It has been suggested that
mercaptans are important factors in the pathogenesis of
hepatic encephalopathy. Using a gas liquid chromatographic technique which uses
propanethiol as internal standard and a sulphur specific detector, blood
methanethiol concentration was found to be significantly risen in encephalopathic patients with
liver disease (13.2 +/- 1.0 nmol/ml; n = 47) compared with control subjects (5.7 +/- 0.3, n = 29; p less than 0.05) and non-encephalopathic patients with
liver disease (7.7 +/- 1.1, n = 35; p less than 0.05) but
ethanethiol and
dimethylsulphide concentrations were similar in the three groups. Blood
methanethiol, however, was not clearly related to
coma grade, similar values being found in deeply comatosed patients to those showing only mild cerebral dysfunction. When rats were injected with 40-120 mumol
methanethiol a range of responses was obtained which varied between normal consciousness and
coma. The minimum blood concentration of
methanethiol associated with
coma (200 nmol/ml) was at least 10-fold greater than in patients with
hepatic encephalopathy but brain concentrations were similar in
comatose rats and those which remained awake. Blood
methanethiol concentrations were similar in control and germ free rats and did not rise in cirrhotics or controls after ingestion of 2 g
methionine. It is concluded that while
methanethiol may accumulate in
hepatic coma, it is unlikely to be of major pathogenetic importance. Endogenous
mercaptans are unlikely to originate from bacterial metabolism in the gut.