Biomedical subjects
Publications and source records attributed to E L Rogers.
Fulminant hepatic failure implies either acute massive destruction of liver tissue or another process that causes rapid deterioration in function of a previously normal liver. The diagnosis in children needs to be differentiated from hepatic failure that occurs as a complication of underlying congenital, anatomical, and metabolic abnormalities.
Significant vitamin A, E, or 25-hydroxy D deficiency occurred in 76% of 40 patients studied up to 6 years after jejunoileal bypass surgery for morbid obesity. Vitamin A was significantly lower in those who had lost 30% of their initial weight than in those who had lost less weight; however, there was no correlation of vitamin A, E, or D levels, time elapsed since surgery, or with daily intake of vitamins as subnormal values were found despite multivitamin supplementation and consumption of twice the recommended daily allowance of vitamin A. Functional derangement of retinal adaptation to darkness secondary to vitamin A deficiency was found in four of nine stable, healthy patients studied at least 18 months after surgery. There was no linear relationship between vitamin A levels and dark adapted final thresholds or with serum albumin, prothrombin time, or degree of steatorrhea. Three patients with abnormal adapted final thresholds were treated with vitamin A. Total daily intake of up to 65,000 IU of vitamin A daily for several months resulted in normalization of function in all.
Twenty-six patients who had typical symptoms of biliary tract disease, e.g. postprandial right upper quadrant pain, nausea and vomiting, fatty food intolerance and flatulence and who had had two or more normal oral cholecystograms were subjected to cholecytokinin cholescystography. Ten patients showed a normal response to the intravenous administration of cholecystokinin, namely prompt and complete emptying of the gallbladder without producing any adverse reaction or symptoms. Sixteen patients demonstrated either no contraction or incomplete contraction of the gallbladder in response to cholecystokinin; several patients had moderate contraction of the gallbladder accompanied by symptoms of biliary colic. This latter group underwent cholecystectomy and operative cholangiography. Fifteen of the 16 patients are asymptomatic or improved, and only one patient continues to have symptoms. All removed gallbladders had histologic evidence of chronic cholecystitis. It is concluded that in some individuals with continuing symptoms suggesting gallbladder disease but normal oral cholecystograms, cholecystokinin cholecystography may be helpful in identifying physiologic dysfunction of the gallbladder.
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