1993
DOI: 10.1136/bmj.307.6905.655
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The fish odour syndrome: biochemical, familial, and clinical aspects.

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Cited by 142 publications
(86 citation statements)
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“…These observations are consistent with the previous report by Dolphin et al (2000) who reported that substitution of a serine for asparagine at the same position (N61S) abolished jpet.aspetjournals.org the capacity of FMO3 to catalyze the N-oxidation of trimethylamine. Thus, similar to the FMO3 N61S variant, the N61K variant is predicted to contribute to the incidence of trimethylaminuria, an autosomal recessive disorder that is characterized by a deficiency in FMO3 enzyme activity and an inability of individuals to metabolize malodorous trimethylamine to the odorless trimethylamine N-oxide (Ayesh et al, 1993). Predictably, the N61K variant was not inferred in any of the common FMO3 haplotypes.…”
Section: Discussionmentioning
confidence: 99%
“…These observations are consistent with the previous report by Dolphin et al (2000) who reported that substitution of a serine for asparagine at the same position (N61S) abolished jpet.aspetjournals.org the capacity of FMO3 to catalyze the N-oxidation of trimethylamine. Thus, similar to the FMO3 N61S variant, the N61K variant is predicted to contribute to the incidence of trimethylaminuria, an autosomal recessive disorder that is characterized by a deficiency in FMO3 enzyme activity and an inability of individuals to metabolize malodorous trimethylamine to the odorless trimethylamine N-oxide (Ayesh et al, 1993). Predictably, the N61K variant was not inferred in any of the common FMO3 haplotypes.…”
Section: Discussionmentioning
confidence: 99%
“…The best understood form of trimethylaminuria is the primary genetic form associated with dysfunctional FMO3 arising from genetic mutations (Cashman et al, 2003). In addition, an acquired form possibly arising from hepatitis (Mitchell and Smith, 2001), childhood forms (Koukouritaki et al, 2002), a transient form associated with menstruation (Ayesh et al, 1993), and substrate or precursor overload or other impaired disease states can lead to trimethylaminuria. The work reported herein is largely related to the form of trimethylaminuria in which abnormal FMO3 enzyme activity is found when a coding region mutation or combination of mutations is present.…”
mentioning
confidence: 99%
“…3 Expert opinion suggests that a short course of low-dose neomycin or metronidazole can be used to suppress production of trimethylamine in the gut. 7 The use of mildly acidic soaps may help to reduce the odour in some patients. 8 Additional therapeutic strategies that may be de veloped in the future include gene therapy, attempts to colonize the human gut with microorganisms engineered with human flavin-containing monooxygenase 3 and enzyme induction with drugs.…”
Section: Treatment Optionsmentioning
confidence: 99%