Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 40 obese patients, the liver function and the morphological picture were examined before and after jejuno-ileostomy. In 94% of the patients, distinct fatty liver was observed already before the small bowel exclusion, and the function tests showed an impaired function of this organ in 25% of the subjects before the operation. No clinical symptoms of liver insufficiency were recorded during the postoperative period. During one to three months after surgery, an increased impairment of the liver function was ascertained but, later on, a gradual improvement. More than one year after jejuno-ileostomy, the function test results were considerably better than before the operation. The degree of steatosis increased in the majority of the patients within 6 months after surgery, and some time later a considerable decrease in fatty liver was observed. Within 18 to 24 months after the jejunoileostomy, the morphological picture of the liver did not differe from the normal. The impaired function and the increased degree of steatosis were noted during diarrhea and rapid loss of body weight. The reson for this is most probably the protein malnutrition caused by the radical reduction in the absorption surface of the small bowel. The improved function and morphological picture of the liver are related to the progress of adaptation changes of the active part of small bowel. The results of the author's research do not confirm the hypothesis of permanent, harmful effect of jejuno-ileostomy on the state of the liver. The symptoms observed are definitely of a periodical and transient character, and are therefore not contra-indicated in the application of this operation in morbid extreme obesity treatment.
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PMID:Function and morphological picture of the liver in obese patients before and after jejunoileostomy. 74 72

Since 1964, 41 patients with strictly defined, severe primary (dietetic) protein malnutrition have been studied under metabolic ward conditions during prolonged periods, initially on a low (20 g) and later on a high (100 g) protein diet. Clinical, nutritional, hematological, intestinal absorptive and histological studies were performed in the malnourished state, during and after protein repletion. Classical signs and symptoms of malnutrition, lasting for at least 4 months, were present in most patients. Mild diarrhea was frequent. All were normoblastically anemic, hypoproteinemic, and hypocholesterolemic; serum folate values were normal or low but serum B12 values were normal or high. Liver biopsy showed fatty liver in the cases where it was performed. Mild malabsorption was detected in over one-half of the patients, with moderate intestinal radiological abnormalities. Malabsorption was independent of concomitant folate deficiency. All the clinical, absorptive and histological abnormalities reversed with treatment consisting only of a high protein diet. In addition to protein lack, another factor has to be invoked in the pathogenesis of the intestinal abnormalities present in severely malnourished adults from rural areas in the tropics.
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PMID:Enteropathy in adult protein malnutrition: a review of the Cali experience. 114 51

A cas is reported of a 23-year-old man who voluntarily took a massive dose of arsenic (at least 8 g). In spite of the ingested amount and the acute nature of the poisoning, the patient survived 8 days. Gastrointestinal, neurologic and cardiac features were predominant including nausea, vomiting, choleroid diarrhoea, encephalopathy, peripheral neuropathy, and finally a fatal toxic cardiomyopathy. Metabolic acidosis, moderate cytolysis and an anticoagulant effect were also observed. This unique characteristic was partly due to a circulating anticoagulant with prothrombinase activity, as well as direct antivitamin K activity. Postmortem examination revealed: a congestive oesophagitis; a necrosing gastritis involving all the stomach wall; diffuse hepatic steatosis; skin lesions with vascular congestion and dermoepidermal detachment; discrete subepicardial congestive lesions. Arsenic was found in all tissues.
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PMID:[Subacute arsenic poisoning]. 185 59

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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PMID:Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs. 188 58

Fluid therapy is practical and beneficial when properly administered to cattle. Mature cattle are more frequently alkalotic than acidotic, so nonalkalizing solutions are usually indicated. Exceptions include cattle with choke, carbohydrate engorgement, diabetes mellitus, and, occasionally, renal disease, diarrhea, and fatty liver/ketosis. Most dehydrated cattle need supplemental potassium and calcium as well as sodium, chloride, and water. Intravenous administration is indicated in patients with obstructive gastrointestinal disease and those with severe dehydration. Oral or intraruminal administration is less expensive and often very effective.
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PMID:Fluid therapy in mature cattle. 217 37

We treated nine infants who unexpectedly developed shock, seizures, and fever, followed by diarrhea, consumption coagulopathy, and hepatorenal dysfunction. Despite vigorous treatment, three infants died and all except one of the six survivors have severe residual neurologic abnormalities. Postmortem findings included cerebral edema, white matter petechial hemorrhages, gastrointestinal hemorrhages, and fatty liver. These clinicopathologic features are similar to those previously described in 10 infants as being due to hemorrhagic shock and encephalopathy, except for the presence of fatty liver in our patients. Based on the combined experience of 19 infants, we propose diagnostic criteria for hemorrhagic shock and encephalopathy that may facilitate recognition and differentiation from other shock syndromes in infancy.
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PMID:Hemorrhagic shock and encephalopathy. Clinical definition of a catastrophic syndrome in infants. 240 86

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

To determine whether depletion of liver glycogen or accumulation of liver fat (steatosis) was associated with the development of hypoglycaemia in children with fatal diarrhoeal illnesses, a case-control study was carried out comparing 17 children who had blood sugars less than or equal to 30 mg/dl with 17 age matched control children who had blood sugars greater than or equal to 59 mg/dl. The most common causes of diarrhoea in the hypoglycaemic children were Shigella sp. and Vibrio cholerae. The mean duration of diarrhoea before admission for the hypoglycaemic children, 7.8 d, was shorter than the 20.7 d for the controls (P less than 0.01). Most children in both groups showed signs of malnutrition, metabolic acidosis, and pneumonia. Liver specimens were obtained at post-mortem examination and stained with haematoxylin and eosin for general assessment and with periodic acid-Schiff stain for glycogen. Glycogen depletion was detected in 9 hypoglycaemic children and in only 3 control children (P less than 0.05). Hepatic steatosis, on the other hand, occurred with equal frequency in both groups but was associated with severe malnutrition in the hypoglycaemic patients (P less than 0.05). This result suggested that hypoglycaemia develops during acute diarrhoeal illnesses because gluconeogenesis fails to maintain the blood sugar concentration after depletion of liver glycogen. Frequent feeding of children with diarrhoea might help to prevent this complication.
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PMID:Depletion of hepatic glycogen in the hypoglycaemia of fatal childhood diarrhoeal illnesses. 261 56

Hepatomegaly, chronic diarrhea, and weight loss in a middle-aged woman were found to be due to massive hepatic steatosis and adult celiac disease. After she was on a gluten-free diet for 1 yr, improvement in clinical, laboratory, and pathological parameters was witnessed. Massive hepatic steatosis complicating adult celiac disease is an uncommon occurrence, differing from other, more frequently encountered hepatopathies in this disease, insofar as pathogenetic and prognostic aspects are concerned.
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PMID:Massive hepatic steatosis complicating adult celiac disease: report of a case and review of the literature. 331 86

Resectability was studied in relation to both the functional reserve of the liver or pancreas and radicality in 112 cases of primary liver cancer and 34 cases of pancreatic head cancer resected in our department over an 11-year period. 1. Primary liver cancer: In extended hepatectomy including one segment beyond the tumor-bearing area, recurrence rate was low with a high long-term survival rate of more than 3 years, although hepatic insufficiency occurred frequently. In limited resection of the segment of the tumor or enucleation, many patients died due to recurrence within 2 years, except for those with small liver cancers. 2. Pancreatic head cancer: Extended surgery especially total pancreatectomy, had higher radicality with a higher 3-year survival rate than for the standard operation, even in case of advanced stage III or IV cancer. However, extended surgery produced a high incidence of postoperative fatty liver due to disturbance of pancreatic exo- and endocrine function, and severe diarrhea following dissection of the nerve plexus. Therefore, it is necessary to select a suitable operative method upon consideration of both radicality and functional reserve of the liver or the pancreas.
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PMID:[Resectability of primary carcinoma of the liver and pancreas, with special reference to radicality and functional reserve]. 338 89


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