious causes of malodor must be ruled out.
2. Epidemiology
Precise epidemiological data are scarce due to underreporting and patient embarrassment. It is estimated that up to 3% of the general population will present complaints related to bromhidrosis at some point in their lives, with a higher prevalence in:
- Young adults (peak between 18 and 35 years)
- Individuals with hyperhidrosis
- Populations with obesity or deep skin folds
- Patients with certain metabolic conditions (e.g., trimethylaminuria)
The condition affects both sexes equally, although axillary odor is more often perceived as problematic in women due to sociocultural factors.
3. Etiology and Pathophysiology
Human sweat is naturally odorless when produced. The characteristic odor of bromhidrosis results from the action of saprophytic bacteria on compounds present in sweat, generating malodorous volatile metabolites.
3.1 Glands Involved
| Gland Type | Secretion | Main Location | Role in Bromhidrosis |
|---|---|---|---|
| Eccrine | Aqueous, rich in NaCl, urea, lactate | Almost the entire body surface | Less relevant – odor occurs only in situations of retention or hyperhidrosis with maceration (e.g., foot odor). |
| Apocrine | Viscous, rich in lipids, proteins, iron | Armpits, anogenital region, nipples, external ear canal | Mainly responsible – bacterial degradation of fatty acids and steroids generates the characteristic odor. |
3.2 Biochemical Mechanisms
Bacteria such as Corynebacterium spp., Staphylococcus hominis, Micrococcus spp., and Cutibacterium spp. hydrolyze odorless precursors present in apocrine sweat:
- Short-chain fatty acids (isovaleric acid – sweaty/cheesy odor)
- Thioalcohols (3-methyl-3-sulfanylhexan-1-ol – sulfurous onion odor)
- Steroids (androst-16-en-3-one – musky/urine odor)
In axillary bromhidrosis, the contribution of trans-3-methyl-2-hexenoic acid (curry odor) has recently been identified as a specific marker.
3.3 Predisposing Factors
- Hyperhidrosis (increase in substrate)
- Poor hygiene (accumulation of secretion and biofilm)
- Occlusion and friction (skin folds, synthetic clothing)
- Hormonal changes (puberty, menopause – influence apocrine secretion)
- Diet (garlic, onion, spices, alcohol – partially excreted in sweat)
- Systemic diseases (trimethylaminuria – fish odor; phenylketonuria – musty odor; isovaleric acidemia – cheese odor)
4. Classification of Bromhidrosis
| Type | Characteristic |
|---|---|
| Apocrine Bromhidrosis | Most common (armpits, anogenital region). Intense odor, appears after puberty. Related to bacterial action on apocrine sweat. |
| Eccrine Bromhidrosis | Rare. Occurs when eccrine sweat is retained on the skin (hyperhidrosis, occlusion) and undergoes degradation by bacteria or fungi. Ex: foot odor (plantar bromhidrosis). |
| Systemic (Metabolic) Bromhidrosis | Endogenous origin: odorous compounds are excreted by eccrine glands or through respiration. Ex: trimethylaminuria, hepatic insufficiency, some intoxications. |
| Psychogenic Bromhidrosis | The patient reports a foul odor that is not objectively confirmed. Usually associated with a delusional disorder (olfactory reference syndrome) or anxiety disorder. |
5. Diagnosis
5.1 Directed Anamnesis
- Location, intensity, worsening/improving factors.
- Age of onset (after puberty suggests apocrine).
- History of hyperhidrosis, obesity, diabetes.
- Use of medications (e.g., some anticonvulsants, cholinesterase inhibitors).
- Dietary history and habits (smoking, alcohol).
- Psychosocial impact.
5.2 Physical Examination
- Inspection of skin folds (maceration, erythema, hyperpigmentation).
- Iodine-starch test (to map hyperhidrosis, when present).
- Evaluation of the odor by the examiner (the use of a disposable mask is recommended for comfort).
6. Therapeutic Approach
The management of bromhidrosis must be gradual, individualized, and multimodal.
6.1 General and Hygiene Measures (First Line)
- Daily hygiene with antiseptic soaps (chlorhexidine 2-4%, triclosan, benzoyl peroxide 5-10%) – reduces bacterial load.
- Complete drying of folds after bathing (using a hair dryer on low heat).
- Natural fiber clothing (cotton, linen) and frequent changing.
- Underarm hair removal (reduces surface area for sweat and bacteria retention).
- Dietary modifications (reduction of garlic, onion, spices, alcohol).
6.2 Topical Antiperspirants
- Aluminum salts (aluminum chloride hexahydrate 10-25% in ethanol) – temporary occlusion of eccrine and apocrine ducts.
- Skin irritation is the main adverse effect.
6.3 Topical Antibacterials
- Clindamycin 1-2% lotion or gel.
- Erythromycin 2-4% solution.
- Metronidazole 0.75-1% gel (effective for anaerobically based odors).
6.4 Minimally Invasive Procedures (Second Line)
- Botulinum Toxin Type A: Cholinergic block of eccrine glands and, indirectly, reduction of the substrate for bacteria. Efficacy is well-established for associated hyperhidrosis; effect lasts 4-6 months.
- Microwaves (miraDry®): Thermal ablation of sweat glands. High efficacy for axillary bromhidrosis; single procedure, permanent results.
7. Conclusion and Practical Recommendations
- Bromhidrosis is a frequent, underdiagnosed condition with a strong social component.
- A careful clinical history and physical examination are sufficient for diagnosis in most cases.
- Treatment should start with hygiene measures and antiperspirants, advancing to minimally invasive procedures in refractory cases.
- Addressing associated hyperhidrosis is fundamental for lasting control.
References
- Kanlayavattanakul M, Lourith N. Body malodours and their topical treatment agents. Int J Cosmet Sci. 2021;43(3):298-311.
- Semprini A, et al. Axillary osmidrosis: pathophysiology and treatment. J Eur Acad Dermatol Venereol. 2019;33(8):1468-1475.
- James WD, Elston D, Treat JR, Rosenbach MA. Andrews' Diseases of the Skin: Clinical Dermatology. 13th ed. Elsevier; 2019.
- Mori N, et al. Classification of axillary osmidrosis and treatment algorithm. Dermatol Surg. 2020;46(5):654-661.