Prevention of Chenodeoxycholic-Acid Toxicity With Lincomycin

Salen, Gerald; Dyrszka, Herbert; Chen, T.; Saltzman, Wendy; Mosbach, Erwin H.

doi:10.1016/s0140-6736(75)91844-9

Cited by 21 publications

(1 citation statement)

References 5 publications

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“…Despite this clear-cut efficacy, clinical testing of this potent agent has expanded only slowly because of dose-related hepatotoxicity observed in the rabbit (Fischer et al, 1974), rhesus monkey (Webster et al, 1975;Dyrszka et al, 1976), and baboon (Morrissey et al, 1975). There is now strong evidence implicating lithocholic acid, the principal bacterial metabolite of chenic acid, as the major factor in chenic acid induced liver injury (Palmer, 1972;Fischer et al, 1974;Morrissey et al, 1975;Salen et al, 1975;Webster et al, 1975;Dyrszka et al, 1976;Gadacz et al, 1976).…”

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confidence: 99%

Lithocholate metabolism during chenotherapy for gallstone dissolution. 1. Serum levels of sulphated and unsulphated lithocholates.

Allan¹,

Thistle²,

Hofmann³

et al. 1976

Gut

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SUMMARY Serum levels of total sulphated and total unsulphated lithocholates were each measured by a specific radioimmunoassay in 66 patients ingesting chenodeoxycholic (chenic) acid for gallstone dissolution and in 35 gallstone patients ingesting either cholic acid or placebo. No changes occurred in serum lithocholate levels in the control groups. In patients ingesting chenic acid, there was a twofold increase in serum levels of total lithocholate, but the percent sulphation (>75 %) remained unchanged during chenotherapy. There was no correlation in the chenic acid treated group between serum lithocholate levels and the proportion of lithocholate in biliary bile acids or changes in serum SGOT. The data suggest that there is effective sulphation of lithocholate in such patients; this may explain the lack of hepatotoxicity observed during ingestion of chenic acid.

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