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)

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

Giant hepatic cavernous hemangiomas are clinically distinct from smaller asymptomatic ones and may be confused with primary or metastatic malignancy. Hemangiomas exceeding 8 cm in diameter (mean, 13.7 cm) were studied in eight women 28-71 years old, six of whom presented with right upper quadrant discomfort and/or hepatomegaly. On unenhanced CT, seven of the masses were less dense than surrounding normal liver and one was slightly more dense than adjacent fatty liver. All masses contained additional stellate or cleftlike low-density zones, and two contained calcification. After bolus IV contrast administration, all exhibited early peripheral enhancement and partial centripetal isodense fill-in. None became completely isodense on delayed scans. Familiarity with these CT characteristics and a high index of suspicion should facilitate correct diagnosis and avert needle biopsy.
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PMID:CT of giant cavernous hemangioma. 349 95

The mortality and the causes of death have been studied in a cohort consisting of 1548 male alcoholics in Stockholm. During the period 1969-1981 there were 542 cases of death in this population. The mortality rates were triple those for males in Stockholm generally. Using the official causes of death there was a highly significant excess mortality in the following diagnostic groups: Cancer in the upper digestive region, primary hepatic cancer, cirrhosis in the liver, pancreatitis, pneumonia, alcoholism and alcoholic poisoning, suicides and other causes of violent death as well as ischemic heart disease. The underlying and contributing causes of death on the death certificates were reclassified according to ICD-rules using clinical records and autopsy protocols. It was found that the underlying cause of death was incorrect in 21.8% of the cases. Important information was withheld in further 19.8%. After validation there was no longer any excess mortality in ischemic heart disease. The number of alcohol-related diagnoses, i.e. alcoholic cardiomyopathy, cirrhosis and fatty liver with alcoholism and alcoholic intoxication, was much greater. It is concluded that there is a underreporting of alcohol-related diseases and injuries which has a great influence on the reliability of death statistics.
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PMID:Validation of diagnoses on death certificates for male alcoholics in Stockholm. 358 75

The major diseases associated with obesity are hypertension, atherosclerosis, and diabetes, as well as certain types of cancer. Less well-known complications include hepatic steatosis, gallbladder disease, pulmonary function impairment, endocrine abnormalities, obstetric complications, trauma to the weight-bearing joints, gout, cutaneous disease, proteinuria, increased hemoglobin concentration, and possibly immunologic impairment. A U- or J-shaped curve illustrates the relation between body mass index and the degree of these various complications. This relationship can be used to provide guidelines for assessing treatment of obesity.
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PMID:Complications of obesity. 406 25

Forty five cases of chronic pancreatitis have been diagnosed between January 1966 to July 1983 in the Hospital A. Posadas. The diagnosis was confirmed by the presence of one or more of the following data: pancreatic calcifications positive in 35, abnormal secretin test 37, ultrasonography and computed tomography pathological findings 10. Surgical operations were carried out in 25 patients and biopsy taken in 5. Thirty nine (86.6%) were males, 6 (13.3%) females, the mean age in each group was 47.4 and 39.8 years. Chronic alcoholism was certain in 41 (91.9) patients, in the remainder 4 no other etiologic factors were found. The main clinical data were: Weight loss 38 (84.4%) diabetes 34 (75.5%) pain 33 (73.3% in 7 as acute pancreatitis) Steatorrhea 23 (51.1%) jaundice 16 (35.5%- 11 by extrahepatic biliary tree obstruction, 5 by hepatic cirrhosis) pseudocysts 12 (26.6%). The more common associated diseases were: hepatic cirrhosis 6, fatty liver 2 (17.7%) gastroduodenal ulcer 6 (13.3%) cancer 4 (8.8%--gastric 1, pancreatic 3). In order to study the frequency of the clinical data the patients were grouped according to the presence or absence of calcifications and the etiologic factor Symptoms and signs were matched and statistic analysis (coefficient association phi) was made. Only a moderate association between acute pancreatitis in no calcified group and diabetes in calcified group were found. The chronologic study of certains clinical data shows that acute pancreatitis, jaundice, pseudo-cyst and surgical operations were significative more frequent in the first five years while diabetes has little more frequency in the second five year period. Twenty six surgical operations were carried out in 25 patients; 20 (76.9%) due to complications, 6 (23.1%) secondary to pain (pancreatic resection 3, pancreatoyeyunostomy 2, exploration 1). Twenty three patients were lost to follow-up, 12 died and 10 are still alive. This last group was followed at regular period, 8 remained asymptomatic and 2 have intermittent abdominal pain related to alcoholic ingestion.
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PMID:[Chronic calcified pancreatitis. Our experience]. 639 6

The precision of CA 19-9 RIA kit was evaluated by recovery, reproducibility and dilution test with very satisfactory results. The CA 19-9 value in sera from 52 healthy individuals and from 224 patients with gastric intestinal cancer and other benign disease, showed an increased positive rate in several cases of gastric intestinal cancer. For example, the positive rate in pancreatic cancer, bile duct cancer, colo-rectal cancer, gastric cancer, esophagus cancer, primary biliary cirrhosis diabetes mellitus, liver cirrhosis and chronic hepatitis was 60%, 75%, 55.6%, 45.6%, 20%, 28.6%, 22.7%, 13.7% and 1.7% respectively. By contrast, values from patients with acute hepatitis, fulminant hepatitis, fatty liver, gastric duodenal ulcer, pancreatitis, and primary liver cancer were within the normal range. In this study, CA 19-9 RIA were found to be significant as an adjunct in the management of patients with gastrointestinal cancer, especially pancreatic cancer, and bile duct cancer.
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PMID:[Serum determination of CA 19-9 in patients with digestive cancers and its diagnostic evaluation]. 658 10

Nonalcohol-induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to cirrhosis but none in the absence of preexisting fibrosis on the index biopsy specimen even when co-existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156. One hundred five patients were initially excluded as having an alcohol-induced cause, and the remaining 51 either were seen in the clinic (37) or had died, in which cases copies of their death certificates were obtained (14). A further 7 patients were excluded after clinic attendance gave evidence of alcohol excess and another 4 after review of their initial biopsy showed the presence of fibrosis or steatohepatitis. The apparent cause of the steatosis in the 40 included patients with strictly nonalcohol-induced pure fatty liver was obesity in 12, diabetes in 4 (1 obese patient), and cachexia associated with extrahepatic malignancy in 6. Four of the remaining 19 had serological evidence of an autoimmune disorder, but none of these had any clinical or histological features of autoimmune liver disease. Nine patients had evidence of hyperlipidemia, 3 of whom were also obese. At a median follow-up of 11 years (7 to 16), 12 of 26 living patients had abnormal results of liver blood tests and had repeat liver biopsies performed. None had progressed to steatohepatitis or cirrhosis; 1 obese patient had developed mild fibrosis 9.8 years after her index biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural history of nonalcoholic fatty liver: a follow-up study. 748 79

Rats fed a choline deficient diet develop foci of enzyme-altered hepatocytes with subsequent formation of hepatic tumors. This is the only nutritional deficiency that, in itself, causes cancer. We suggested that carcinogenesis is triggered, in part, because of abnormalities in cell signals which regulate cell proliferation and cell death. Because choline deficient rats develop fatty liver (choline is needed for hepatic secretion of certain lipoproteins), we examined whether an important lipid second messenger involved in proliferative signaling, 1,2-sn-diacylglycerol, accumulated in liver and resulted in the prolonged activation of protein kinase C. We observed that 1,2-sn-diacylglycerol accumulated in the plasma membrane from the non-tumor portion of livers of rats fed a choline deficient diet, and that unsaturated free fatty acids, another activator of protein kinase C, also accumulated in deficient livers. Protein kinase C in the hepatic plasma membrane and nucleus of choline deficient rats was elevated for months; this is the only model system which exhibits such prolonged activation of protein kinase C. Premalignant, abnormal hepatic foci were detected only in the deficient rats, and 15% of deficient rats (none of the controls) had hepatocellular carcinoma at 1 year on the diet. In rats, an early event in choline deficiency is an increase in the rate of cell death. In liver from choline deficient rats, we observed an increase in the numbers of liver cells with fragmented DNA (characteristic of programmed cell death; apoptosis). We used a cell culture model (immortalized rat hepatocytes) to study the effects of choline deficiency on apoptosis. Liver cells grown in a choline deficient medium became depleted of choline, accumulated triacylglycerol and 1,2-sn-diacylglycerol, and had increased DNA fragmentation and other morphologic and biochemical changes associated with apoptosis. This model has great potential as a tool for studying the underlying link between choline deficiency and the regulation of the balance between cell proliferation and cell death. We suggest that choline deficiency altered the cell proliferation signals mediated by protein kinase C within liver, and altered cell apoptosis. These changes in cell signaling may be the triggering events which result in hepatic carcinogenesis.
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PMID:Choline and hepatocarcinogenesis in the rat. 764 29

Thus, the pathologic consequences of feeding a CD diet are fatty liver, liver cell death, liver cell proliferation, and liver cell cancer. The fatty liver with CD is similar to that with other types of fatty liver in that the most attractive current hypothesis is based on some interference with the production and output of VLDL by the liver. The induction of cell death appears to be consistent with quite a different hypothesis, genesis and/or increase in liver free radicals leading to both acute necrosis and initiation of carcinogenesis. Especially noteworthy is the low incidence of liver cirrhosis, even after 2 years of exposure to the CD diet. The feeding of the CD diet reproducibly induces severe and persistent fatty liver coupled with extensive cell death, a combination that is frequently considered to be appropriate for the induction of "micronodular" (fatty) cirrhosis in humans. The findings with the LD diet, the high incidence of cirrhosis, with severe persistent fatty liver without significant cell death, together with the low incidence of cirrhosis with the CD diet, stand out as unpredictable and strange, according to current concepts of the pathogenesis of human cirrhosis. The CD model offers an unusual opportunity to explore in increasing detail the possible roles of free radicals in two important problems in pathology and medicine-acute cell injury and neoplasia. The challenges include mechanistic studies on how the free radicals are generated and how they relate to the biological consequences. The relatively slow sequential changes in the induction of cell injury and neoplasia makes the CD model one of the best for mechanistic studies relating to free radicals.
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PMID:Choline deficiency, lipotrope deficiency and the development of liver disease including liver cancer: a new perspective. 768 Jul 28

Liver fatty acid binding protein (L-FABP), a cytoplasmic 14 kDa protein previously termed Z protein, is conventionally considered to be an intracellular carrier of fatty acids in rat hepatocytes. The following evidence now indicates that L-FABP is also a specific mediator of mitogenesis of rat hepatocytes: a. the synergy between the action of L-FABP and unsaturated fatty acids, especially linoleic acid, in the promotion of cell proliferation; b. the specific requirement for L-FABP in induction of mitogenesis by two classes of nongenotoxic hepatocarcinogenic peroxisome proliferators (amphipathic carboxylates and tetrazole-substituted acetophenones); c. the direct correlation between the binding avidities of different prostaglandins for L-FABP and their relative growth inhibitory activities toward cultured rat hepatocytes; d. the temporal coincidences between the covalent binding to L-FABP by chemically reactive metabolites of the genotoxic carcinogens, 2-acetylaminofluorene and aminoazo dyes, and their growth inhibitions of hepatocytes during liver carcinogenesis in rats; e. and f. the marked elevations of L-FABP in rat liver during mitosis in normal and regenerating hepatocytes, and during the entire cell cycle in the hyperplastic and malignant hepatocytes that are produced by the genotoxic carcinogens, 2-acetylaminofluorene and aminoazo dyes. These actions of L-FABP are consistent with those of a protein involved in regulation of hepatocyte multiplication. Discovery that L-FABP, the target protein of the two types of genotoxic carcinogens, is required for the mitogenesis induced by two classes of nongenotoxic carcinogens points to a common process by which both groups of carcinogens promote hepatocyte multiplication. The implication is that during tumor promotion of liver carcinogenesis, these genotoxic and nongenotoxic carcinogens modify the normal process by which L-FABP, functioning as a specific receptor of unsaturated fatty acids or their metabolites, promotes the multiplication of hepatocytes.
Cancer Metastasis Rev 1994 Dec
PMID:Modulation of mitogenesis by liver fatty acid binding protein. 771 94


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