Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Liver morphology and biochemistry were investigated in 61 morbidly obese subjects selected by defined criteria. Median overweight was 82 per cent (range 61 to 170 per cent), and median duration of overweight was 20 years (range two to 45 years). No patient had more than a moderate alcohol consumption and only one was diabetic. Four biopsies (7 per cent) showed normal liver tissue, while fatty change was the main diagnosis in most cases (85 per cent). Increasing degrees of fatty change was significantly (P less than 0.02) associated with presence of lipogranulomas (found in 54 per cent of the biopsies), focal necroses (found in 28 per cent), slight parenchymal inflammation (found in 33 per cent), and Kupffer cell proliferation (found in 49 per cent). Slight portal inflammation was seen in 23 per cent but portal fibrosis in only 2 per cent of the biopsies. No case of cirrhosis was registered. Patients with moderate or severe fatty change, lipogranulomas , focal necroses or with parenchymal inflammation were significantly more obese than patients without these changes (P less than 0.05). Even in absence of fatty change, obese subjects showed a markedly decreased serum albumin concentration and an elevated serum alkaline phosphatase activity (P less than 0.0001) compared with non-obese controls. Serum lactate dehydrogenase and aspartate aminotransferase were significantly raised only in patients with fatty change. With respect to serum bilirubin and plasma cholesterol concentrations no significant differences were detected between patient subgroups and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The liver in consecutive patients with morbid obesity: a clinical, morphological, and biochemical study. 672 92

In 64 patients suffering from chronic inflammatory liver disease (alcoholic hepatitis, chronic active hepatitis, chronic persistent hepatitis) significantly increased values of blood glucose and insulin, free fatty acids and C-peptide were observed during a 100 g oral glucose load. Fasting values of blood glucose, free fatty acids and C-peptide were also increased, while serum growth hormone remained unchanged. In patients with chronic active hepatitis the C-peptide/insulin-ratio, a measure for hepatic insulin degradation, was significantly lowered after glucose uptake. During oral load there were no discernible differences between the different types of chronic inflammatory liver disease concerning blood glucose, serum insulin and free fatty acids. In normal weight and in overweight patients suffering from liver disease blood glucose and serum insulin values were increased to the same extent. As it is known from the liver cirrhosis chronic inflammatory liver disease lead to an insulin resistance, to which elevated free fatty acid levels contribute. Increased body weight has no influence on the insulin resistance observed in chronic liver inflammation. From the changes of the C-peptide and the C-peptide/insulin-ratio it can be deduced, that the hyperinsulinism in patients with chronic inflammatory liver disease is due to both insulin hypersecretion and diminished hepatic insulin degradation.
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PMID:[Hyperinsulinaemia and impaired glucose tolerance in chronic inflammatory liver disease (author's disease)]. 722 67

In man, the assay of insulin receptors is performed on circulating monocytes or erythrocytes. In physiology, insulin binding decreases with age; it is lower in women during the luteal phase of the menstrual cycle or during administration of oestrogen-progestogen oral contraceptives; it exhibits diurnal variation; it increases after physical training; it depends on the diet, being inversely correlated with its carbohydrate content; finally, rapid variations in binding affinity are observed after glucose ingestion or after breakfast. In pathology, obese people are resistant to the effects of insulin and they have decreased numbers of receptors on blood cells; short-term fasting induces an increase in the binding affinity, while a long term hypocaloric diet leads to an increase in receptor numbers. Similarly non-insulin-dependent, maturity onset diabetics, even without overweight, have low numbers of binding sites, which are increased by diet or after treatment by sulfonylureas. In the syndrome of insulin resistance and acanthosis nigricans, there is a decrease in hormone binding, which is either primary (Type A) or is secondary to the effects of circulating antibodies to the insulin receptor (Type B). In acromegaly, insulinomas, liver cirrhosis and acute viral diseases the binding of insulin is decreased. On the contrary, variable results have been reported in cases of lipoatrophic diabetes, leprechaunism, uremia and glucocorticoid administration. Finally, an increase in insulin receptors has been observed in anorexia nervosa and in insulino-penic diabetes.
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PMID:[The insulin receptors of the blood cells and their study in disease states in man (author's transl)]. 734 Jun 95

AIMS. 1) To evaluate the nutritional status of a group of alcohol abusers, relatively to their liver function and morphology, and 2) to compare these data with those of a previous study carried out by out team ten years ago. According to their body weight, 135 alcohol abusers were divided into three groups: normal-weight, over-weight and under-weight. The severity of their hepatopathy was defined as: 1. slight hepatopathy; 2. alcohol-induced hepatitis; 3. alcohol-induced hepatitis plus cirrhosis; 4 child A cirrhosis; 5. child B cirrhosis. RESULTS. 1. The overweight group was homogeneously distributed among the several degrees of compensated hepatopathy. 2. There was a marked reactivity to skin tests (Multitest) in patients with alcohol hepatitis without cirrhosis, independently of nutritional disorders. 3. Only decompensated cirrhosis may cause caloric-protein malnutrition; consequently, nutritional disorders due to alcohol abuse appear late and they are unlikely to play a leading role in the pathogenesis of liver disease due to alcohol abuse. Obesity, on the other hand, may facilitate the onset of liver steatosis.
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PMID:[Nutritional status of patients with alcoholic liver diseases: comparison of the situation in the seventies and at present]. 764 38

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
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PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8

When compared to 32 healthy normal weight normolipidemic control subjects, plasma protein C antigen and serum cholinesterase activity were significantly decreased in 17 patients with decompensated cirrhosis of the liver and in 29 critically-ill surgical patients displaying the acute phase reaction, most of them without evidence of consumption coagulopathy. The low levels of these variables are considered to be subsequent to impaired and dysregulated hepatic protein synthesis. On the contrary, plasma protein C and serum cholinesterase were increased in 20 nephrotic patients and in 20 overweight hypertriglyceridemic subjects, a finding highly suggestive of enhanced hepatic synthesis probably related to an accelerated turnover of triglycerides. A discrepancy between low serum cholinesterase activity and normal or even high plasma protein C antigen was noted in 15 patients with cholestasis. This was particularly evident in 7 subjects with extrahepatic cholestasis and an abnormal pattern of hepatic protein synthesis or impaired clearance of plasma protein C would appear to develop in such pathological conditions.
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PMID:Clinical studies on plasma protein C. Correlation with serum cholinesterase. 829 22

We describe three men and two women, aged 18-50, with an occasional finding of increased aspartate and alanine aminotransferase and gamma-glutamyl transpeptidase levels in the absence of any drug treatment and past or current alcohol abuse. Two patients were overweight (body mass index 29 and 32, respectively) and physical examination was normal in all but one case. Tests for hepatitis A, B and C, Epstein-Barr virus, cytomegalovirus, toxoplasma and autoimmune hepatitis were negative and metabolic diseases (Wilson's disease, haemochromatosis, alpha-l-antitrypsin deficiency) were excluded by specific tests. Ultrasound liver scan revealed massive steatosis in all patients. Liver histology showed diffuse steatosis and parenchymal inflammation in all cases, with concomitant fibrosis and Mallory bodies in three of them. Findings were consistent with non-alcoholic steatohepatitis, a rare condition with potential progression to cirrhosis in a minority of cases. This disease, for which no treatment is currently available, must be considered in all subjects with elevated aminotransferases, in the absence of known causes of liver damage.
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PMID:Non-alcoholic steatohepatitis. Report of five cases and review of the literature. 878 33

Though the hepatotoxicity of ethanol has been established, only 8% to 20% of chronic alcoholics develop cirrhosis. The aim of this study was to assess whether being overweight is a risk factor for alcoholic liver disease. One thousand six hundred four alcoholic patients were studied. According to the liver biopsies, 194 patients had a normal liver; 402 had steatosis without fibrosis; 281 presented with fibrosis, with or without steatosis; 119 presented with acute alcoholic hepatitis (AAH) without cirrhosis; 232 indicated cirrhosis without AAH; and 179 presented with cirrhosis with AAH. One hundred ninety-seven patients had clinically obvious cirrhosis. In the study, five variables were studied as risk factors: age, sex, daily consumption of alcohol during the previous 5 years, the total duration of alcohol abuse, and tendency to be overweight (body mass index [BMI] > or = 25 in women and > or = 27 in men). The BMI was calculated according to the minimum weight over the 10 previous years. In the first stepwise logistic regression analysis, age, being overweight for at least 10 years, being of the female sex, and the total duration of alcohol abuse were independently correlated with the presence of cirrhosis. In the second analysis, female sex being overweight were the two independent risk factors of AAH. In the third analysis, being overweight for at least 10 years was the only independent risk factor of steatosis. These results show that the presence of excess weight for at least 10 years is a risk factor for cirrhosis, AAH, and steatosis. Our results suggest that there is a possible potential for the metabolic effects of ethanol ingestion caused by excess weight in patients with alcoholic liver disease.
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PMID:Excess weight risk factor for alcoholic liver disease. 898 74

Recurrence of hepatitis C virus (HCV) after orthotopic liver transplant (OLT) may be mild or may lead to progressive liver disease requiring retransplantation (re-OLT). Results of re-OLT for hepatitis C are not well known. We analyzed outcomes in 14 patients retransplanted for recurrent hepatitis C. All had evidence of recurrent hepatitis on multiple biopsies. Polymerase chain reaction (PCR) was performed in blood or tissue samples from 12 patients when recurrence was suspected; all 12 were positive for HCV-RNA. Explants showed chronic hepatitis with bridging necrosis in 3 patients, hepatitis with transition to cirrhosis in 2, hepatitis and cirrhosis in 3, and cirrhosis alone in 2. In 2 patients, in whom immunosuppression had been withheld for 4 to 6 weeks, there was also evidence of chronic rejection. Four died of sepsis perioperatively (median, 32.5 days; range, 9-59); pre-OLT, 3 of 4 had renal failure, and 1 had fever with no obvious source of infection. Ten patients did well early after OLT and were discharged. One patient was readmitted 6 weeks after discharge and died of cytomegalovirus (CMV) infection 127 days after re-OLT. One patient with concomitant vanishing bile duct syndrome, probably due to chronic rejection, developed recurrent hepatitis and died of progressive liver failure 161 days after re-OLT. Eight patients are well at a median of 926 days (range, 315-1930) after re-OLT. Three have evidence of mild recurrent hepatitis on liver biopsy, one is overweight with severe steatosis on biopsy, and four have no evidence of recurrent hepatitis. Retransplantation for hepatitis C should be considered a viable option for patients who develop end-stage hepatic dysfunction secondary to recurrent disease and should be performed before development of infectious complications and renal insufficiency.
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PMID:Retransplantation for recurrent hepatitis C. 934 26

In this article, as part of an evaluation of the future of medical education in California, we characterize the distribution of disease and injury in California; identify major factors that affect the epidemiology of disease and injury in California, and project the burden of disease and injury for California's population to the year 2007. Our goal is to elucidate the major causes of illness and disability at present and in the near future in order to focus state resources on the interventions likely to have the greatest impact. Data from various governmental agencies were utilized; the base year, 1993, is the most recent year with sufficient information available when this report was prepared. Several major risk factors have decreased, including smoking (30% decline from 1984 to 1993) and drinking and driving. However, hypertension prevalence has not changed, and overweight has increased dramatically. Poverty continues to burden about 15% of Californians, with poverty highest among children. During 1993, 220,271 Californians died, with 3 major causes accounting for 61% of these deaths: coronary heart disease (31%), cancer (23%), and stroke (7%). In terms of potential years of life lost (years lost before age 65), the most important causes of death in 1993 were unintentional injury (756 years lost/100,000 population), cancer (632 years), and the acquired immunodeficiency syndrome (AIDS; 491 years). Mortality rates were highest among blacks and lowest among Asians. Overall mortality in California has been declining for decades; in just 1 decade, from 1980 to 1991, mortality declined from 780 to 680 deaths per 100,000 population. Several major causes of death have declined, including coronary heart disease, stroke, unintentional injury, cirrhosis, and suicide, while others have increased, for example, chronic obstructive lung disease and diabetes mellitus. Death from AIDS increased dramatically in the past decade, but is leveling off, and death from cancer is beginning to decline. Rates for overall mortality and morbidity, and for most specific conditions, should continue to decline. A projected 28% population increase by 2007 will yield a corresponding increase in the absolute level of disease cases and death; a disproportionate increase in younger and older groups will yield increased conditions affecting young (unintentional injury, AIDS) and older (heart disease, cancer, stroke, diabetes mellitus) people. Californians should experience overall improved health in coming years, reaping benefits of reduced environmental and behavioral risk factors as well as improved medical treatment and rehabilitation. Coordinated strategies for health promotion, disease prevention, delivery of medical treatment, and rehabilitation are needed to maintain and improve present levels of health across the life span.
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PMID:Disease and injury in California with projections to the year 2007. Implications for medical education. 961 96


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