The condition can be known medically as bromhidrosis, apocrine bromhidrosis, osmidrosis, ozochrotia, fetid sweat, body smell, or malodorous sweating.James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. p. 779. .
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Osmohidrosis is excessive odor from apocrine sweat glands (which are overactive in the axillae). Osmidrosis is thought to be caused by changes in the apocrine gland structure rather than changes in the bacteria that acts on sweat.
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Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. p. 707. . Osmidrosis or bromhidrosis is defined by a foul odor due to a water-rich environment that supports bacteria, which is caused by an abnormal increase in perspiration (hyperhidrosis).
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Sweat builds up in the duct, causing enough pressure to rupture the duct where it meets the epidermis. Sweat also escapes the duct to adjacent tissues (a process called milaria). Hypohydrosis then follows milaria (postmiliarial hypohydrosis). ; Osmidrosis: Often called bromhidrosis, especially in combination with hyperhidrosis.
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This can be particularly strong when it happens in the axillary region (underarms). In this case, the condition may be referred to an axillary osmidrosis. Trimethylaminuria (TMAU), also known as fish odor syndrome or fish malodor syndrome, is a rare metabolic disorder where trimethylamine is released in the person's sweat, urine, and breath, giving off a strong fishy odor or strong body odor.
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ATP-binding cassette transporter sub-family C member 11, also MRP8 (Multidrug Resistance-Related Protein 8) is a membrane transporter that exports certain molecules from inside a cell. It is a protein that in humans is encoded by gene ABCC11. The gene is responsible for determination of human cerumen type (wet or dry ear wax) and presence of underarm osmidrosis (odor associated with sweat caused by excessive apocrine secretion).
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In addition to earwax phenotype, the ABCC11 genotype has been found to be associated with colostrum secretion from the breasts as well as normal axillary odor and osmidrosis (excessive axillary malodor). A functional ABCC11 protein has been found to be essential for the presence of the characteristic strong axillary odor, with the 538G→A SNP leading to a loss of secretion of axillary malodorous precursors and a nearly complete loss of axillary odor in those who are homozygous for the polymorphism. Specifically, the secretion of the amino-acid conjugates 3M2H-Gln, HMHA-Gln, and Cys-Gly-(S) 3M3SH, which are precursors of key axillary malodorous compounds including the unsaturated or hydroxylated branched-chain fatty acids 3M2H and HMHA and the sulfanylalkanol 3M3SH, has been found to be abolished in homozygotic carriers of the SNP, and the odoriferous androstane steroids androstenone and androstenol and their precursors DHEA and DHEA-S have been found to be significantly reduced as well. Patients with axillary osmidrosis (538G/G or 538G/A genotype) were found to have significantly more numerous and relatively large axillary apocrine glands compared to controls with the A/A genotype.
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Indeed, it has been noted that there is currently no evidence that sweat secretion glands nor sweat production varies across ethnicities. Indeed, one large study failed to find any significant differences across ethnicity in residual compounds on the skin, including those located in sweat. Indeed, if there were observed ethnic variants in skin odor, one would find sources to be much more likely in diet, hygiene, microbiome, and other environmental factors. Research has indicated a strong association between people with axillary osmidrosis and the ABCC11-genotypes GG or GA at the SNP site (rs17822931) in comparison to the genotype AA.
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These respectively code for glycine and arginine in the gene's protein product. Dominant inheritance of the GG or GA genotype is observed while the AA genotype is recessive. The phenotypes expressed by the genotypes include cerumen type (wet or dry ear wax), osmidrosis (odor associated with sweat caused by excessive apocrine secretion), and possibly breast cancer risk, although there is ongoing debate on whether there is a real correlation of the wet ear wax phenotype to breast cancer susceptibility. The GG or GA genotype produces the wet ear wax phenotype (sticky and brown colored) and acrid sweat odor and is the dominant allele.
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