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)

The incidence of post-transfusion hepatitis (PTH) in recipients of blood products is reviewed. PTH was observed in 10%-12% of recipients of blood products in the United States, 2%-4% in northern Europe and 15%-20% in southern Europe. All studies indicate that 80%-90% of all PTH cases are attributed to non-A/non-B. At least 40% of the patients with PTH non-A/non-B will develop chronic hepatitis or cirrhosis. No specific tests for the detection of the non-A/non-B agent(s) exist. However, several independent studies indicate that part of the donors carrying the infectious non-A/non-B agent have increased levels of alanine amino transferase (ALT). When donors are excluded with elevated ALT values, it is estimated that about 30% of the PTH non-A/non-B cases would be prevented. Some studies indicate that anti-hepatitis B core (anti-HBc) positive donors may carry an increased risk to transmit the non-A/non-B agent, but more recent studies do not confirm this. There is hope that a specific non-A/non-B test will be developed soon.
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PMID:Blood transfusion and hepatitis: still a threat? 264 93

The present study investigated whether or not, in addition to the oral glucose tolerance test, oral alanine loading was a useful diagnostic tool for hormonal and metabolic diseases. Fifty g of L-alanine was administered orally in 14 normal, 12 diabetic, and 8 liver cirrhotic subjects. The influence of oral alanine loading on hormones and metabolites was compared with the results of 100 g oral glucose loading. The results obtained were as follows: 1) In the normal subjects and cirrhotics, lactate and pyruvate concentrations gradually increased with time and reached their peak levels at 60 min, whereas they remained unchanged throughout the course in the diabetic group at glucose loading. 2) Alanine administration accelerated ureogenesis but did not affect blood glucose levels. 3) In both glucose and L-alanine administration, free fatty acid, glycerol and ketone body levels declined nonspecifically in all groups. 4) Serum glucagon levels during L-alanine loading increased in all groups, especially in liver cirrhotics. 5) L-alanine was a potent stimulus for insulin secretion in diabetics, while no insulin release during glucose loading was observed. 6) The molar ratio of insulin levels (during glucose loading)/glucagon levels (during L-alanine loading) was a good indicator of systemic glucose homeostasis from the hormonal aspect. It is suggested that, in addition to the oral glucose tolerance test, the oral administration of L-alanine can be a useful tool for the diagnosis of the status in diabetes mellitus and cirrhosis.
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PMID:Pancreatic alpha- and beta-cell function and metabolic changes during oral L-alanine and glucose administration: comparative studies between normal, diabetic and cirrhotic subjects. 267 46

Plasma amino acid levels were determined in 23 patients in comparison with 16 normal subjects and 17 patients with liver cirrhosis. Patients with hepatocellular carcinoma had elevated levels of the aromatic amino acids and lowered levels of the branched-chain amino acids, as seen in liver cirrhosis; however, they had lowered levels of alanine and glutamine as compared with normal subjects and with liver cirrhosis patients. Following treatment with intraarterial chemotherapy and/or transcatheter arterial embolization, plasma levels of alanine and glutamine recovered. These results suggest that the consumption of alanine and glutamine increase in hepatocellular carcinoma.
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PMID:Plasma amino acid patterns in hepatocellular carcinoma. 282 52

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.
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PMID:Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis. 289 85

Eleven acute rejections were found in 9 patients with liver transplantation due to end-stage liver cirrhosis. The rejections were diagnosed with fine-needle aspiration biopsy (FNAB) giving the cellular picture of immunoactivation in the liver graft when compared to a simultaneous sample of peripheral blood. s-Alkaline phosphatase and s-bilirubin increased within 1 week after onset of rejection in 7 and 10 cases, respectively. s-Alanine amino-transferase and b-ammonium were of no value in the diagnosis of acute rejection. A core biopsy was obtained only in a case of severe liver damage, mainly to estimate the need for retransplantation. One year after grafting, 6 out of 7 cirrhotic patients are well, all with normal liver function. Two have died of sepsis. One patient died from pulmonary metastases of occult liver carcinoma 6 months after the transplantation. FNAB seems helpful in detecting early acute rejection and also excluding such an event in the liver graft.
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PMID:Diagnosis of acute rejection in liver transplantation. 304 94

We describe a case of liver cirrhosis lacking the expected increase in serum thyroxin (T4)-binding globulin (TBG) despite abrupt, severe increases in aspartate and alanine aminotransferases (ASAT and ALAT) in serum. Sequential change in serum T4, triiodothyronine (T3), and TBG concentrations were also measured retrospectively in serum of 10 hospitalized patients with acute viral hepatitis. Although their mean T4 and TBG concentrations significantly exceeded those in 40 normal subjects (P less than 0.002 and P less than 0.001, respectively), these values were within the normal reference intervals in five patients. ASAT and ALAT concentrations were not significantly different in patients with increased TBG and patients with normal TBG, whereas mean concentrations of serum albumin and cholinesterase and mean prothrombin times (in percent) in the former group were significantly higher than those in the latter group (P less than 0.05, P less than 0.05, and P less than 0.001, respectively). For 60 samples with increased ASAT and ALAT, TBG and albumin or cholinesterase correlated significantly (r = 0.49, P less than 0.001 and r = 0.50, P less than 0.001, respectively), but not TBG and ASAT or ALAT. Collectively, these results suggest that the increase in serum TBG in acute hepatitis may reflect its synthesis in regenerating hepatocytes rather than a simple leakage from damaged hepatocytes.
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PMID:Are increases in thyroxin-binding globulin in patients with acute hepatitis ascribable to synthesis by regenerating hepatocytes? 312 18

The ratio of the serum aspartate to alanine amino-transferase levels (AST/ALT) is often used as a clue to the etiology of the underlying liver disease. This ratio is usually greater than 2.0 in alcoholic liver disease and less than 1.0 in patients with chronic hepatitis and chronic cholestatic syndromes. We analyzed the AST/ALT ratio in 177 patients with various forms of nonalcoholic chronic liver disease who underwent medical evaluation and percutaneous liver biopsy. In the majority of cases of chronic viral hepatitis, the AST/ALT ratio was less than 1.0. However, there was a statistically significant correlation between the AST/ALT ratio and the presence of cirrhosis. Among 100 patients with chronic type B hepatitis, the mean AST/ALT ratio was 0.59 in those without cirrhosis and 1.02 in those with cirrhosis. Furthermore, the AST/ALT ratio often rose to greater than 1.0 when cirrhosis first became manifest. Thus, the finding of an AST/ALT ratio of greater than 1.0 in a patient with nonalcoholic liver disease should suggest the presence of cirrhosis. In addition, the use of the AST/ALT ratio as a means of separating alcoholic and nonalcoholic liver disease must be tempered with the knowledge that this ratio may be less helpful in the presence of cirrhosis.
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PMID:Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis. 313 26

Non-A, non-B of hepatitis (NANBH) may occur following blood transfusions or administration of blood products. The causative agent(s) is still not identified and the symptoms are usually mild. The only indication of infection may be increased serum alanine transferase levels. The incidence of posttransfusion NANBH has been reported as high as 4-12% in the US (average 7%) while in Sweden it is according to recent studies on the average 2%. An estimated 2-3% of Swedish blood donors are probably carriers of the NANBH agent(s). Of patients acquiring posttransfusion NANBH, 40-60% will develop chronic hepatitis which in 15-20% will progrediate to cirrhosis.
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PMID:Transfusion transmitted non-A, non-B hepatitis. 314 65

The long-term follow-up of 80 heart transplant patients (70 men, 10 women) from January 1982 to July 1985 who had received cyclosporine (CsA) showed a high incidence of mild to severe liver dysfunction. Fifty patients (62.5%) had long-lasting postoperative biological disturbances (alanine amino transferase greater than 2N and/or alkaline phosphatase greater than 1.5N for 3 months or more). Most patients were asymptomatic; eight were icteric, and one had arthralgia. The most common biological feature consisted of isolated elevation of ALAT (27 cases). Assessment of causes led to a definite etiology in 42 patients: 7 cardiac failure, 13 HBsAg-positive liver disease (26%) (chronic persistent hepatitis 8, chronic active hepatitis 2, subacute necrosis 2). Fourteen patients (28%) sustained non-A, non-B (NANB) hepatitis (chronic persistent hepatitis 5, chronic active hepatitis 1, cirrhosis 1), and 7 (14%) sustained a drug-related hepatitis. Liver biopsy and complete virus screening was contributive to the diagnosis in nearly all patients. Additionally, prolonged impairment of liver function tests occurred in 62% of heart transplant recipients, mostly during the first 6 postoperative months. Hepatitis B virus (HBV) and NANB hepatitis accounted for 26% and 28% of the cases of liver dysfunction, respectively; drug-induced hepatitis may have been involved in 14% of the cases. Complete hepatitis virus screening should be performed before heart transplant and in any case of abnormal liver function posttransplantation. HBV vaccination prior to heart transplant is recommended in HBsAg- and HBcAb-negative candidates for heart replacement. Long-term follow-up of these patients is mandatory to assess the severity of these liver dysfunctions.
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PMID:Prevalence and causes of long-lasting hepatic dysfunction after heart transplantation: a series of 80 patients. 329 31

Gluconeogenesis and alanine metabolism of normal and cirrhotic rats were studied in view of partial hepatectomy. Liver cirrhosis was made by repeated injection of thioacetamide in rat. Partial hepatectomy was performed by modified method of Higgins-Anderson. Liver glycogen and fructose-2, 6-bisphosphate were decreased after hepatectomy and recovered within 7 days in normal groups, while those of cirrhotic group reduced even in preoperative state were further decreased and hardly recovered after hepatectomy. Gluconeogenesis of perfused liver in cirrhosis was increased from both lactate and alanine preoperatively, but gluconeogenesis from alanine was not increased in both hepatectomized rats. ATP and energy charge were decreased after hepatectomy and recovered within two weeks. These level were lower in cirrhotic group, and decreased further and hardly recovered after hepatectomy. Alanine utilization to CO2 in vivo was not impaired in cirrhotic group either preoperatively or postoperatively. ATP and energy charge were increased by alanine injection in hepatectomized rats of both normal and cirrhotic group. In conclusion, glucose-insulin therapy of sufficient amounts is important to improve decreased glycolysis and abnormal gluconeogenesis on both post-hepatectomy period of normal and pre and post-hepatectomy period of cirrhosis. Also alanine is effective for stimulating decreased energy production.
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PMID:[Changes of gluconeogenesis and alanine metabolism following partial hepatectomy in normal and cirrhotic rats]. 339 28


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