Oxindole in pathogenesis of hepatic encephalopathy
1998; Elsevier BV; Volume: 351; Issue: 9119 Linguagem: Inglês
10.1016/s0140-6736(05)78807-3
ISSN1474-547X
AutoresFlavio Moroni, Raffaella Carpenedo, Ivo Venturini, Mario Baraldi, Maria Luisa Zeneroli,
Tópico(s)Tryptophan and brain disorders
ResumoThe pathogenesis of hepatic encephalopathy is largely unknown. While ammonia is the substance most often incriminated in this encephalopathy, other compounds such as mercaptans, short-chain fatty acids, amines, endorphins, glutamate, GABA, and endogenous benzodiazepine agonists have been proposed as contributing factors. 1 Blei AT Butterworth RF Hepatic encephalopathy. Sem Liver Dis. 1996; 16: 233-239 Crossref Google Scholar It has also been shown that the concentrations of tryptophan are significantly increased in blood and brain of animal models of hepatic encephalopathy, and that the consumption of tryptophan-rich meals by patients with hepatic disorders affects their behaviour and may precipitate coma. 2 Bengtsson F Bergqvist PBF Neuropsychiatric implications of brain tryptophan perturbations appearing in hepatic encephalopathy. in: Allegri Filippini G Costa CVL Bertazzo A Recent Advances in Tryptophan Research. Plenum Press, New York1996: 387-397 Crossref Scopus (16) Google Scholar It is therefore reasonable to suppose that tryptophan or its metabolites may be involved in the pathogenesis of this syndrome. Significant changes in the synthesis, release, and blood or brain concentrations of several tryptophan metabolites able to affect central nervous system function, such as 5-OH-tryptamine, quinolinic or kynurenic acids, have been reported in hepatic encephalopathy models, but no clear evidence that any of these compounds play a major pathogenetic role is available.
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