Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients on haemodialysis for 6 months to 3 years contracted AgHBs positive hepatitis, 9 being also Ag e positive. They continued to carry the same antigens. Histological surveillance was begun from the 6th month of the disease onwards, with 2 to 4 repeated biopsies in 1,5 to 3,5 years in 9 patients, the last 3 having only one biopsy between the 8th and the 15th month. In 6 patients, the first biopsy revealed chronic persistent hepatitis (CPH) and in other 6 (5 male and 1 female) chronic aggressive hepatitis (CAH). Subsequent biopsies revealed cirrhosis in a patient treated with alphamethyldopa (Ag e +), the absence of any changes in 7 other patients (4 CPH including 3 Ag e + and 3 CAH including 2 Ag e +), and an improvement in the last. Long term surveillance of hepatitis B by repeated biopsies in haemodialysed patients reveals that histological lesions are stable at 2 years, that certain drugs may have an aggravating role and that Ag e has no prognostic value.
Nouv Presse Med 1978 Sep 23
PMID:[B virus chronic hepatitis in the haemodialysed uraemic patient. Correlation between hepatic lesions and the presence of antigen e in 12 patients (author's transl)]. 71 64

In an attempt to evaluate the role of renin-angiotensin system in the contols of blood pressure and aldosterone secretion in the patients with cirrhosis and asictes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity. These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or palasma renin activity.
Jpn Heart J 1978 Sep
PMID:Role of renin-angiotensin system in the controls of blood pressure and aldosterone in patients with cirrhosis and ascites. 73 36

Analysis of data on death certificates indicates that the value of P (the percentage of all deaths due to cirrhosis of the liver that can be attributed to alcoholism) in the Jellinek estimation formula is a function of sex, race and whether or not an autopsy was performed.
J Stud Alcohol 1978 Sep
PMID:Some considerations in using cirrhosis mortality rates as indicators of the prevalence of alcoholism. 73 24

47 cases of viral hepatitis with HBs antigenemia, who were diagnosed by peritoneoscopy and biopsy, were studied. 41 cases were males, and 6 cases were females. The onset ages were mostly in 25--29 years old. The histories of blood transfusion were found in only 4.3%. On the other hand, the families clustered with HBs antigen were found in 68%. Recidivums were often seen (76%), and yet the intervals between recidivum were short (the neighborhood of 8 months). The transaminases at the recidivums were not so high (200 units or thereabout). 20 cases whom biopsies were performed more than twice, were studied histologically. 14 cases were prognessive. 5 were stationary. 1 was improved. In all of progressive cases, sublobular hepatic necrosis was seen. But in other cases, sublobular necrosis was not seen. After this sublobular necrosis, various distortion of the lobule architecture was appeared, and some of them progressed to liver cirrhosis. As to GOT and GPT, GPT was dominant before sublobular neerosis, but GOT was liable to be dominant after sublobular necrosis. Peritoneoscopically, peculiar red spots were found on liver surfaces at the time of sublobular necrosis.
Hokkaido Igaku Zasshi 1978 Sep
PMID:[Studies on development of viral hepatitis with HBs antigenemia (author's transl)]. 74 63

Vitamin A absorption tests using vitamin A palmitate and alcohol separately in oil and oil-water emulsions were done on 43 patients with cystic fibrosis. Patients were given 7,000 units of vitamin A per kilogram of body weight with a fatty breakfast. Pancreatic enzymes were not given with the test meal and were withheld for five hours from start of test. Blood was drawn before administration of the vitamin and at three and five hours after administration. Serum vitamin A levels were estimated using the Carr-Price technique. The percentages of patients with normal vitamin A absorption were 85 with vitamin A alcohol in oil-water emulsion, 61 with vitamin A alcohol dissolved in oil, 64 with vitamin A palmitate in oil-water emulsion, and 19 with vitamin A palmitate in oil. The number of stools per day is an inverse indicator of retention time in the intestine. Absorption of fat soluble vitamins is always abnormal when a patient has four or more stools a day. The observations that cystic fibrosis patients with abnormal liver biopsies have poor absorption of vitamin A were not statistically significant. The question of the effect of cirrhosis in cystic fibrosis on vitamin A absorption remains unresolved.
Clin Pediatr (Phila) 1976 Sep
PMID:Absorption of vitamin A in patients with cystic fibrosis. Absorption is best with emulsified vitamin A alcohol. 78 64

This paper describes immunofluorescence studies on liver cell surface localization of hepatitis B surface antigen (HBsAg) and of IgG in acute and chronic hepatitis and in cirrhosis. In acute hepatitis B, HBsAg was found at the surface of hepatocytes in an early phase of the disease, but not during the recovery. This finding is consistent with the hypothesis that immune reactions to HBsAg may be responsible for the liver cell lysis. In HBsAg-positive chronic hepatitis and cirrhosis the antigen was found in the cytoplasm, but not on the surface of the hepatocytes, while in HBsAg-negative cases the antigen could not be detected in the liver cells. Both in HBsAg-positive and in HBsAg-negative chronic active hepatitis (CAH) and cryptogenic cirrhosis IgG bound to the membrane of the hepatocytes could be detected, suggesting a role of antibodies in the pathogenesis of the disease.
Clin Exp Immunol 1976 Sep
PMID:Liver cell surface localization of hepatitis B antigen and of immunoglobulins in acute and chronic hepatitis and in liver cirrhosis. 78 18

The authors report a case of major acanthocytosis which regressed spontaneously in a cirrhotic patient. The usual lipid abnormalities: considerable rise in free red cell cholesterol and lesser rise in phospholipid, regressed concommitantly to the disappearance of acanthocytes. No change in the main liver function tests was, however, observed. The etiological mechanisms of acanthocytosis in cirrhosis are probably multiple, and their interactions are compplex. The exchange of abnormal lipoproteins between the plasma and the red cell membrane is the last theory to be considered. On the other hand, no argument could explain the disappearance of the acanthocytosis, this phenomenon is considered up to now irreversible and a sign of the gravity of hepatic lesions.
Pathol Biol (Paris) 1976 Sep
PMID:[Transient acanthocytosis in a patient with liver cirrhosis. Study of red cell and plasma lipids (author's transl)]. 79 Feb 72

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
Diabete Metab 1975 Sep
PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
Diabete Metab 1975 Sep
PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Liver function and the presence of HBsAg and anti-HBsAg were studied in 90 hypertransfused thalassaemic children. Increased serum transaminases were found in 62 patients, and persisted from more than 6 months in 45 cases. Liver biopsy in this latter group led to a diagnosis of 14 cases of chronic persistent hepatitis, 9 cases of aggressive hepatitis, and 3 cases of hepatic fibrosis. In Italy thalassaemic children undergoing hypertransfusion therapy frequently encounter SH virus infection, with a consequent hepatitis that is generally anicteric and unrecognized unless systematically sought. In a liver already stressed by the concomitant iron overload, hepatitis infection might thus play a key role in the evolution of cirrhosis which frequently affects thalassaemics.
Arch Dis Child 1976 Sep
PMID:Role of chronic hepatitis in development of thalassaemic liver disease. 79 38


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