Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perforation of the gallbladder is a life-threatening complication of acute cholecystitis that is often difficult to diagnose at an early stage. Standard radiographic and laboratory tests have not been reliable in identifying patients with this complication. In contrast, biliary sonography correctly diagnosed pericholecystic abscesses preoperatively in three patients with acute cholecystitis. The ultrasonic appearance of acute cholecystitis with a pericholecystic abscess was similar in all three patients. There was an extraluminal fluid collection located contiguous to a thick-walled gallbladder in the fundic region. The fluid collection was constant in location and could be seen in at least two different views. Two of these three patients had acalculous cholecystitis; the initial clinical diagnosis in one was pancreatitis, and in the other alcoholic hepatitis. Biliary sonography, by demonstrating a thickened gallbladder wall in the absence of ascites, strongly suggested that these two patients had acute acalculous cholecystitis, and not hepatitis or pancreatitis. The ultrasonic examination was a critical factor in the decision for prompt surgery instead of continued nonoperative management in these patients. These data suggest that not only can biliary sonography aid in the diagnosis of acute cholecystitis, calculous as well as acalculous, but can also visualize a pericholecystic abscess when it is present.
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PMID:Ultrasonic detection of acute cholecystitis with pericholecystic abscesses. 701 38

Four cases of fulminant hepatic disease caused by lymphoreticular infiltration are described. All 4 patients died within a few weeks and clinical diagnoses included viral hepatitis, alcoholic hepatitis, and drug hepatitis. A diagnosis of malignancy was made prior to autopsy in only 1 of the 4 patients. Autopsies revealed typical malignant histiocytosis in 3 patients and the fourth had a primitive lymphoreticular malignancy with malignant histiocytosis the favored diagnosis. The extent of the liver infiltrate as judged histologically was mild compared with the severe clinical illness. Randomly scattered foci of necrosis associated with the malignant infiltrate were seen in the 2 patients who had marked elevations of serum glutamic oxaloacetic transaminase.
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PMID:Lymphoreticular malignancy presenting as fulminant hepatic disease. 705 34

Among 112 patients with alcoholic liver injury, 45 had alcoholic fibrosis. The incidence of alcoholic fibrosis was 40.2% which was the highest among various types of alcoholic liver injury (fatty liver; 3.6%, alcoholic hepatitis; 2.7% and liver cirrhosis; 31.3%). Clinical features of alcoholic fibrosis were milder than those of liver cirrhosis and more severe than those of fatty liver. The mean laboratory values in alcoholic fibrosis were significantly different from those in fatty liver and liver cirrhosis. The laboratory data were well correlated with the presence of pericellular fibrosis and thickening of the terminal hepatic venule, but only partially with hepatic cell necrosis and not with fatty metamorphosis. Two patients with alcoholic fibrosis who developed cirrhosis without any clinical and histological features of hepatitis were observed during 5-yr follow-up. These results indicate that alcoholic fibrosis is the most common type of alcoholic liver injury in Japan and is an independent clinicopathological entity distinct from the classical types of alcoholic liver injury. Pericellular fibrosis and thickening of the terminal hepatic venule which are the main histological features of alcoholic fibrosis may play an important role in its transition to liver cirrhosis.
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PMID:Clinicopathological study of alcoholic fibrosis. 711 30

Acetaldehyde in non-toxic doses (15.6 micrograms per start) causes in the inhibition test of the migration of leucocytes an inhibition of the migration in 6/13 of the patients with alcoholic hepatitis, a stimulation of the migration in 6/11 of alcohol cirrhoses. Healthy (n = 16) persons, patients with alcoholic fatty degeneration of the liver (n = 3) as well as non-alcoholic liver diseases (chronic persisting hepatitis, n = 11; chronic active hepatitis, n = 8, cirrhosis, n = 7) did not show this cellular immune reagibility. The inhibition of the migration and the stimulation of the migration, respectively, might develop by hapten autoantigen complexes (altered cytoskeleton?) with release of the factors of inhibition of migration and stimulation of migration, in which case the role of a hapten belongs to acetaldehyde. The results of the tests did not correlate with functional and histological findings of the liver, with the actual consumption of alcohol and also not with haptoglobin phaenotypes. When it is postulated that by acetaldehyde also the release of further lymphokines is mediated, origin and progression of alcoholic hepatitis and alcoholic cirrhosis might be explained immunopathogenetically.
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PMID:[Acetaldehyde-induced leukocyte migration inhibition in alcoholic liver diseases]. 712 38

Serum levels of alpha-tocopherol (vitamin E) were determined in various types of liver diseases, and as a results, it was revealed that serum alpha-tocopherol was significantly depressed in acute hepatitis (p less than 0.01, n = 22), alcoholic hepatitis (p less than 0.001, n = 9) and fulminant hepatitis (p less than 0.001, n = 6). There was a significant correlation between serum levels of alpha-tocopherol and beta-lipoprotein (r = 0.92, p less than 0.001, n = 17). Though there was no correlation between serum levels of alpha-tocopherol and triglyceride, there was a significant correlation between alpha-tocopherol and cholesterol (r = 0.57, p less than 0.01, n = 21), and phospholipid (r = 0.49, p less than 0.05, n = 18). There was no correlation between serum levels of alpha-tocopherol and other liver function tests. These facts suggested that the diminished serum vitamin E in patients with liver diseases is ascribable to the depression in blood level of beta-lipoprotein that results from liver disorders, because the liver is the major supply source of beta-lipoprotein.
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PMID:alpha-Tocopherol level in liver diseases. 715 92

Nonalcoholic steatohepatitis is a poorly understood and hitherto unnamed liver disease that histologically mimics alcoholic hepatitis and that also may progress to cirrhosis. Described here are findings in 20 patients with nonalcoholic steatohepatitis of unknown cause. The biopsy specimens were characterized by the presence of striking fatty changes with evidence of lobular hepatitis, focal necroses with mixed inflammatory infiltrates, and, in most instances, Mallory bodies; Evidence of fibrosis was found in most specimens, and cirrhosis was diagnosed in biopsy tissue from three patients. The disease was more common in women. Most patients were moderately obese, and many had obesity-associated diseases, such as diabetes mellitus and cholelithiasis. Presence of hepatomegaly and mild abnormalities of liver function were common clinical findings. Currently, we know of no effective therapy.
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PMID:Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. 2901 67

Ninety-two British, caucasian, alcoholic patients with liver disese were grouped on the basis of hepatic histology into fatty change, hepatitis with or without cirrhosis, and cirrhosis alone. Men with alcoholic hepatitis with or without cirrhosis showed an increased incidence of the histocompatibility antigen HLA-B8 (P less than 0.02). Increased measles antibody titres were found in patients without cirrhosis with or without hepatitis and were associated with the B8 phenotype in both sexes. Rubella antibody titres and percentage DNA-binding were raised in patients with cirrhosis and showed no association with the B8 phenotype. Concentrations of IgM and IgA were were raised in patients with stetosis and with hepatitis, while in patients with cirrhosis IgG concentrations were also increased. Low titres of autoantibodies were found in all histological groups. It is possible that the development of hepatitis in response to alcohol abuse may be influenced, at least in men, by a gene linked to the B locus. Otherwise, immune processes associated with alcohol-related liver disease are probably secondary phenomena.
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PMID:HLA-B8, immunoglobulins, and antibody responses in alcohol-related liver disease. 740 Mar 47

Caffeine elimination was studied in 419 patients with cirrhotic and noncirrhotic liver disease of different etiology (hepatitis B virus infection n = 79; hepatitis NANB virus infection n = 74; ethanol-induced liver damage n = 143; primary biliary cirrhosis I-IV n = 63; cryptogenic liver cirrhosis n = 60) following oral administration of 366 mg caffeine. Caffeine clearance in the control group was 69 +/- 33 ml/min (age-matched healthy volunteers and patients without liver disease). Caffeine clearance in acute hepatitis B (70 +/- 60 ml/min) chronic persistent hepatitis B (81 +/- 56 ml/min), chronic aggressive hepatitis B (107 +/- 66 ml/min), posthepatitic liver cirrhosis B (84 +/- 62 ml/min), acute hepatitis NANB (94 +/- 69 ml/min), chronic persistent hepatitis NANB (122 +/- 60 ml/min), chronic aggressive hepatitis NANB (87 +/- 52 ml/min) and posthepatitic cirrhosis NANB (59 +/- 26 ml/min) is not reduced in comparison with controls. In patients with alcoholic fatty liver (127 +/- 71 ml/min, p < 0.05) caffeine clearance is enhanced, in alcoholic hepatitis (57 +/- 72 ml/min) comparable to controls and in alcoholic cirrhosis reduced (36 +/- 44 ml/min, p < 0.05). In primary biliary cirrhosis I-IV caffeine clearance is higher than in controls (117 +/- 59 ml/min, p < 0.05). In cirrhotic liver disease of different origin caffeine clearance is inversely related to the serum bilirubin level. However, the absolute value is determined in addition by the underlying disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine elimination in cirrhotic and non-cirrhotic liver disease of different etiology. 748 16

In three alcoholic patients, two men aged 30 and 42, and a woman aged 52, hepatitis was diagnosed after the use of disulfiram. In all cases, there was a close temporal relationship between the occurrence of symptoms and disulfiram intake. Other possible causes were excluded. The 30-year-old man died from liver damage. Biopsy showed massive hepatic necrosis without signs of alcoholic hepatitis. In the other patients, symptoms subsided quickly and liver function returned to normal after discontinuation of disulfiram, but there was no confirmation by biopsy. The possibility of drug-induced hepatitis should always be considered in an alcoholic patient treated with disulfiram.
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PMID:[Liver damage attributed to the use of disulfiram]. 750 Oct 79

The pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remains unclear. It has been proposed that a direct viropathic effect, the host immune response, or both mediate cell damage. To address this issue, the immunophenotype of the inflammatory infiltrate in the liver of 18 patients with abnormal liver function tests and serologically detectable hepatitis C virus antibodies was compared with seven control patients (three cases with hepatitis B virus infection, two with alcoholic hepatitis, and one patient each with primary biliary cirrhosis and autoimmune hepatitis). The immunohistochemical markers included UCHL1, L26, Ham-56, Mac-387, CD68, Leu-M1, and cathepsin B. We found that T cells represent the predominant cell type in both histopathologic patterns of hepatitis C, ie, chronic active hepatitis and chronic persistent hepatitis, but the intensity of the T-cell infiltrate displayed marked differences. B-cell infiltrates were only seen in the germinal centers of lymphoid follicles in portal tracts. Furthermore, significant numbers of CD68-positive macrophages/monocytes were seen in the more aggressive form of hepatitis C viral infection. These data suggest that the T-lymphocyte-mediated host immune response is similar in chronic active and chronic persistent hepatitis patterns of hepatitis C viral infection, but varies in its intensity. In addition, macrophages/monocytes may play a role in hepatocyte and bile duct injury in chronic hepatitis C.
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PMID:Chronic hepatitis C. Analysis of host immune response by immunohistochemistry. 753 56


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