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Abstract:
It would appear from these observations that the morbidly obese human has an abnormal liver at the time of surgical intervention. This abnormality exists whether the operation performed is an intestinal shunt procedure or a gastric restrictive procedure. In the early period after an intestinal shunt, during the phase of most rapid weight loss, there is a selective malabsorption of fats and proteins with an increase in the proportion of calories absorbed in the form of carbohydrate. It would also appear that there is an overgrowth of bacteria, predominantly anaerobes, in the excluded limb of intestine. Although the production of liver dysfunction after an intestinal shunt is almost certainly multifactorial, it would appear from the evidence presented that the excluded limb of intestine plays a significant role in the production of this syndrome. It would seem reasonable to propose that the already compromised liver is insulted further by protein calorie malnutrition. This insult is compounded by the effect of some type of toxin produced within the excluded limb of intestine. The most likely candidate for this latter agent would appear to be an endotoxin. To date, in the human, no antimicrobial has been demonstrated to be effective in protecting the liver from this damage. Many similarities can be drawn between the histologic changes seen in alcoholic liver disease and the liver disease produced by an intestinal bypass. It is possible that these two disease states share, in part, a common pathway. This pathway may involve a state of malnutrition (maldistribution of a caloric source) but may also be associated with a toxin. Although this toxin may be alcohol or a breakdown product affected by alcohol, we should also consider the possibility that alcohol might have an effect on the intestinal mucosa, allowing the absorption of some other type of toxin. If this latter hypothesis has any validity, then a tenuous link between the two disease states could be proposed.