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

Four hundred and four patients (273 men, 131 women) aged 3 to 85 years with chronic Hepatitis B virus (HBV) infection seen during a five year period were analysed. At presentation, 177 patients (44%) were Hepatitis B e Antigen (HBeAg) positive (mean age 32 years) and 217 patients (54%) were anti-HBe-positive (mean age 40 years). Ten patients (2%) were negative for HBeAg and anti-HBe. Serum HBV-DNA was detected in 169 patients (42%). 85% of the HBeAg-positive patients had detectable serum HBV-DNA and 9% of the HBeAg-negative patients were positive for serum HBV-DNA. The mean serum Alanine amino-transferase (ALT) and Aspartate amino-transferase (AST) levels were higher in HBeAg-positive patients (75 and 52 iu/l) than in HBeAg negative patients (46 and 37 iu/l) (P less than 0.001). Liver biopsies were performed in 135 patients. Fifty-three (39%) had minimal changes, 61 (45%) chronic hepatitis (CPH, CLH & CAH) and 21 (16%) cirrhosis. There was no significant difference in the histologic distribution between HBeAg-positive and HBeAg-negative groups. Two hundred and fifty eight patients were followed up for a mean duration of 2 years (range 3 to 108 months). The cumulative probability of clearing HBeAg at the end of the first, second and third year were 14%, 16% and 18% respectively. Of these, the cumulative probability of developing anti-HBe over one, two and three years were 8%, 9% and 11% respectively. Reversion to HBeAg occurred in 1.5% of patients who were HBeAg-negative at presentation and 11% of HBeAg-positive patients who cleared HBeAg.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Chronic hepatitis B infection in Singapore. 179 64

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.
 ...
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

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.
 ...
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.
 ...
PMID:Diagnosis of acute rejection in liver transplantation. 304 94

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.
 ...
PMID:[Changes of gluconeogenesis and alanine metabolism following partial hepatectomy in normal and cirrhotic rats]. 339 28

The subcellular localization of alanine-glyoxylate aminotransferase (EC 2.6.1.44 L-Alanine: glyoxylate aminotransferase) of adult human liver was examined by sucrose density gradient centrifugation. The enzyme sedimented at the same density as catalase, indicating that it was localized in the peroxisomes. Alanine-glyoxylate aminotransferase activity in the liver of patients with cirrhosis was about 65% of that of normal liver or 71% of that from patients with chronic hepatitis, but its activity in the serum of patients with cirrhosis was higher than that from patients with chronic hepatitis. Patterns of activity of alanine-glyoxylate aminotransferase in liver and serum differed from those of aspartate-2-oxoglutarate aminotransferase and ornithine carbamoyltransferase that have a different intracellular location. Serum immunoreactive alanine-glyoxylate aminotransferase (Im-AGT) was measured by enzyme-linked immunoadsorbent assay (ELISA). The Im-AGT levels (mean +/- SEM) in acute (80 +/- 13 micrograms/L) and chronic (72 +/- 4 micrograms/L) hepatitis were higher than those of normal controls (44 +/- 1 micrograms/L). However, the difference between acute and chronic hepatitis was not statistically significant. The level in liver cirrhosis (54 +/- 3 micrograms/L) was lower than those of the hepatitides but higher than that of normal controls. The apparent half-life of serum Im-AGT of patients who underwent liver lobectomy by a microwave tissue coagulation method was approximately 3-4 days.
 ...
PMID:Peroxisome localized human hepatic alanine-glyoxylate aminotransferase and its application to clinical diagnosis. 405 44

Splanchnic arteriovenous differences for several intermediary metabolites of carbohydrate and lipid metabolism were determined simultaneously with hepatic blood flow in seven normal subjects, eight patients with cirrhosis, and six patients with cirrhosis after surgical portosystemic shunt ( SPSS ) after an overnight fast. Arteriovenous differences in the legs were also determined together with flux measurement. The individual turnover rates of acetoacetate (AcAc) and 3 hydroxybutyrate (beta OHB) were also determined by means of isotopic techniques. Splanchnic gluconeogenic precursors and FFA uptakes were lower in cirrhotic patients with SPSS than in normal subjects (P less than 0.05 and P less than 0.01, respectively). Splanchnic triglyceride output was also lower in cirrhotic patients with SPSS than in normal subjects (P less than 0.01), whereas no significant differences were found for AcAc, beta OHB, and glucose release. In the group of cirrhotic patients without SPSS , those patients with negligible signs of portal systemic shunt and normal splanchnic blood flow had uptake of gluconeogenic precursors and of FFA normal or higher than that of normal subjects, whereas those patients with signs of spontaneous portal systemic shunt behaved like cirrhotic patients with SPSS . Alanine release from the leg was lower in both cirrhotic patient groups. Tracer determined hepatic output of AcAc and beta OHB was higher in cirrhotic patients with SPSS (P less than 0.05). Plasma clearance rates of AcAc and beta OHB were significantly elevated in both cirrhotic patient groups. Close agreement was found between tracer and catheterization techniques in the evaluation of ketone body production in cirrhotic patients with SPSS , whereas in cirrhotic patients without SPSS tracer determined hepatic output was slightly lower, possibly because of extrahepatic splanchnic tissue ketone body uptake. In conclusion, our data in patients with cirrhosis indicate that: 1) splanchnic uptake of gluconeogenic precursors and of FFA was related to the degree of portal systemic shunt, e.g. to the degree of effective hepatic blood flow; 2) liver triglyceride but not ketone body output was decreased by the impaired FFA (and glycerol) liver uptake; 3) the higher circulating levels of gluconeogenic precursors (except alanine) and of FFA appeared at least partially due to lower hepatic removal of these metabolites; and 4) peripheral use of ketone bodies was increased and alanine release from the leg reduced in patients with cirrhosis.
 ...
PMID:Carbohydrate and lipid metabolism in cirrhosis. Evidence that hepatic uptake of gluconeogenic precursors and of free fatty acids depends on effective hepatic flow. 637 11

beta-Blockers are widely used to prevent gastrointestinal hemorrhage in cirrhosis. The metabolic effects of treatment are scarcely studied: hepatic function reportedly does not change significantly, but beta-adrenoceptors have been reported to regulate protein and amino acid metabolism. We studied hepatic nitrogen metabolism in response to constant alanine infusion in seven patients with cirrhosis before and 7 to 10 days after treatment with oral propranolol (60 to 100 mg/d). Beta-blockade was effective: it decreased heart rate by 25%, abolished orthostatic tachycardia, and reduced portal blood flow by 20%. Alanine-stimulated urea nitrogen synthesis rate (UNSR) was higher in patients with propranolol treatment, without any difference in aminonitrogen concentration. The kinetics of hepatic conversion of amino acid nitrogen into urea--ie, functional hepatic nitrogen clearance (FHNC)--increased by 30%, from (mean +/- SD) 17.0 +/- 4.1 to 22.0 +/- 6.6 L/h (P < .01). Increased urea production during alanine infusion resulted in negative nitrogen exchange even at the peak of alpha-aminonitrogen concentration. Basal insulin level was only slightly reduced during propranolol treatment, whereas the insulin response to alanine was significantly blunted. No differences in glucagon and cortisol were demonstrated. Epinephrine and norepinephrine levels were high-normal and did not vary after treatment. Increased urea production and stimulation of hepatic nitrogen clearance during beta-blockade may be mediated by relative hypoinsulinemia or by direct involvement of beta-adrenoceptors in the control of nitrogen metabolism, possibly by regulation of amino acid uptake and release in peripheral tissues.
 ...
PMID:Effects of beta-blockade on hepatic conversion of amino acid nitrogen and on urea synthesis in cirrhosis. 761 49

Among 211 patients who, between 1985 and 1990, underwent liver resection in Kyushu University Hospital, uncontrollable ascites occurred in 53 (25%). A univariate analysis revealed that postoperative death with liver failure occurred more frequently in patients with intractable ascites (p < 0.05). Alanine amino transferase levels were significantly higher in patients with intractable ascites (p < 0.05), but serum bilirubin, alkaline phosphatase and serum albumin levels did not differ significantly. Portal pressure (p < 0.05), the operation time (p < 0.01) and blood loss (p < 0.01) were significantly higher in patients with intractable postoperative ascites. A multiple analysis showed a correlation between the operation time, portal hypertension and postoperative intractable ascites. Postoperative histology revealed that a larger number of patients with cirrhosis had intractable ascites (p < 0.05). We conclude that cirrhosis, portal pressure and operating time are the most important factors related to intractable ascites in the case of hepatectomy. Areas of the liver to be resected should be limited in cirrhotic patients with portal hypertension.
 ...
PMID:Liver resection and intractable postoperative ascites. 846 21

Open (OC) or laparoscopic (LC) cholecystectomy is considered a relative contraindication in patients with liver cirrhosis. The effect of LC and OC on the hepatic catabolic stress response was studied in patients with postnecrotic liver cirrhosis and chronic hepatitis to define the most suitable procedure from a metabolic point of view. Altogether 14 patients with cirrhosis and 14 with chronic hepatitis were randomized to LC or OC (n = 7 in each group). The increase in the functional hepatic nitrogen clearance (FHNC) was quantified. Changes in glucose, insulin, glucagon, cortisol, epinephrine, norepinephrine, and prostaglandin E(2) (PGE(2)) were observed. There was no difference in FHNC between LC and OC in any of the patients. Among cirrhotic patients OC caused a 132% increase in FHNC (p < 0.05) and among the hepatitis patients a 69% increase (p < 0.05). In contrast, there was no significant increase following LC in any of the patients. OC increased fasting glucose and insulin in the hepatitis patients (p < 0.01 and p < 0.001, respectively) and in the cirrhosis group (p < 0.01 and p < 0.05, respectively). Alanine stimulation increased glucose in hepatitis patients after OC (p < 0.05) and after LC (p < 0.01). Stimulated glucagon increased after OC in the hepatitis group (p < 0.05). During stimulation cortisol was higher following LC in hepatitis patients (p < 0.01) and cirrhotic patients (p < 0.05). Fasting PGE(2) was down-regulated after LC in hepatitis patients (p < 0.05) and cirrhotic patients (p < 0.01) and after OC in the hepatitis group (p < 0.001). FHNC is similar after LC and OC. Thus from a metabolic point of view, LC has no advantage over OC.
 ...
PMID:Postoperative hepatic catabolic stress response in patients with cirrhosis and chronic hepatitis. 1065 74


1 2 Next >>