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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver biopsies from 60 patients with acute alcoholic hepatitis (AAH) developing against the background of steatosis, chronic hepatitis and cirrhosis were studied histologically, histochemically and electron microscopically. AAH is characterized by necrosis of hepatocytes with deposition of alcoholic hyalin, obesity of the organ, and polymorphonuclear leukocyte infiltration. Hyperplasia of the smooth endoplasmic reticulum, the appearance of megamitochondria, and an increased amount of peroxisomes reflect the participation of MEOS and the catalase system in alcohol metabolism with a progressive decrease in the activity of alcoholdehydrogenase. Acute alcoholic hepatitis is a connecting link between steatosis and cirrhosis of the liver in which the accompanying autoimmune mechanism and microcirculation disorder followed by activation of lipofibroblasts are conducive to the progression of the pathologic process.
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PMID:[Morphological characteristics of acute alcoholic hepatitis]. 7 56

The pathology of the liver in 19 cases of malabsorption is reported. Five of these were proven to have adult coeliac disease, in the others that diagnosis was presumed by exclusion of other causes of malabsorption and by the coincidence of other conditions known to be associated with coeliac disease. Of these cases, three had liver changes of chronic hepatitis and two of these were in the proven coeliac group, including a case with cirrhosis and a hepatoma. In addition, less severe liver changes such as portal tract fibrosis and portal tract infiltration by inflammatory cells were present greatly in excess to that of the controls. The reasons for the occurrence of liver damage in coeliac disease are outlined and discussed in relation to the liver disorders associated with jejunoileal bypass used in the treatment of obesity. Possible mechanisms of liver injury in coeliac disease are described.
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PMID:The liver in coeliac disease. 21 Jan 3

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
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PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

This study evaluates the correlation between long-term weight history and health risks. One thousand three hundred and sixteen male subjects of normal weight (-5%(-)+5% by Broca's obesity index) at age twenty, were studied. The average age of the subjects was 43.7 +/- 6.5 (M. +/- S.D.) years old. According to their long-term weight history, the subjects were classified into four groups: weight lost (N = 35), weight stable (N = 502), mild weight gain (N = 187), severe weight gain (N = 592). Odds ratios for systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, uric acid, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, hyperperspiration, angina pectoris, and hypertension were significantly higher in the severe weight gain group than in the stable weight group. Stepwise logistic regression analysis was performed by choosing weight history, obesity index, age, and smoking and drinking habits as the independent variables. Weight history was shown to be a significant variable in systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, chronic hepatitis and liver cirrhosis. Odds ratios for factors suspected of promoting atherosclerosis were significantly higher in the severe weight gain group. Results of this study indicate that a weight gain of over 7 kilograms appears to be the critical level that is associated with health risks.
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PMID:[Health risk assessment of long-term weight history]. 213 52

A health survey of adults aged 30 years or more was carried out in southwest Taiwan to determine the prevalence of gallstones and to study risk factors associated with gallstones. Blood samples were collected and abdominal sonographic examination and anthropometric measurements were performed on a total of 923 people. The 40 gallstone cases detected resulted in a prevalence of 4.3%. The risk factors explored included age, sex, hepatitis, obesity, hyperlipidemia, and diabetes mellitus (DM). Age and DM were the only significant factors associated with gallstones in our study. With a reference group of 30-39-year-olds as a comparison, multiple logistic regression analysis showed a trend effect with odds ratios of 1.73, 3.74, and 6.32 for age groups of 40-49, 50-59, and 60 or above, respectively. The odds ratio for DM was as high as 2.59. However, sex, body weight index, chronic hepatitis B, and hyperlipidemia were not significantly associated with gallstones.
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PMID:Risk factors for gallstones among Chinese in Taiwan. A community sonographic survey. 222 97

Portal blood flow was measured by means of direct bolus imaging (DBI), a method of measuring flow velocity with magnetic resonance imaging. DBI allows immediate visualization of fluid movement, thereby enabling calculation of a flow velocity from fluid displacement. In a study of 14 healthy male volunteers, portal blood flow was measured with electrocardiographic gating during the 18 seconds subjects could suspend respiration. These measurements showed a close correlation (r = .968) with those obtained by means of Doppler ultrasound (US). Increases in portal blood flow after oral administration of ethanol and glucose were measured with DBI. Glucose caused a statistically greater increase in portal blood flow volume in healthy control subjects than in patients with chronic hepatitis. Blood sugar, on the other hand, showed a significantly greater increase in these patients, possibly reflecting the greater vascular resistance of the liver. DBI is a useful noninvasive method of measuring portal blood flow without the limitations imposed on Doppler US by obesity and intestinal gas.
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PMID:Portal blood flow: measurement with MR imaging. 268 71

Serum beta 2-microglobulin was determined in 53 patients with chronic liver diseases. No elevation was shown in fatty liver due to obesity or alcoholism. Serum beta 2-microglobulin was abnormal only in 4% of the patients with chronic hepatitis. Determination of serum beta 2-microglobulin seems not useful for the differential diagnosis between chronic hepatitis and fatty liver due to obesity or alcoholism. Serum beta 2-microglobulin was elevated in 29% of the patients with alcoholic liver cirrhosis, in 41% of those with non-alcoholic liver cirrhosis, and in 75% of those with primary liver carcinoma. The average serum beta 2-microglobulin concentration was significantly higher in non-alcoholic liver cirrhosis than in alcoholic liver cirrhosis. There was a significant correlation between serum beta 2-microglobulin and gamma-globulin concentrations in liver cirrhosis.
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PMID:Serum beta 2-microglobulin in chronic liver diseases. 617 12

Pretreatment variables that could predict the response of chronic hepatitis C to interferon alfa treatment have not been fully assessed. Eighteen baseline variables were evaluated in a series of 100 consecutive patients treated with a 12 month course of interferon alfa. For the purposes of this study, response was defined as the return to normal of aminotransferase activities before the third month of treatment. Seventy per cent of the patients responded to treatment. Six variables were associated with an increased likelihood of response assessed by univariate analysis. With stepwise multiple regression analysis assessment, however, only three variables remained independently predictive of response: low gamma glutamyltransferase (gamma GT) activities (p < 0.001), absence of obesity (p = 0.005), and absence of cirrhosis (p = 0.01). The response rate in patients with gamma GT activities < 0.66 mu kat/l (n = 55) was 78% and 60% in patients with values > 0.66 mu kat/l (n = 45) (p = 0.048). Response was attained in 75% of non-obese patients (n = 80), compared with only 50% of obese patients (n = 20) (p = 0.03). Finally, 80% of patients without cirrhosis (n = 76) responded, while among those with cirrhosis (n = 24) the response rate was only 37% (p < 0.001). All 23 patients without cirrhosis, <40 years old, and with gamma GT activities <0.66 mu kat/l responded to treatment, while only 28.5% of 14 patients with cirrhosis, >40 years old, and with gamma GT activities >0.66 mu kat/l responded to interferon alfa (p<0.001). Those findings may be useful when evaluating interferon alfa trials and it is suggested that this treatment should be applied early in the course of chronic hepatitis C.
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PMID:Prediction of the response of chronic hepatitis C to interferon alfa: a statistical analysis of pretreatment variables. 790 52

To evaluate if any pretreatment characteristics of patients with chronic hepatitis C (HCV) can be used to predict response to the current recommended dose (3 million units three times a week) and higher doses of interferon-alpha (IFN), we retrospectively assessed the response of 37 patients with HCV who were treated with IFN. Sixteen patients (43%) responded to the standard dose of IFN with normalization of ALT. Weight and liver histology were found to be significant factors for response. The responders weighed significantly less than nonresponders (161.8 +/- 35.5 lb versus 200.3 +/- 45.4 lb, P = 0.008). Seventy-five percent of patients with chronic lobular or persistent hepatitis were responders, whereas only 28% of patients with more advanced hepatitis responded (P = 0.01). There was no correlation between the degree of bile duct damage or steatosis and response rate. This study suggests that obesity and severe histologic injury are negative predictive factors of response to the current recommended dose of IFN. The adequacy of the current recommended dose of IFN in overweight patients needs to be investigated.
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PMID:Clinical and histologic predictors of response to interferon-alpha in patients with chronic hepatitis C viral infection. 799 93

Elevated aminotransferases activities are frequent in medical practice. In acute elevations, the mains causes are generally easily found (viral, drug-induced, toxic, ischemic). In moderate or prolonged elevations, the most frequent causes are steatosis (alcoholic, diabetes, obesity) and chronic hepatitis (viral B, D, C, drug-induced and auto-immune diseases.
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PMID:[Increase of aminotransferases]. 819 Nov 1


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