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Query: UMLS:C0011849 (diabetes)
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The prevalence of HBsAg and anti HBs was studied in 1062 inpatients in the city of Rio de Janeiro. HBsAg positivity rates were as follows: a) acute viral hepatitis: 37.8% b) chronic hepatitis 46.67% c) chronic liver disease without hepatitis: 7.69% d) diabetes 3.08% e) lepromatous leprosy 2.35% f) others 2.01%. The carrier state is emphasized. Anti HBs was less frequent in patients with acute viral hepatitis than in patients with other diseases (hepatic or not). The highest levels were: a) lepromatous leprosy: 57.65% b) drug addicts: 46.15% e) diabetes: 43.3%. The high anti HBs positivity is discussed.
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PMID:Infection by the hepatitis B virus in patients of a general hospital. 54 81

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

When the serum insulin valves during a 50-gm oral glucose tolerance test were expressed as the function of glucose concentrations, a good linear relationship was found in normal subjects and in patients with diabetes, hyperthroidism, hypothroidism or chronic hepatitis. The insulin index calculated from the line representing this relationship was less than 100 in all 19 diabetic patients and most of the 13 hyperthyroid patients with oxyhyperglycemia, whereas it was more than 100 in the 14 normal subjects, the 4 hypothyroid patients, and the 8 patients with oxyhyperglycemia due to chronic hepatitis. The insulin index decreased with increasing maximal blood glucose concentration during the glucose tolerance test in diabetic patients. Furthermore, improvement in the insulin index was correlated with the effectiveness of sulfornylurea drugs in the diabetic group.
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PMID:A device for expressing the serum insulin glucose relationship in diabetes, hyper- or hypothyroidsm, and chronic hepatitis. 84 55

Peculiarities of clinical picture of diabetes mellitus in its combination with chronic hepatitis and cirrhosis of the liver were studied in 60 patients. Diabetes mellitus developed mostly against the background of chronic affection of the liver, preceding it. Glucose tolerance disturbances according to the type of latent and manifest diabetes were revealed in 28% of 132 patients with chronic hepatitis and cirrhosis of the liver. Histological study of the pancreas in 63 patients who died of cirrhosis of the liver demonstrated marked fibrosis of hepatic parenchyma without any noticeable changes in the pancreatic islets. The blood insulin and growth hormone levels were significantly greater in 132 patients examined than in healthy persons. The mentioned changes in the glycemia level, of the insulin and growth hormone level after glucose administration were more pronounced in cirrhosis of the liver than in chronic hepatitis, and in late stages of portal cirrhosis than at its early stages. The leading role played by insulin sensitivity reduction of the peripheral tissues in the pathogenesis of carbohydrate metabolism in cases with chronic diseases of the liver is supposed.
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PMID:[Clinical picture and pathogenesis of diabetes mellitus in chronic hepatitis and cirrhosis of the liver]. 90 62

The urinary excretions of L-xylulose, xylitol and D-glucarate after the oral administration of glucuronolactone (5 g) were measured in normal healthy persons, patients with diabetes mellitus, acute hepatitis in recovery stage, chronic hepatitis and liver cirrhosis. In normal subjects, the mean value of L-xylulose excretion was 14.6 +/- 1.4 mumol/2 h with a range from 6.5 to 21.8. Marked increase of L-xylulose excretion was observed in cirrhotic patients, the mean value was 97.1 +/- 19.8 with a range from 22.0 to 236.6. Though some cases of acute and chronic hepatitis showed higher values than the normal range, no case exceeded 50 mumol/2 h. The urinary excretion of xylitol in cirrhotic patients was also higher than normal no increase was observed in D-glucarate excretion. The values of L-xylulose excretion in cirrhosis were correlated with the values of serum total bilirubin, albumin, albumin/globulin ratio, lactate dehydrogenase and prothrombin time. These findings indicate that the measurement of L-xylulose in urine after the oral glucuronolactone loading provides a useful tool for evaluation of the severity of liver cirrhosis.
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PMID:Increased urinary excretion of L-xylulose in patients with liver cirrhosis. 124 50

Septic arthritis of the hip caused by Campylobacter fetus subsp. fetusis very rare. The authoris isolated C. fetus subsp. fetus from a specimen of the left hip. The patient was a 53-year old man with a history of heavy drinking, diabetes, and chronic hepatitis, and had been suffering from avascular necrosis of both femoral heads. It was considered that the organism invaded already damaged tissue of the joint. The patient was treated with intravenous antibiotics and later received successful total hip replacement.
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PMID:Pyogenic arthritis of the hip due to Campylobacter fetus--a case report. 150 34

The responses of serum IRI, serum IRG, and blood sugar levels to 75 g oral glucose and serum IRI to glucagon injection were investigated in 26 chronic hepatitis, 20 liver cirrhosis, 5 primary sclerosing cholangitis (PSC) and 8 healthy volunteers served as controls. The results obtained herein were as follow: 1) The frequency of the glucose intolerance in PSC was higher than the other liver diseases. The mean values of the insulinogenic index (delta IRI/delta BS 30 min) in PSC was lower than control subjects. No suppression of IRG by glucose was observed in PSC. 2) The maximum IRI value (max delta IRI) in PSC during glucagon test was lower than that in control subjects. 3) In one case of 5 PSC ICSA was founded to be positive. These data suggest that we should pay much attention to suffering from diabetes mellitus in natural history of PSC.
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PMID:[Studies on the glucose tolerance and the endocrine function of the pancreas in primary sclerosing cholangitis]. 151 43

The case of a 68-year-old man with chronic hepatitis C who developed worsening of liver disease with jaundice when he was treated with alpha interferon is described. His disease activity appeared to improve when interferon was stopped but flared again with reinstitution of treatment. Subsequent treatment with prednisone resulted in partial resolution of disease. The patient had antibody to hepatitis C virus and hepatitis C virus RNA detectable in serum; titers of these viral markers did not change with treatment. In addition, he had insulin-dependent diabetes and antinuclear antibodies, suggesting that he had a pre-existing autoimmune diathesis that may have predisposed him to developing an autoimmune hepatitis with interferon therapy.
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PMID:Acute exacerbation of liver disease during interferon alfa therapy for chronic hepatitis C. 155 49

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

Insulinemia, concentration of C-peptide and glucagon in the blood was studied in chronic hepatitis patients showing moderate tolerance disorders to glucose and diabetes mellitus developed against the background of chronic pancreatitis. Both groups showed hyperglucagonemia. Basal hypoinsulinemia and reduction of the C-peptide level revealed only in patients suffering of chronic pancreatitis with secondary diabetes mellitus. Reduced reaction of beta-cells of the pancreas to physiologic stimulation by pancreosozymin were observed also in less significant disorders of tolerance to glucose. The authors discuss the significance of changes in the sequential development of different degrees of disorders of the carbohydrate metabolism in patients with chronic recurrent pancreatitis.
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PMID:[The indices of pancreatic incretory activity in patients with chronic pancreatitis and disordered carbohydrate metabolism]. 209 92


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