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: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to compare the clinical and immunological characteristics of the hepatitis B surface antigen (HBsAg)-positive and HBsAg-negative (cryptogenic) forms of chronic active hepatitis. The data of 48 patients with chronic active hepatitis, 24 with persistent HBs antigenemia and 24 without HBsAg, were analysed. HBsAg was detected by counter-immunoelectrophoresis and radioimmunoassay. The clinical features, biochemical liver function tests, immunoglobulins, complement C3, antoantibodies, and cell-mediated immunoreactivity of the two forms of the disease were compared. Cirrhosis was found to occur more frequently at the time of diagnosis in the HBsAg-negative group, and the serum alkaline phosphatase level was raised significantly compared to the HBsAg-positive form. The elevation of the IgG level was greater in the cryptogenic form, but the difference was not statistically significant compared to the HBsAg-positive patients. There was a marked difference in the frequency of the mitochondrial antibodies, but not of the antinuclear factor and other autoantibody-like serum factors. Lymphoblastic transformation revealed a similar diminution in response to phytohaemagglutinin stimulation in both groups of patients compared to the normal controls. An increase of the 3H-thymidine incorporation was seen after stimulation with human liver mitochondrial antigen, and leukocyte migration inhibition could be observed with this antigen in both forms of chronic active hepatitis.
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PMID:Chronic active hepatitis in patients with and without hepatitis B surface antigenemia. 91 64

(1) Liver cirrhosis was induced in male rats by treatment with carbon tetrachloride and phenobarbitone for 130-142 days. Detailed histological examination showed all livers from rats treated with carbon tetrachloride had annular fibrosis, necrosis, loss of normal hepatic architecture and other features that were consistent with an established micronodular cirrhosis. (2) Plasma biochemical analysis showed a significant reduction in total protein concentration (13%), which was due entirely to a reduction in plasma albumin (29%). There were also large increases in the plasma activities of alkaline phosphatase (110%) and aspartate aminotransferase (159%), when compared to phenobarbitone-treated controls. Plasma cholesterol was also increased (67%), but other plasma analytes were not significantly altered. (3) The soleus (Type I), plantaris (Type II) and gastrocnemius (Types I and II) muscles were dissected and examined for possible differential effects. There were minor reductions in all three muscle weights, but these changes did not reach statistical significance. The protein, RNA and DNA concentrations, total muscle content and content relative to body weight in cirrhotic rats were also not significantly altered in any of the muscles. Cirrhosis did not cause any perturbations in derived parameters, i.e. amount of synthetic apparatus per cell, RNA/DNA ratio, apparent cell size, protein/DNA ratio and the capacity for protein synthesis or RNA/protein ratio. (4) The gastrocnemius was fractionated into soluble, stromal and myofibrillar proteins. The concentrations and contents of all three proteins were unaltered in cirrhotic animals, compared to controls. (5) It is concluded that in this experimental model of cirrhosis there were no effects on those skeletal muscle variables which are strikingly altered by chronic alcohol feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver histology, blood biochemistry and RNA, DNA and subcellular protein composition of various skeletal muscles of rats with experimental cirrhosis: implications for alcoholic muscle disease. 170 23

Portal hypertension with varices developed in 18/675 patients with chronic myeloid leukaemia (CML) in a randomized trial comparing busulphan with busulphan and thioguanine. All 18 had received the drug combination and none busulphan alone (P less than 0.0001). Ascites was also seen significantly more often in the combination arm (P less than 0.05). These results strongly suggest that the addition of thioguanine was responsible for the development of portal hypertension. The histological features were predominantly those of non-cirrhotic portal hypertension--either idiopathic portal hypertension with minimal morphological abnormalities, nodular regenerative hyperplasia or in two cases leukaemic infiltration only was noted. Cirrhosis was present in 3/16 cases studied. Both treatment groups developed abnormal liver function tests during the chronic phase, but particularly with progression of the disease. During chronic phase abnormalities were significantly more frequent in those receiving busulphan and thioguanine-alkaline phosphatase (P less than 0.02), transaminases (P less than 0.04), bilirubin (P less than 0.05), multiple abnormalities (P less than 0.01). The development of portal hypertension was often associated with abnormalities of these tests; however, lack of specificity precludes their use as a predictor of subsequent clinical problems. Thioguanine confers no survival advantage in this disease. In view of its hepatotoxicity it should not be used routinely for maintenance of control in chronic phase CML.
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PMID:Thioguanine used in maintenance therapy of chronic myeloid leukaemia causes non-cirrhotic portal hypertension. Results from MRC CML. II. Trial comparing busulphan with busulphan and thioguanine. 195 75

We studied a consecutive series of 204 patients who were admitted to a hospital for addictive diseases during 40 months and who had a liver biopsy. Parenteral drug abusers (n = 34) were significantly younger than alcohol abusers (n = 23) or abusers of both (n = 147) and had lower levels of serum alkaline phosphatase, total bilirubin, and aspartate aminotransferase than the other two groups. Chronic active hepatitis and chronic persistent hepatitis were more frequent (p less than 0.001) in abusers of parenteral drugs alone, whereas cirrhosis was found most often (p less than 0.001) in abusers of both alcohol and parenteral drugs. Cirrhosis was present in 10 of 39 (26%) simultaneous abusers of alcohol and parenteral drugs compared with 58 of 96 (60%) alcohol-abusing former parenteral drug abusers (p less than 0.001). Methadone maintenance treatment was not associated with cirrhosis. Thus, methadone-maintained patients who abuse alcohol and develop cirrhosis should remain in methadone maintenance treatment and receive concomitant alcoholism treatment. Also, these data further support the hypothesis that abusers of both alcohol and parenteral drugs have an increased risk of developing cirrhosis.
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PMID:Chronic liver disease in abusers of alcohol and parenteral drugs: a report of 204 consecutive biopsy-proven cases. 354 73

A standardized clinical, laboratory, and histological assessment was carried out on 85 patients with primary biliary cirrhosis within 1 year of developing symptoms. Presenting symptoms included pruritus (n = 30), jaundice (n = 9), variceal bleeding (n = 6), ascites (n = 5), fatigue (n = 4), and abdominal pain (n = 4). Ten patients had symptoms not immediately suggestive of hepatic etiology and a further 17 were asymptomatic, the diagnosis being made fortuitously. Eighty four percent were not incapacitated and 52 were anicteric. Less than half were pigmented, 22% had xanthoma, and only 12% were deeply jaundiced. In contrast, all had significant laboratory abnormalities with alkaline phosphatase activity greater than 400 IU/L in 60% and IgM greater than 2.5 g/L in 75%. Mitochondrial antibody was detectable in 83% with a titer greater than 1:160 in 70%. Cirrhosis was present in 24 patients, nine of whom were anicteric and a further 11 had fibrosis or scarring.
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PMID:Early features of primary biliary cirrhosis: an analysis of 85 patients. 400 76

An experimental animal model designed specifically to simulate liver fibrosis and cirrhosis in childhood is described. Phenobarbitone was administered continuously from the 4th day of life and carbon tetrachloride intermittently from the 13th day to developing rats for 10 weeks. Treated animals showed hepatic necrosis, hepatic regeneration and a progressive increase in hepatic fibrosis; cirrhosis developed before the animals reached sexual maturity at 72 days or were fully grown. Hepatic prolyl hydroxylase activity increased to a maximum level after 20 days of treatment, before increased hepatic collagen could be detected, and fell to a lower level as cirrhosis became established. Serum activities of alkaline phosphatase, aspartate aminotransferase and alanine aminotransferase gave a similar pattern, a marked increase at 20 days of age followed by a fall to near normal levels as hepatic damage became more severe. By the 26th day of life hepatic collagen levels were increased significantly and rose thereafter progressively as fibrosis became more widespread throughout the liver. Cirrhosis developed between the 38th and 75th days. Cirrhosis remained 10 weeks after discontinuation of treatment with phenobarbitone and carbon tetrachloride treatment.
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PMID:Carbon tetrachloride-induced hepatic fibrosis and cirrhosis in the developing rat: an experimental model of cirrhosis in childhood. 630 21

Liver damage was produced in male Wistar rats aged 15 weeks by daily oral administration of 40 mg/kg thioacetamide over a period of 24 weeks. All of the animals were weighed once a week. Furthermore, the duration of hexobarbital anaesthesia and the activities of the enzymes ASAT, ALAT, GIDH, LDH, LAP and alkaline phosphatase in the serum were determined in 6 experimental and 4 control animals after 3 d and 1, 2 and 4 weeks, and then at intervals of 4 weeks. For the purpose of comparison the same investigations were performed (under identical experimental conditions) both in rats fed normally and rats starved for 24 h to which a single dose of thioacetamide was applied. The histological study of the livers revealed destruction of the lobule architecture and profuse bile-duct proliferations after 12 weeks. Cirrhosis was observed after 16 weeks. The activities of ASAT, ALAT, GIDH and LDH increased for a short time and then returned closely to normal. During the whole experimental period, the LAP and alkaline phosphatase activities remained in the pathological range, as well as the duration of hexobarbital anaesthesia. Enzyme diagnosis is not suitable for assessing the degree of severity of a liver damage produced by thioacetamide.
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PMID:[Enzyme activities in the blood serum from rats with chronic liver damage. part 3: Effect of thioacetamide]. 686 88

Mastocytosis is a disease of mast cell hyperplasia that may involve several organ systems, including liver. Between 1988 and 1991, we conducted a retrospective-prospective study of 41 patients with mastocytosis and found 61% had evidence of liver disease. Hepatomegaly was detected in 24%, splenomegaly in 41%, and elevated serum alkaline phosphatase, serum aminotransaminases, 5'nucleotidase, or gamma-glutamyltranspeptidase (GGTP) in 54% of the patients. Alkaline phosphatase levels directly correlated with GGTP levels, hepatomegaly, splenomegaly, and liver mast cell infiltration and fibrosis. Elevated alkaline phosphatase levels and splenomegaly were observed more frequently in patients with categories II and III mastocytosis. Five patients in combined disease categories II or III developed ascites or portal hypertension and died of complications of mastocytosis; three had hypoprothrombinemia at the time of death. Thirty-five liver biopsy specimens from 25 patients were examined. Mast cell infiltration was commonly observed in the biopsy specimens, more severe in those patients with either category II or III disease, and correlated with hepatomegaly, splenomegaly, alkaline phosphatase levels, and GGTP levels. Mast cells were often only detected by using special stains (toluidine blue and chloracetate esterase). Increased portal fibrosis was seen in 68% of the biopsy specimens and correlated with mast cell infiltration and portal inflammation. Cirrhosis was not observed. Nodular regenerative hyperplasia, portal venopathy, and venoocclusive disease was observed in eight biopsy specimens and may have been the cause of the portal hypertension or ascites in four patients. These findings demonstrate that liver disease with mast cell infiltration is a common finding in patients with mastocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic involvement in mastocytosis: clinicopathologic correlations in 41 cases. 755 67

Investigations of liver function and histology were undertaken in thirty four patients with Fibrocalculous Pancreatic Diabetes (FCPD). The data obtained were compared with those of similarly aged members of a diabetic control group comprising twelve patients with Protein Deficient Diabetes Mellitus (PDDM), twelve with Type 1 diabetes or Insulin Dependent Diabetes Mellitus (IDDM) and four young patients with Type 2 Diabetes of Non-Insulin Dependent Diabetes Mellitus (NIDDM). None of them had apparent past or present liver disease. Elevations of serum ALT (SGPT) and alkaline phosphatase levels were fairly common and was often associated with mild fatty changes and occasionally with focal necrosis and inflammatory changes. Cirrhosis and inflammatory changes per se were infrequent and fatty changes per se did not occur. In contrast patients belonging to the other diabetic subsets were very occasionally afflicted with hepatic abnormalities or not afflicted at all. We propose that loss of hepatotrophic actions mediated by insulin and glucagon could initiate and/or enhance hepatic abnormalities in FCPD where deficiencies of insulin and glucagon coexist.
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PMID:Observations on hepatic structure and function in fibro-calculous pancreatic diabetes (FCPD) vis-a-vis other diabetic subtypes. 967 Jun 24

The files of 122 patients hospitalized for hepatocellular carcinoma (HCC) were reviewed retrospectively to study survival as a function of treatment and different peri-therapeutic factors. Cirrhosis was certain or probable in 69 cases. Laparotomy was performed 77 times (13 exploratory, 64 excisions). Chemoembolization with Adriamycine was performed 18 times. Median survival was 11.6 months. The factors influencing survival in monovariate analysis were the Child-Pugh stage (p < 0.0001), the Okuda stage (p < 0.0001), ascites (p < 0.001), a post-operative complication (p < 0.0001), gamma-glutamyltransferase level (p < 0.0037), tumor site (p < 0.004), albuminemia (p < 0.008), alkaline phosphatase concentration (p < 0.0087), number of tumors (p < 0.01), portal thrombosis (p < 0.01) and alpha-foetoprotein level (p < 0.01). In multivariate study, the Okuda stage (p < 0.001), age (p < 0.001) and portal thrombosis (p < 0.037) remained significant. The Okuda 1 group was also considered in multivariate study, in which case only patient age and the possibility of therapeutic excision were significant factors. In our opinion, the Okuda classification, which is easy to establish, should be adopted for pretherapeutic evaluation of patients with hepatocellular carcinoma.
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PMID:[Uni- and multivariate analysis of predictive survival factors in hepatocellular carcinoma. A study of a series of 122 patients]. 968 58


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