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)

An electrophoretically slow-moving band of alkaline phosphatase (ALP) isoenzyme was found in four patients with chronic liver disease and in one with ulcerative colitis. Immunoelectrophoretic studies revealed that the slow band was a complex containing alkaline phosphatase and an immunoglobulin G of the lambda class. Its molecular weight was approximately 280 000. A complex molecule consisting of one molecule of immunoglobulin G and one molecule of alkaline phosphatase was proposed. The complex was similar to the liver and bone alkaline phosphatases in functional properties. Serum containing the complex was capable of binding liver and bone alkaline phosphatase isoenzymes but not the intestine or placenta alkaline phosphatase isoenzymes from normal controls. The presence of an abnormal immunoglobulin which binds liver and bone alkaline phosphatases appears to be responsible for the development of the complex. In one case of chronic liver disease, the complex disappeared after a few months.
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PMID:Formation of an alkaline phosphatase-immunoglobulin G complex in human sera. 48 7

The clinical course is reported in 17 patients in whom the histological picture of subacute hepatic necrosis ("bridging hepatitis") was found on needle liver biopsy or at autopsy. The patients' ages ranged from 10-71 years, 12 patients being less than 40 years old. Ten patients were males. Jaundice lasted 2-4 months in nine cases and over six months in two, one of the latter having developed cirrhosis. In five patients a relapse of jaundice occurred within three months. Hepatitis B antigen was found in one of 13 patients tested. Two patients died in fulminant hepatic failure, one developed cirrhosis. These three patients and an additional two received prednisone therapy. Twelve of the remaining patients were followed for periods of 8-81 months; an additional two patients' follow-up was incomplete. None developed clinical evidence of chronic liver disease, and laboratory data at the last examination were normal except for slight elevation of alkaline phosphatase in six cases. Repeat biopsies showed persistent hepatitis in one case, slight portal fibrosis in one, cirrhosis in one and at autopsy in a patient who died of unrelated causes two years after hepatitis no evidence of chronic liver disease was found. This relatively good outome of subacute hepatic necrosis is probably due to the young average age of the patients, and the low incidence of B hepatitis in this series.
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PMID:The clinical course of subacute hepatic necrosis. 74 11

Fasting serum bile acid (SBA) was measured by the enzymic fluorimetric method coupled with the NAD-resazurin system in 23 controls, 35 asymptomatic carriers of HIs antigen including 4 e antigen carriers and 91 patients with various liver diseases. All GHBs and e antigen carriers showed SBA within the normal range. SBA was most significantly correlated with serum bilirubin (gamma=0.74) and was a more sensitive index for impaired liver function than bilirubin or alkaline phosphatase in 164 radomly chosen samples from the liver disease group. In serial determinations of SBA with reference to GOT, GPT, changing patterns of these two parameters were classified into the parallel type and the discrepant type. Thirty two out of 40 cases with chronic liver disease belonged to the parallel type. SBA remained abnormal even after the normalization of transaminase in 12 out of 20 resolving episodes in cases of the parallel type, regardless of diagnosis. Since SBA changes according to the stage of the disease activity, serial and simultaneous estimation of SBA and GOT, GPT was found to be helpful in the observation of liver diseases. Maximum values of SBA elevation in an endogenous bile acid tolerance test after eating two egg yolks were higher than controls in 4 out of 7 cases with liver disease, who were associated with normal fasting SBA.
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PMID:Evaluation of fluorimetrically estimated serum bile acid in liver disease. 84 3

Primary biliary cirrhosis is a rare chronic liver disease in Taiwan, which eventually causes mortality. As yet, no safe and effective treatment has been found. To investigate the safety and therapeutic efficacy of recently introduced ursodeoxycholic acid (UDCA) in the treatment of primary biliary cirrhosis, an uncontrolled trial was conducted in 6 patients in the early stages (I-II) and 5 patients in the late stages (III-IV). Five patients in stage I and one patient in stage II were treated with 10-15 mg/kg/day UDCA for a mean administration period of 13 +/- 9 months. Levels of laboratory tests including serum alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) improved significantly within one month and were sustained at the new lower levels for the period of observation. The symptoms of one patient with pruritus were reduced after long-term therapy. No major side effects were found during the treatment period. In contrast to early-stage patients, patients with late-stage primary biliary cirrhosis who received UDCA therapy for a mean duration of 25 +/- 5 months showed no beneficial effects either clinically or biochemically. From these preliminary results, UDCA appears to be safe and effective in the treatment of early-stage primary biliary cirrhosis, although further controlled clinical trials in conjunction with histological follow-up are mandatory to evaluate the critical role of UDCA in primary biliary cirrhosis.
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PMID:Therapeutic effect of ursodeoxycholic acid on early-stage primary biliary cirrhosis. 168 79

Serum level of osteocalcin (OC) is believed to be a specific biochemical parameter of bone formation. Decreased serum OC has been reported in alcohol-intoxicated subjects, in patients with primary biliary cirrhosis and in patients with chronic alcoholic liver disease. The question was, whether lower OC level could be detected in patients with nonalcoholic and non-cholestatic chronic liver disease. The serum OC was measured by RIA developed in our laboratory. Results were compared to age and sex matched controls. Decreased OC level was found in 35 out of 47 (74%) patients with non-alcoholic and non-cholestatic liver disease as chronic persistent hepatitis, chronic active hepatitis, fatty liver and cirrhosis, in 21 out of 26 (80%) patients with alcoholic liver disease and in 8 out of 15 (53%) primary biliary cirrhosis. None of the patients had elevated value. There was no correlation between the decreased OC level and the duration or severity of the liver disease and the laboratory parameters as bilirubin, AST, ALT, alkaline phosphatase, albumin, prothrombin, and serum 25-OH-D3 vitamin level. Decreased OC was found also in the patients without cirrhosis. The possible causes are discussed. Relying upon these findings it is supposed that chronic liver disease by itself can influence the osteoblast activity also by some unknown mechanism.
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PMID:[Decreased serum osteocalcin level in non-alcoholic and alcoholic chronic liver diseases]. 185 6

The medical records and liver biopsies of nine sickle cell patients with chronically elevated liver function tests were retrospectively reviewed to determine the etiology of chronic liver disease. There were eight women and one man with a mean age of 30 yr. All patients had hemoglobin SS. Eight patients were referred for elevated aminotransferases and one for an elevated alkaline phosphatase. Hemosiderosis was present in all of the biopsies. Two patients had cirrhosis. Chronic hepatitis was noted in two patients, and five patients had cholestasis. Two patients had serologic markers demonstrating HBV exposure but no patients were HBsAg positive. Erythrophagocytosis, sinusoidal dilatation, and Kupffer cell hyperplasia were present in all of the liver biopsies. Transfusion-related causes were the most common significant pathologic findings in our patients, and appeared to be the etiologies of chronic liver disease in sickle cell patients.
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PMID:Transfusion-related chronic liver disease in sickle cell anemia. 188 2

To identify the types of liver disease in which osteopenia is a prominent feature and to understand the mechanisms of bone loss, bone mineral density was measured in the lumbar spine and hip, bone alkaline phosphatase, osteocalcin, and biochemical markers of calcium homeostasis were measured in 42 women, aged 33 to 52, with chronic liver disease and in 299 healthy women of similar age. In control women, bone alkaline phosphatase and osteocalcin correlated negatively with bone density at all sites (p less than 0.05). In women with liver disease, osteocalcin correlated negatively with bone density in the lumbar spine (p less than 0.007), whereas bone alkaline phosphatase did not correlate with bone density at any site. Bone alkaline phosphatase correlated positively with osteocalcin in control women (p = 0.001) and negatively with osteocalcin in women with liver disease (p = 0.03). Serum bone alkaline phosphatase in women with liver disease was increased significantly over serum bone alkaline phosphatase of control women, probably because of decreased clearance owing to defective function or decreased numbers of hepatic asialoglycoprotein receptors. Bone density was lower in the lumbar spines and hips of women with primary sclerosing cholangitis, primary biliary cirrhosis, and chronic active hepatitis or fibrosis without cirrhosis than in the lumbar spine and hips of control women. However, the differences were not significant, possibly because of the small sample size. It is concluded that, in liver disease, osteocalcin is a more reliable marker of osteoblastic function than bone alkaline phosphatase. Although our results show that bone density may decrease in women with cholestatic liver disease, larger studies are needed to determine the degree of osteopenia.
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PMID:Osteocalcin and bone alkaline phosphatase in the serum of women with liver disease. 195 79

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.
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PMID:[Estimation of portal pressure using the theory of quantification]. 201 41

Recent studies have established the clinical efficacy of S-adenosyl-L-methionine (SAMe) in the treatment of cholestasis associated with hepatic diseases, pregnancy and the administration of estrogen-containing oral contraceptives. In 4 clinical trials involving a total of 639 patients with cholestasis due to acute or chronic liver disease, SAMe in an intravenous dose of 800 mg/day or an oral regimen of 1.6 g/day for 2 weeks was superior to placebo in relieving the symptom of pruritus and in restoring serum total bilirubin and serum alkaline phosphatase towards normal. The drug is also effective in intrahepatic cholestasis of pregnancy (ICP), with intravenous administration of 800 mg/day for 2 weeks producing a substantial reduction in pruritus and an improvement in abnormal liver function indices. Moreover, SAMe treatment decreases the incidence of premature labour. SAMe appears to be the first safe and effective approach to the treatment of this syndrome, and also protects against the adverse hepatic effects of small doses of estrogen in patients with a history of ICP by normalising liver biochemistry and the oversaturated biliary lipid composition of the gallbladder bile. In animal models, SAMe reverses the pathological liver changes induced by xenobiotics such as taurolithocholate and alpha-naphthyl-isothiocyanate (ANIT) and the antipsychotic chlorpromazine. Several cooperative mechanisms appear to underlie the anticholestatic action of SAMe, the most important being the restoration of normal hepatocyte membrane fluidity and Na+, K+ ATPase activity, through a reversal of the reduction in phospholipid methylation produced by hepatotoxic agents. In addition, SAMe may act by promoting trans-sulphuration pathway reactions and consequently improving the detoxifying capacity of this metabolic system.
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PMID:Role of S-adenosyl-L-methionine in the treatment of intrahepatic cholestasis. 208 76

Parenteral S-adenosylmethionine proved to be effective in reversing intrahepatic cholestasis in pregnant women. Based on these findings, a prospective multicenter, double-blind, placebo-controlled trial was planned to assess whether oral S-adenosylmethionine is effective in cholestatic patients with chronic liver disease. Accordingly, 220 inpatients (26% chronic active hepatitis, 68% cirrhosis, 6% primary biliary cirrhosis) with stable (1 month or more) at least twofold increases in serum total and conjugated bilirubin and alkaline phosphatase volunteered for the trial. Serum markers of cholestasis significantly (P less than 0.01) decreased after oral S-adenosylmethionine administration (1600 mg/day), and their values were significantly (P less than 0.01) lower than the corresponding values in the placebo group. S-adenosylmethionine significantly (P less than 0.01) improved subjective symptoms such as pruritus, fatigue, and feeling of being unwell, whereas placebo was ineffective. Two patients in the S-adenosylmethionine group and 9 controls (P less than 0.05) withdrew from the trial for reduced compliance because of inefficacy of treatment. Oral S-adenosylmethionine was tolerated to the same extent as placebo. In conclusion, short-term administration of oral S-adenosylmethionine is more effective than placebo in improving clinical and laboratory measures of intrahepatic cholestasis and offers a new therapeutic modality for the symptomatic management of this syndrome.
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PMID:Oral S-adenosylmethionine in the symptomatic treatment of intrahepatic cholestasis. A double-blind, placebo-controlled study. 218 71


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