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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A community health survey of 923 residents aged 30 years or more was performed in Putai Township of Taiwan. To elucidate the relationships between hepatitis C virus (HCV) and surrogate tests for non-A, non-B hepatitis in hyperendemic areas of hepatitis B virus (HBV) serum levels of alanine aminotransferase (ALT), triglycerides, cholesterol, hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) were examined. Glucose tolerance tests and the history of diabetes treatment were used to define the diabetes status. Fatty liver was diagnosed by sonography. The prevalence of anti-HCV was 2.6% (95% confidence interval, 1.6-3.6%). Elevated ALT and fatty liver were significantly associated with anti-HCV in univariate analysis. Anti-HCV was not an associated factor for fatty liver after adjusting for serum triglycerides and cholesterol, sex, body mass index and diabetes status through multiple logistic regression. However elevated ALT was still associated with anti-HCV after adjusting for serum triglycerides, sex, body mass index, HBsAg and age through multiple linear regression. The anti-HCV prevalence was similar between HBsAg-positive and negative subjects. Aggregation of HCV infection was found among spouses. It was concluded that elevated ALT and intimate contact with HCV carriers might be associated factors for HCV infection, and that HBV infection and fatty liver were not related to HCV infection in Taiwan.
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PMID:Relationship between fatty liver, alanine aminotransferase, HBsAg and hepatitis C virus. 138 55

A 57-year-old man had suffered from poorly controlled diabetes mellitus and liver cirrhosis due to alcohol and hepatitis C for about 10 years. He developed fever and swelling of the right cheek and neck due to periodontal infection. The symptoms worsened in spite of antibiotic therapy and were accompanied by dyspnea. He was therefore referred to our hospital. Chest radiographs and computed tomographs revealed widening of the superior mediastinum, pulmonary infiltrates and right pleural effusion. He was diagnosed as having mediastinitis, right pyothorax and pneumonia caused by periodontal infection. Tracheotomy and mechanical ventilation were performed. Antibiotic therapy resulted in improvement of the mediastinitis and pyothorax. However, renal and liver dysfunction developed and the patient died of multiorgan failure after 35 days of hospitalization. Death due to periodontal infection is rare. We give a review of the literature.
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PMID:[A fatal case of acute mediastinitis caused by periodontal infection]. 146 87

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

We report here two cases of mixed cryoglobulinemia showing renal involvement associated with hepatitis C virus (HCV) infection. The subjects were 62- and 63-year-old males. Both patients presented with purpura on the legs, which was diagnosed as allergic vasculitis by skin biopsy. Case 1 followed a clinical course of progressive nephrotic syndrome with mild hematuria. He also had diabetes mellitus and hypertension. In contrast, case 2 showed only mild hematuria without proteinuria at the time of the renal biopsy. Both cases had immunological disarrangements, such as severe hypocomplimentemia and seropositive rheumatic factor. Recently, it was reported that patients with type II mixed cryoglobulinemia had HCV seropositivity, and revealed membranoproliferative glomerulonephritis. These facts strongly suggested that renal lesions are the result of direct damage mediated by cryoglobulinemia and an activated complement pathway through an immune complex mechanism related to HCV.
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PMID:[Glomerular lesion in patients with type II mixed cryoglobulinemia having antibodies to hepatitis C virus]. 747 12

This study was carried out to determine the prevalence of hepatitis C virus (HCV) antibodies and the epidemiologic factors associated with HCV infection in patients with chronic renal failure before the onset of ESRD. Sex, age, type of renal disease, level of renal function, and history of blood transfusions and invasive procedures were analyzed in 226 patients with renal disease, compared with a population of 1,244 normal subjects and 124 patients with impaired immunity (patients having autoimmune diseases and receiving chemotherapy treatment). Eighteen seropositive patients with renal disease (prevalence, 7.9%) were found, which was significantly higher than the prevalence in the normal population (1.03% in blood donors, 0.98% in pregnant women; P < 0.001, chi 2). There was no significant association of sex, number of blood transfusions, or history of invasive procedures with the presence of HCV antibodies. The prevalence of HCV antibodies was higher (16.6%) in patients with glomerulonephritis compared with patients diagnosed with interstitial nephritis, pyelonephritis, nephrosclerosis, diabetes mellitus, polycystic kidney, and miscellaneous renal diseases (P < 0.01, chi 2). There was a higher prevalence of HCV antibodies in patients with creatinine clearance lower than 30 mL/min (13%) compared with patients with creatinine clearance higher than 30 mL/min (2.7%) (P < 0.01, chi 2). These data suggest that HCV infection may be associated with the pathogenesis of glomerulonephritis. Alternatively, glomerulonephritis or severe renal insufficiency may increase the likelihood of HCV infection.
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PMID:Epidemiology of hepatitis C virus infection in patients with renal disease. 752 63

Hepatitis C virus antibodies were studied in sera coming from 39 patients with porphyria (cutanea tarda in 17, variegate in 8, intermittent acute in 4, coproporphyria in 2 and protoporphyria in 8). Nine of 17 patients with porphyria cutanea tarda had positive antibodies, but none of the patients with other types of porphyria. All subjects with porphyria cutanea tarda had histological or laboratory liver abnormalities. There was no relationship between the presence of antibodies and frequency of alcoholism, diabetes, or carbohydrate intolerance. Family background of porphyria was significantly less frequent among patients with positive hepatitis C virus antibodies. In 13 patients, a liver biopsy was performed, always showing signs of chronic hepatitis, whose magnitude was higher in those with positive antibodies. It is concluded that, as reported previously, hepatitis C virus may be an activating factor for porphyria cutanea tarda or may potentiate its accompanying liver disease.
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PMID:[Hepatitis C virus infection in patients with porphyria]. 752 36

Moderate elevations of serum transaminases are frequently found in patients with diabetes mellitus and are often attributed to fatty infiltration of the liver without further investigation. Recent studies of patients with end-stage liver disease have suggested a possible association between Hepatitis C virus (HCV) antibody positivity and the development of diabetes (mostly Type 2). As a first step in the examination of any potential association between HCV and Type 2 diabetes in subjects without overt liver disease, we examined 200 British patients with Type 2 diabetes (100 White Caucasians, 50 Asians, and 50 Afro-Caribbeans), recruited from the United Kingdom Prospective Study of Diabetes, half of whom had a significant elevation of alanine aminotransferase (ALT) on at least two occasions and half of whom had consistently normal ALT levels. In Afro-Caribbean Type 2 diabetic subjects 7/25 (28%) patients with abnormal ALT and 1/25 (4%) with normal ALT were HCV antibody positive. Among White Caucasian subjects 6/50 (12%) patients with abnormal LFTs and 0/50 with normal LFTs were HCV antibody positive and in Asians the prevalence was 2/25 (8%) and 0/25, respectively. This study suggests that persistent mild to moderate elevation of serum transaminases in a patient with Type 2 diabetes should not automatically be attributed to the metabolic disturbances of diabetes. Particularly in Afro-Caribbean subjects, HCV infection is a major diagnostic consideration. The question of whether HCV infection itself may have a diabetogenic action is worthy of further investigation.
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PMID:High prevalence of hepatitis C infection in Afro-Caribbean patients with type 2 diabetes and abnormal liver function tests. 753 25

We report a case of nephrotic syndrome which mimicked membranoproliferative glomerulonephritis (MPGN) and was associated with hemophagocytic syndrome after renal death. A 41-year-old Japanese man was referred to our hospital because of nephrotic syndrome in February 1979. He had no signs, symptoms nor laboratory data suggestive of liver damage. He was diagnosed as idiopathic MPGN and administered prednisolone and cyclophosphamide (total dose of about 50,000mg). He developed end-stage renal disease, and dialysis therapy was initiated in February 1992. Simultaneously, he was diagnosed as hepatitis C virus (HCV)-positive liver cirrhosis. In August 1994, he died because of reactive homophagocytic syndrome, which occurred in the setting of immunosuppression due to chronic renal failure, liver cirrhosis, and sesecondary diabetes. In this case, we can not deny the possibility that radical therapeutic intervention against "idiopathic MPGN" had a negative effect on the clinical course of chronic HCV infection.
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PMID:[A case of nephrotic syndrome mimicking membranoproliferative glomerulonephritis (MPGN) and associated with reactive hemophagocytic syndrome after renal death]. 760 13

Abnormalities of carbohydrate metabolism, including hyperinsulinaemia and insulin resistance, are well recognised complications of cirrhosis. While diabetes mellitus can be explained in many instances on the basis of coincident pancreatic disease, in most the characteristic glucose intolerance of cirrhosis is not readily explicable. A previous clinical observation that hepatitis C virus infection and diabetes mellitus appeared to be associated was formally tested by a retrospective review of 100 consecutive adult patients with cirrhosis undergoing assessment for liver transplantation. Hepatitis C virus was diagnosed by conventional serological and histological criteria. Twenty-three patients had diabetes mellitus, of whom 18 were being treated with insulin. Of the 34 patients with hepatitis C virus-related cirrhosis, 17 (50%) had diabetes mellitus, in contrast to just six (9%) of the 66 patients with cirrhosis unrelated to hepatitis C virus (chi2 = 19.1, p < 0.0001) with an odds ratio for hepatitis C virus by diabetes mellitus status 10.0 (95% confidence interval 3.4 to 29.3). Hierarchical loglinear model analysis of those factors of potential relevance to the development of diabetes mellitus revealed that only hepatitis C virus interacted significantly with diabetes mellitus while the relation between diabetes mellitus and origin, sex, body mass index and severity of cirrhosis was conditional. By multiple logistic regression analysis of diabetes mellitus status in relation to the same variables, only hepatitis C virus status was statistically significant (p < 0.0001). Origin, sex, severity of cirrhosis, body mass index and therapy were not significantly associated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for a link between hepatitis C virus infection and diabetes mellitus in a cirrhotic population. 877 23


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