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)

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.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Various parameters of the insulin secretion in man may be appreciated and calculated by studying the insulin response to an intravenous pulse of glucose followed 120 minutes later by one of tolbutamide. The relative insensitivity of the B cell to glucose, probable marker of a constitutional pancreatic predisposition to diabetes may be assessed in a given individual whatever his age and body weight. The glucose intolerance per se is due to, or accompagnied by various B cell dysfunctions according to its etiology. This is illustrated by the results observed in chronic pancreatitis, liver cirrhosis, aged or obese subjects.
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PMID:[A method of studying insulin secretion in humans: the glucose stimulation test, followed by tolbutamide]. 79 23

The karyomgrams of normal human livers (50 biopsides from patients of varied age) and of fatty livers (350 biopsies from patients with diabetes, alcoholism, and fatty cirrhosis) were investigated. The nuclear diameters were measured with an analyzer of particle size--the "TGZ-3 Zeiss"--, the cut surface of the nuclei was determined and the nuclei categorized accordingly. 1. The normal liver in each age group is characterized by a well-defined nuclear pattern that is specific for this organ. In the 3rd decade nuclei of the main class predominate. In later decades 2 classes of large nuclei gradually appear and reach their mximum after the 50th year. In the 7th decade a reduction of the cut nuclear surface takes place in all the categoreis, presumably determined by a reduction of function. 2. The increase in the number of large nuclei is explained by abortive karyokineses which in the course of the normal turnover of cells ("Zellmauserung"), increasingly replace normal mitoses. This is This is attributed to disturbances of the achromatic apparatus that occur with increasing age. 3. Alcoholic, and even more so diabetic, fatty change leads to the formation of particularly large nuclei. This appears to depend on the volume of the individual fat droplet within the individual cell rather than on the degree of fatty change of the whole liver. 4...
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PMID:[The karyogram of normal and of fatty livers in man (author's transl)]. 80 91

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

Statistically there exists an increased coincidence between liver cirrhosis and diabetes mellitus. The higher frequency of cirrhosis in diabetics compared with the normal population is to be explained partly from the higher risk of hepatitis. In addition to this the diabetic suffers from disturbances which further the development of cirrhosis, such as fatty degeneration of the liver, abuse of alcohol, more frequent inflammatory diseases of the bile duct and others. When a diabetes mellitus exists in liver cirrhosis it is to be differed between a diabetes due to absolute or relative insulin deficit and disturbances of carbohydrate clearance which are associated with normal or increased insulin levels. The latter form can be denoted as so-called liver diabetes. Main cause of this carbohydrate intolerance is an insulin resistance, partly by deminution of the metabolically active liver parenchyma, partly by the diminished reactivity of the peripheral tissues. By prophylactic measures and differentiated therapy may be favourably influenced lesions of the liver in diabetes mellitus as well as disturbances of the carbohydrate metabolism.
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PMID:[Liver cirrhosis and diabetes mellitus]. 85 43

Postmortal histologic examinations of the synovial membrane of both knee joints were conducted in 85 selected cases. The following conditions were given priority: diabetes mellitus, advanced renal insufficiency, liver cirrhosis with ascites, chronic insufficiency of the right heart, vericose syndrome of the lower extremities, tumours compressing organs of the pelvis minor as well as a few rare infectious and tumerous diseases. Comparison of the histomorphologic findings revealed consistancies such as pronounced ultravillous branching of the synovial membrane with villous hyalinosis in diabetes mellitus, increased, coarse villi formation in renal insufficiency and liver cirrhosis, edema of the synovial membrane in chronic insufficiency of the right heart and renal insufficiency as well as a number of nonspecific reactions of the synovial membrane in obstruction of venous drainage. In the context of generalized fibrotic processes such as in Ormond's disease and scleroderma, similar reactions of the synovial membrane are pronounced. Arthralgic complaints and secondary arthroses in those systemic diseases not primarily involving joints can be at least partially clarified by histomorphologic findings.
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PMID:[Reaction of synovial membranes in knee joint with primary extra-articular systemic diseases (author's transl)]. 85 62

Idiopathic hemochromatosis is an iron-storage disease more common in men than in women. It is characterized clinically by diabetes mellitus, cirrhosis of the liver, pigmentation of the skin and cardiac failure. The diagnosis may be overlooked when the presenting symptoms do not follow the pattern. A case is reported which was diagnosed after an onset that featured neurologic symptoms.
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PMID:Idiopathic hemochromatosis: case report of a patient presenting with neurologic symptoms. 86 79

Data on 40 patients with Staphylococcus aureus endocarditis treated with appropriate antibiotics in adequate dosage at the University of Cincinnati Medical Center hospitals between January 1961 and June 1975 were analyzed. The overall mortality was 40 per cent. The mortality was 11.1 per cent in patients under 50 years old and 63.6 per cent in patients over 50 years old (p less than 0.01). Seven patients were narcotic addicts who had no underlying disease and were under 50 years old; all survived. For patients without underlying diseases, the mortality was 0 per cent in those under 50 years old and 75 per cent in those over 50 years old. Patients who died had a greater number of major underlying diseases (pre-existing cardiac disease, diabetes mellitus, alcoholism and/or cirrhosis) than the survivors. Patients over 50 years old had significantly more major underlying diseases than patients under 50 years old (p less than 0.001). Among patients over 50 years old, those who died had more complications than the survivors while the number of underlying diseases were comparable. A group of patients treated with gentamicin during the first two to three weeks of therapy in addition to a penicillin was compared to a similar group treated with a single antibiotic. The mortality of both groups was 40 per cent.
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PMID:Prognostic factors in Staphylococcus aureus endocarditis and results of therapy with a penicillin and gentamicin. 87 Nov 33

It is reported on the dispensary care of 789 patients suffering from infectious hepatitis. Of these patients 92.86% healed completely of hepatitis during observation. 2.91% developed sequels after hepatitis, among them 1.03% a posthepatitic hyperbilirubinaemia, 1.03% a chronic persistent hepatitis, 0.17% a chronic aggressive hepatitis, 0.34% a liver cirrhosis, 4.25% had concomitant diseases, such as fatty degeneration of the liver, diseases of the bile duct, pancreatitis, and ventricular ulcer. The probable associations of these diseases with infectious hepatitis are discussed. Three patients suffered from diabetes mellitus. One of these patients developed a chronic aggressive hepatitis and finally an incipient cirrhosis.
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PMID:[Results of 10 years hepatitis follow-up]. 87 28

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


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