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)

Nine hundred and ninety nine patients were admitted in our Department (the Third Department of Internal Medicine, School of Medicine, UOEH) during the five years more since the opening date of the University Hospital (July, 9, 1979), and 864 cases in them (86.2%) suffered from the various digestive diseases. Most of the in-patients with digestive diseases in our Department are resident in Kitakyushu city and its suburbs, especially in Yahatanishi-ku, Wakamatsu-ku and Onga county, therefore, it may be possible to investigate the ecological characteristics of the in-patients of our Department in the relation to the outbreak, clinical course and outcome of the digestive diseases. Namely, it may be assumed that the incidence and prevalence of the idiopathic inflammatory bowel disease (IBD) including ulcerative colitis and Crohn's disease are relatively high in this area (Kitakyushu city and its suburbs) as compared with the average of all Japan. Although the true causes of these illness are still unknown, the inclination of haptoglobin phenotypes (HP) which include 2-2, 2-1 & 1-1 type 1-1 strongly suggests to the association with some genetical factors on the high incidence of these diseases (IBD). In this connection, Hp type 1-1 were recognized 4 in 11 cases (36.4%) with ulcerative colitis, and 3 in 7 cases (42.9%) with Crohn's disease in our Department whereas only 3-5% in normal controls. Secondly, the patients with carcinoma of the biliary tree (bile duct and gall bladder) are relatively more, namely, 17 cases of bile duct cancer and 3 cases of gall bladder cancer were admitted in our Department during this term. It is interesting to note that hepatohilar type of the bile duct cancer was observed comparatively high (4 in 17 cases, 52.9%) in the past five years-more although the etiology is unknown. Finally, several characteristics in liver diseases particularly in viral hepatitis were illustrated in this study, namely, the ratio of transient HBV infection to whole (transient and persistent) HBV infection in the patients with acute viral hepatitis (due to HBV) is high (80.9%), HBeAg positivity is high in chronic B-hepatitis (44.9%), the ratio of alcoholic cirrhosis to whole liver cirrhosis is relatively high (34.9%) and HBsAg positivity is lower in liver cirrhosis due to non-alcoholic origin (mainly due to hepatitis virus) than the average of this country, and also, hepatocellular carcinoma (HCC) without liver cirrhosis is higher (23.0%) than the average of whole Japan (less than 15%) statistically.
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PMID:[Ecological approach to the patients with digestive diseases in Kitakyushu City and its suburbs]. 372 13

Seven males with liver cirrhosis associated with hepatitis and one with schistosomal liver fibrosis were studied for hypophyseal gonadal dysfunction and compared to six age matched controls. Cirrhotics as a group had higher serum 17 beta estradiol levels (22.1 +/- 6.3 vs 7.8 +/- 0.8 pg/ml, p less than 0.05) which did not rise after four days of human chorionic gonadotropin (hCG) stimulation. Conversely, there was an adequate rise in serum testosterone level after hCG stimulation (332.8 +/- 99.7 ng/dl baseline to 887.6 +/- 67.1 ng/dl, p less than 0.01). Compared to the controls, cirrhotics had lower baseline serum follicle stimulating hormone (FSH) (3.6 +/- 1.7 vs. 10.2 +/- 1.5 mIu/ml, p less than 0.02) and higher serum prolactin (13.5 +/- 2.5 vs. 6.8 +/- 1.0 ng/ml, p less than 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to luteinizing hormone releasing hormone (LHRH) in four out of eight subjects tested. We conclude that the mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common in alcoholic cirrhosis.
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PMID:Hypophyseal-gonadal dysfunction in men with non-alcoholic liver cirrhosis. 392 49

The two major constituents of basement membranes are type IV collagen and laminin. Specific radioimmunoassays are described here for two structural domains of these proteins (7-S collagen and the fragment P1, respectively) that allow the related antigens to be quantified in human serum. The serum 7-S collagen antigen was uniform in size, whereas the laminin P1 antigenicity was heterogeneous. These proteins were measured in sera from sixty-three alcoholics, divided on the basis of liver histology into four groups: normal light microscopy, fatty liver, alcoholic cirrhosis with hepatitis and inactive cirrhosis. The group with cirrhosis and hepatitis had clearly elevated values in both assays, differing significantly from the others. A few pathological results were also seen in the other groups. The increases noted in 7-S collagen concentration were larger than those in laminin P1. During follow-up of a patient with cirrhosis and hepatitis the 7-S collagen level in particular seemed to reflect the course of the disease. The elevated basement membrane protein concentrations in serum may be associated with the formation of real basement membranes in the perisinusoidal space, a process known as capillarization of the sinusoids which is found during the development of liver cirrhosis.
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PMID:Type IV collagen and laminin-related antigens in human serum in alcoholic liver disease. 392 6

Of 20 patients with alcoholic liver cirrhosis and a superimposed episode of acute viral hepatitis, 12 developed hepatic encephalopathy or ascites or both. Four died of hepatic failure. Seventeen patients had received blood transfusions within 6 months before the acute hepatitic episode. Two patients were HBsAg-positive; the other 18 were presumptively diagnosed as having non-A, non-B hepatitis. However, hepatitis A virus infection was excluded in only three of the 18 patients. Histologic examination performed in 13 cases disclosed necrotizing inflammatory activity, which is commonly observed in acute viral hepatitis. The distinctive histologic feature was a meager regenerating activity. We conclude that patients with alcoholic cirrhosis complicated by acute viral hepatitis frequently develop hepatic failure and have a high fatality rate (20% in our series).
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PMID:Acute viral hepatitis superimposed on alcoholic liver cirrhosis: clinical and histopathologic features. 393 97

Most pathologic studies of liver disease in sickle cell anemia and its variants were performed retrospectively on autopsy specimens, and, because of the prominent histologic features of intrasinusoidal sickling and Kupffer cell erythrophagocytosis, hepatic dysfunction was attributed to the intrahepatic sickling of erythrocytes in this hemoglobinopathy. We compared the liver histology from 19 patients who had liver biopsies to the autopsy specimens from 32 patients who succumbed to the complications of the hemoglobinopathy. In the former, nine patients had histological evidence of viral hepatitis. Four of these patients had both serological and immunohistochemical evidence of hepatitis B surface antigen. The features of biliary tree obstruction were found in two cases and alcoholic cirrhosis and sarcoid granuloma in one case each. Only one patient, who had recovered from septic shock, showed ischemic necrosis. In five patients incidentally biopsied during cholecystectomy, no significant lesions were found. Fourteen of the autopsy specimens showed ischemic necrosis, a result which was significantly different from the biopsy group. Ten cases had no significant morphologic changes other than heavy iron deposits. There were two cases with chronic active hepatitis, two with diffuse fibrosis, and one case each of cirrhosis, acute viral hepatitis, cholestasis, and giant cell hepatitis. Intrahepatic sickling and erythrophagocytosis were seen in almost all specimens and did not correlate with liver disease or transaminase elevation. Other than the patient with septic shock, ischemic necrosis was found only in postmortem material. These histological features may represent red cell destruction rather than the etiology of liver disease in these patients.
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PMID:Pathological spectrum of liver diseases in sickle cell disease. 394 29

A consecutive series of 1002 jaundiced adult patients covering 23 different causes of jaundice is presented. Patients were followed up for 2 to 7 years. The survival for the 784 patients included during their first episode of jaundice was calculated for each diagnostic category. Examples of decreased survival as compared with the general population were (figures indicate 3 months' and 5 years' survival, respectively): alcoholic cirrhosis 0.81, 0.35; cryptogenic cirrhosis 0.78, 0.32; pancreatic carcinoma 0.54, 0.04; cholangiocarcinoma 0.26, 0.00; and heart failure with liver congestion 0.47, 0.07. Ten of 172 patients with acute viral hepatitis died, 1 of fulminant hepatitis and 9 because of suicide or accidents. Of 105 patients with gallstones 37 died during the study period, but in only 9 of these could death be attributed to the gallstone disease. New diagnostic methods and types of treatment for jaundiced patients have been developed during recent years. To justify fully these diagnostic and therapeutic modalities, knowledge of the prognosis for the various causes of jaundice is essential.
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PMID:Survival after jaundice: a prospective study of 1000 consecutive cases. 399 72

The precise nature of the relationship between cirrhosis and HCC remains to be elucidated. However, it seems likely that no single explanation will cover the various forms the association takes in different parts of the world. In the high HCC incidence regions of sub- Saharan Africa and the Far East, an etiology common to the two disorders, HBV and possibly other hepatitis viruses, seems to account for the majority of cases. The role of aflatoxin in these areas is uncertain because it appears not to cause cirrhosis in man. In populations in which HCC is uncommon, alcoholic cirrhosis is the most frequent association of HCC. There is no convincing evidence to support a shared etiology in this situation because alcohol has not thus far been proved to be directly oncogenic for the liver. Possibly, cirrhosis renders the hepatocytes more susceptible to environmental carcinogenic factors. The same explanation may apply to hemochromatosis. There is at present little evidence for the postulate that HCC is an inevitable consequence of the hyperplasia of cirrhosis.
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PMID:Relationship between hepatocellular carcinoma and cirrhosis. 608 59

The reason why similar amounts of alcohol consumption cause different types of organ damage in alcoholics is obscure. Recent studies indicate that hepatitis B virus infection may influence the development of liver cirrhosis in alcoholics. We investigated the prevalence of markers of viruses known to cause hepatitis (HAV, HBV, EBV, CMV) in two groups of patients, one with alcoholic pancreatitis without known liver cirrhosis and one with alcoholic liver cirrhosis without known pancreatitis. We found signs of past infection with HAV and HBV more often in alcoholics with liver cirrhosis than in patients with alcoholic pancreatitis or in age-matched controls.
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PMID:Prevalence of markers of hepatotrophic viruses in alcoholics with symptomatic liver cirrhosis or pancreatitis. 608 3

In most cases, primary liver carcinoma in tropical areas remains an hepatoma. The high incidence of this malignant tumor of the liver in some regions, and especially in black Africa, is still unexplained. As compared with the form found either in the European or in the North-African, this hepatoma shows special features since it occurs in younger people (35 years), follows a bursting-out course and is precipitously associated not to an alcoholic cirrhosis but to a post-hepatitic one. An humoral syndrome leading to a presomptive diagnosis consists of hypoglycemia, hypercholesterolemia, hyperlipemia, and high blood level of alcaline phosphatases. In 85% of the cases, these tumors secrete an alpha fetoprotein determined by radioimmunoassay. A major etiologic factor is the oncogenous activity of hepatitis virus B which could be either an induction factor or a "co-factor" which would initiate, facilitate or increase the activity of the carcinogen. In this respect, aflatoxin has to be regarded as a "co-factor" too. The best treatment, when it is possible, is an exeresis carried out through a partial hepatectomy. If such a surgical intervention is unadvisable, chemotherapy is the only possibility. Immunization against viral hepatitis has raised hope for the prophylaxis of hepatoma. But it will not be possible to evaluate it before the year 2.000.
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PMID:[Primary liver cancer in the tropical environment. Classical and current data]. 619 92

The propensity to develop alcoholic cirrhosis is probably, at least in part, genetically determined. A striking similarity exists histologically between perhexiline and alcohol-related hepatitis and both are potentially precirrhotic lesions. Liver damage due to perhexiline is associated with impaired drug oxidation capacity which is genetically determined and tested by use of debrisoquine. Oxidation phenotyping might be used to predict susceptibility to perhexiline liver damage; it might also predict the potential to develop alcoholic cirrhosis. Oxidation phenotyping was therefore undertaken, using debrisoquine in 100 alcoholic patients, 30 of whom had only fatty liver despite prolonged alcohol abuse, while the remaining 70 had alcoholic hepatitis and/or cirrhosis. One hundred patients with nonalcoholic chronic liver disease served as controls. The number of patients with severely impaired drug oxidation capacity (poor metabolizer phenotype) was similar in the alcoholic group (8%) and the nonalcoholic control group (7%). In particular, the incidence of the poor metabolizer phenotype was similar in alcoholics with severe liver disease (10%) and in those with only fatty change (3%). There appears to be no association between the susceptibility to develop alcoholic cirrhosis and drug oxidizing capacity.
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PMID:Oxidation phenotyping in alcoholics with liver disease of varying severity. 639 Dec 52


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