Protective Effect Of Bile Acids Preparations Against Endotoxin Shock

On the basis of the above experiments therapeutic preparations of bile acids (DETERTOXON-S and B) have been produced which seem to be beneficial for the treatment of entero-endotox-aemia in newborns [27], Comparative pathological studies conducted during these therapeutic trials demonstrated that these preparations were able to decrease mortality due to E. coli diarrhoea. For instance, in a cattle herd 195 calves received conventional treatment and 23 of them died, whereas after the treatment of 234 calves with the bile acid preparation only 6 were lost because of E. coli diarrhoea. Essentially similar results were obtained during the trial in other herds. The results were similar though inferior in a pig farm where 120 piglets were lost out of 2027 untreated animals, whereas 68 died of 1803 bile acid treated animals due to E. coli diarrhoea [28],

These results are significant because of the experience gained during several decades that the treatment of entero-endotoxaemic newborn animals with drugs or vaccines is of limited value. Vaccines provide protection only against specific strains that have been used for its production and become useless against other strains that frequently occur in a given population. This is a serious limitation, as approximately 150 different E. coli strains are known simply on the basis of O serotypes. For this reason the induction of specific immunity seems impossible. Perhaps the new, so-called pilus antigen vaccines or the use of DNA vaccines will improve the situation [29,30]. The problem is similar when antibacterial agents (antibiotics, sulphonamides) are used for treatment. Resistance will occur within a short period of time, which renders these drugs ineffective. One may hope, on the basis of our results, that this disease could be prevented by the restoration of bile acid deficiency. Current evidence indicates that in E. coli diarrhoea the entero- and protein toxins [30] could facilitate the translocation of endotoxin by causing damage to the gut mucosa. Such damage would inhibit or prevent the secretion of cholecystokinin, which in turn would lead to bile retention and allow the absorption of endotoxin into the bloodstream, resulting in endotoxaemia and shock. This explanation is compatible with those views that emphasise the fundamental pathogenic role of endotoxin in these conditions.

The above examples of animal disease have comparative pathological significance and serve as models for human conditions. It is well known that a significant proportion of the human population suffers from problems of bile secretion and of gallbladder function (Bertok Jr. and Bertok, unpublished observations). It is possible that the use of bile acid preparations would be of advantage in such patients.

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