Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year old female patient with anorexia nervosa developed a severe toxic liver injury after parenteral hyperalimentation. Over a period of five days she received a total amount of carbohydrates of 0.47-1.07 g/kg/hr consisting of glucose, fructose and the polyalcohols sorbitol and xylitol. A steep rise in SGOT, SGPT, and GLDH were noted as well as prolongation of the prothrombin time and decrease of the clotting factors; uric acid and lactate increased, serum phosphate decreased. After termination of parenteral hyperalimentation a laparoscopy and liver biopsy were performed. The liver biopsy revealed by light- and electronmicroscopy signs of a severe toxic liver injury. After reduction of total carbohydrates and later oral feeding a complete remission occurred. The cause of the toxic liver lesions was believed to be due to an overdosage of fructose and sorbitol.
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PMID:[Severe toxic liver injury after overdosage of parenteral administered carbohydrates: a case report (author's transl)]. 40 17

Between October 1988 and May 1989, four cancer patients treated by broad-spectrum antibiotics developed a hemorrhagic diathesis induced by vitamin k (VK) deficiency. Activated partial thromboplastin time (APTT), prothrombin time (PT), factor II (FII) and protein induced by vitamin k absence of antagonist-II (PIVKA-II) were measured after administration of antibiotics and VK in all 4 patients. All these patients had been receiving intravenous hyperalimentation (IVH) and antibiotics for various infections. But all or them developed hemorrhagic diathesis within five days after the initiation of broad-spectrum cephem antibiotics (LMOX or CMNX). The abnormalities were 1) marked decrease of F II (6-18%), 2) prolongation of APTT (58.4-200 seconds), 3) prolongation of PT (7-21%), 4) marked increase of PIVKA-II (17-80 less than AU/ml). After being treated by intravenous administration of VK, hemorrhagic diathesis and abnormalities of coagulation tests except for PIVKA-II were corrected quickly in three evaluated patients. The measurement of PIVKA-II seemed to be useful to diagnose the hemorrhagic diathesis caused by VK deficiency in the patients during administration of antibiotics.
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PMID:[Acquired coagulopathy caused by administration of parenteral broad-spectrum antibiotics]. 190 Nov 16

We performed a controlled trial of peripheral hyperalimentation in moderate and severe alcoholic hepatitis to determine whether improvement in survival and liver function could be obtained. Twelve patients with moderate and 22 with severe alcoholic hepatitis were randomized to 28 days of peripheral parenteral nutrition (PPN) or standard therapy (ST). In the moderate group, six were treated with each therapy. In the severe group, 10 were treated with PPN and 12 with ST. Routine liver tests, hepatocyte function (galactose elimination capacity), estimated hepatic blood flow (galactose clearance) and assessment of ascites and encephalopathy were performed at randomization and at 28 days. Groups were equally matched at randomization. In the moderate group PPN produced no improvement in morbidity (liver tests) and mortality (no deaths). In the severe group there were seven deaths (4 PPN, 3 ST). PPN produced greater improvement than ST in serum bilirubin and transferrin concentrations and a trend toward greater improvement in prothrombin time, serum albumin and galactose elimination capacity. PPN had no deleterious effect on encephalopathy or ascites as only ST patients developed ascites or encephalopathy after randomization. We conclude that PPN compared to ST (1) provides no benefit in moderate alcoholic hepatitis, but (2) did more rapidly improve morbidity (liver tests) and probably liver function in severe alcoholic hepatitis; (3) PPN did not improve early mortality, and (4) it had no deleterious effect on encephalopathy or ascites.
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PMID:A randomized controlled study of peripheral parenteral nutrition in moderate and severe alcoholic hepatitis. 314 49