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)

Furosemide is frequently used for ascites and causes adverse reactions (AR). In an intensive prospective drug monitoring study of 1,920 patients, 172 (8.9%) had cirrhosis of the liver and received furosemide. Mean age was 53 years, and 66.3% were male; and 87% had alcoholic cirrhosis. Eighty-eight (51.2%) had 221 events that by consensus of the monitoring team and attending physicians were either definitely of probably related to furosemide. No AR was fatal but 24% of patients had severe reactions. Almost all reactions were dose-related (96%). The most common were electrolyte disturbances (23.3% of patients) and volume depletion (14%). Furosemide-induced coma occurred in 20 (11.6%) patients and was more frequent in patients with prior hepatic encephalopathy (p less than 0.0005). Higher total doses (p less than 0.001), hyerbilirubinemia (p less than 0.05), prolonged prothrombin time (p less than 0.02), and longer hospital stay (p less than 0.001) were associated with higher frequencies of AR to furosemide. The frequency of hypokalemia did not decrease when potassium chloride or potassium-sparing diuretics were added to furosemide therapy. Frequdncy of AR did not correlate with age, sex, renal impairment, serum albumin, transaminase, or alkaline phosphatase.
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PMID:Furosemide-induced adverse reactions in cirrhosis of the liver. 75 67

Diversion of portal blood in congenital portosystemic shunts (CPSS) results in liver atrophy and passage of toxins into the systemic circulation causing hepatic encephalopathy. In some dogs, there is indirect evidence for hepatic insufficiency, but histologic findings are equivocal. This study determined whether hepatocyte integrity in PSS is comprised at a subcellular level using analytical subcellular fractionation of liver biopsies. Six dogs with CPSS had hypoproteinemia (6/6), increased serum alkaline phosphatase (6/6) and alanine aminotransferase (4/6) activity, hypocholesterolemia (6/6), and decreased blood urea (2/6). Liver biopsy specimens had increased activities (mU/mg protein) of alkaline phosphatase (17.9 +/- 10.1; controls 5.1 +/- 5.3: P less than 0.01), but not of other plasma membrane enzymes. There were increased activities of endoplasmic reticular (neutral alpha-glucosidase: 1.67 +/- 0.7; controls 0.86 +/- 0.2: P less than 0.01) and lysosomal enzymes (N-acetyl-beta-glucosaminidase: 12.6 +/- 2.3; controls 6.24 +/- 2.7: P less than 0.01; alpha-mannosidase: 0.85 +/- 0.5; controls 0.39 +/- 0.3: P less than 0.05). Subcellular fractionation on reorientating sucrose density gradients showed a high-density peak of alkaline phosphatase suggestive of a specific increase in the biliary canalicular component of enzyme activity. Neutral alpha-glucosidase was shifted to denser fractions, indicative of an increase in the proportion of rough-to-smooth endoplasmic reticulum and consistent with enhanced synthesis of membranous enzymes. There was also evidence for increased fragility of intracellular organelles, particularly lysosomes. In contrast, histology showed either no abnormalities or minor degenerative changes compatible with hepatic underperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic organelle pathology in dogs with congenital portosystemic shunts. 161 98

Progressive changes in serum enzyme activity and liver histologic features were monitored in calves fed tansy ragwort (Senecio jacobaea)-contaminated pellets. The experiments were designed to simulate natural intoxicant ingestion conditions in relationship to the dose and duration of exposure to the toxic plant to correlate early laboratory diagnostic changes with the natural progression of the disease, thereby facilitating early diagnosis and intervention by veterinary clinicians. Eight calves were fed tansy ragwort and 4 additional calves served as controls. In group 1, 4 calves were continuously fed dried tansy ragwort mixed in a pelleted feed at a 5% concentration by dry weight until terminal liver disease developed. Serum liver enzyme (alkaline phosphatase, glutamate dehydrogenase, and gamma-glutamyltransferase) activities were monitored at weekly intervals in these calves and in the 2 controls. In group 2, 4 calves were fed the same contaminated feed for only 60 days, with return to normal feed for the duration of the trial. Two additional calves served as controls. Their liver enzyme activities were monitored every other week in conjunction with percutaneous liver biopsies. All 8 calves fed tansy ragwort-contaminated pellets developed terminal hepatopathy in either a chronic pattern (n = 6) or a chronic-delayed pattern (n = 2), with the onset of a moribund state or sudden death at 11 to 17 weeks and 27 to 51 weeks, respectively. The calves were euthanatized when classic terminal signs of hepatic encephalopathy first became evident. The clinicopathologic patterns of chronic and chronic-delayed toxicoses were typical of over 5,000 cases of field tansy toxicosis diagnosed at the diagnostic laboratory. Serum glutamate dehydrogenase was the first enzyme to increase in most animals, with a short-term increase to peak values followed by a rapid return to normal. This enzyme change was followed by increases in alkaline phosphatase and gamma-glutamyltransferase. Serum enzyme changes preceded development of recognizable histologic lesions. Vacuolar changes in hepatocyte nuclei, biliary hyperplasia, and fibrosis sequentially developed in liver biopsy specimens from each animal, whereas megalocytosis was not a predominant feature until necropsy. On the basis of our findings, we suggest that the optimal tests for diagnosis of pyrrolizidine alkaloid intoxication should consist of liver biopsy and determination of concurrent serum liver-enzyme activities.
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PMID:Serum liver enzyme and histopathologic changes in calves with chronic and chronic-delayed Senecio jacobaea toxicosis. 168 78

The pathophysiological changes occurring with increasing grade of encephalopathy were examined in 93 consecutive episodes in 44 patients with liver cirrhosis (37 posthepatic). The incidence of gastrointestinal bleeding and leukocytosis increased significantly when the grade advanced from 1 to 5. The following variables showed a trend for change that did not reach statistical significance: rising serum bilirubin, SGOT, and BUN levels; decreasing serum sodium and chloride levels; and increased incidence of infection. The mean values of the following variables were significantly different in 25 fatal episodes and 68 survivors, implicating a bad prognosis: high serum bilirubin, alkaline phosphatase, and BUN levels; low serum albumin, sodium, and chloride levels; and a higher incidence of severe infections (sepsis, infected ascitic fluid). Because increasing grade of encephalopathy is the most important factor in determining the prognosis of hepatic encephalopathy (mortality 0, 10, 5, 19, and 85 percent in grades 1 to 5, respectively), more efforts should be made to understand and prevent the pathophysiological changes associated with advancing grades of encephalopathy.
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PMID:Pathophysiological changes associated with increasing grade of hepatic encephalopathy. 324 14

The aim of this paper is to evaluate the relationships among the increase of serum bile acids (SBA) and other common liver function tests in subjects with liver cirrhosis. Our results show that SBA levels are well-correlated with the seriousness of the disease (classified according to Child's criteria), and with the presence of ascites, of oesophageal varices, of hepatic encephalopathy and with the gamma-globulin level. SBA also appear to be well-correlated with total bilirubinemia, and, at a lower extent, with cholesterolemia and albuminemia; no significant linear correlation was found among SBA and cholestasis (alkaline phosphatase, gamma-glutamyl-transpeptidase) or cytolysis (transaminases) indexes. In conclusion, the SBA increase in liver cirrhosis without evidence of cholestasis (as in our patients) seems to be related to liver cell reuptake disturbances and to the presence of porto-systemic shunts, with consequent alterations in entero-hepatic bile salt recirculation.
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PMID:[Serum bile acids in cirrhosis: correlation with liver function parameters and with the severity of the disease]. 367 66

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
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PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

The EEG, grades of hepatic encephalopathy, and biochemical indices of 16 beagles with portacaval anastomosis were recorded throughout their lives and correlations between these parameters were investigated. The degree of deterioration of some biochemical indices, such as the ammonia concentration, glutamate oxaloacetate transaminase and alkaline phosphatase activities in the plasma, and percentage loss of body weight showed a progressive increase parallel to the severity of the hepatic encephalopathy (HE) grade (grading scale O-IV), but other biochemical indices such as the concentrations of aromatic or branched-chain amino acids, the molar ratio of branched-chain to aromatic amino acids, or the total protein concentration in the plasma did not show such relationship. The SW ratio, an index of the incidence of slow-waves in the EEG, was calculated from frequency distribution histograms which were obtained by frequency analyses of EEG recordings. A slight but significant correlation was found between the SW ratio and the plasma ammonia concentration. In addition, the SW ratio consistently increased with increase in the HE grade, although the SW ratio in HE grade IV was below the normal range for beagles. These results show that only the ammonia concentration in the plasma correlates with deterioration of the HE grade and of the SW ratio, suggesting that changes in ammonia concentration in the plasma should be of diagnostic value in assessing changes in mental state and the EEG in patients with liver cirrhosis. The importance of ammonia in pathogenesis of HE is stressed.
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PMID:Correlation between electroencephalogram, hepatic encephalopathy grade, and biochemical indices in beagles with portacaval anastomosis. 400 21

Measurements of the key parameters of cholesterol homeostasis and the mass of the body pools of cholesterol were carried out in two patients with familial hypercholesterolemia (FH), one homozygote and one heterozygote, before and 28 and 18 months, respectively, after portacaval anastomosis (PCA). In both patients the procedure significantly reduced the plasma concentrations of total and low density lipoprotein cholesterol and the daily rate of whole body cholesterol and bile acid synthesis. In addition, PCA caused a net efflux of accumulated tissue cholesterol as demonstrated by reductions in the rapidly exchangeable and total exchangeable masses of body cholesterol. Shunt patency was verified by demonstration of increased bile acids in serum from fasting patients and from patients 2 hr after a meal and by increased plasma glucagon before and after arginine infusion. Other than a persistently increased level of serum alkaline phosphatase, liver function tests have fallen within the normal range in both patients; there has been no evidence of hepatic encephalopathy. In the homozygous patient there has also been a striking resolution in xanthoma size and distribution. These multiple effects on cholesterol homeostasis and pool sizes strongly suggest that PCA can reverse the progressive accumulation of cholesterol in body tissues of FH patients.
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PMID:Treatment of familial hypercholesterolemia by portacaval anastomosis: effect on cholesterol metabolism and pool sizes. 657 6

A newly recognized clinical and morphologic pattern of acute alcoholic liver disease is described. Twenty-one patients, having the hepatic morphologic features of alcoholic foamy degeneration, were retrospectively analyzed. All patients had a significant history of chronic alcoholism. Jaundice and hepatomegaly were usually present. Hepatic encephalopathy, ascites, bleeding esophageal varices, or functional renal failure occurred in less than 10%. Usually this was the first episode of decompensation. Laboratory studies revealed a pattern of very transiently marked elevation of serum aminotransferase and more prolonged elevation of alkaline phosphatase activity and bilirubin levels. In the majority of cases, leukocytosis was absent, and serum cholesterol was elevated. The laboratory profile differed significantly from that of acute sclerosing hyaline necrosis. Serologic markers of acute viral hepatitis A and B were absent. Needle biopsy specimens of the liver revealed intact lobular architecture except for 1 case of cirrhosis. The perivenular hepatocytes revealed foamy fatty change characterized by striking cell swelling with massive accumulation of microvesicular fat, bile pigment deposition in the cytoplasm, and no displacement of the nucleus to the periphery of the cell. Megamitochondria were frequently identified. Multiple foci of hepatocyte dropout without significant parenchymal neutrophilic exudation and delicate intrasinusoidal collagen fibers were present in the perivenular area. Macrovesicular fatty change coexisted to a variable degree. The affected hepatocytes had extensive disorganization of the organelles by electron microscopy and decreased or absent functional activity by enzyme histochemical staining. These changes appear to be a purely degenerative process without inflammatory reaction. All patients in the present series showed a rapid recovery upon abstaining from alcohol.
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PMID:Alcoholic foamy degeneration--a pattern of acute alcoholic injury of the liver. 682 80

Idiopathic hepatic fibrosis was diagnosed by liver biopsy in 15 young dogs, of which nine were German shepherds. Clinical signs included ascites, anorexia, weight loss and hepatic encephalopathy. Erythrocyte microcytosis was a consistent clinical feature, and clinical chemistry generally revealed hypoproteinaemia and high serum activities of alkaline phosphatase and, to a smaller extent, alanine aminotransferase. Fasting blood ammonia and serum bile acid concentrations were increased in most dogs examined, and all the dogs tested had prolonged retention of sulfobromophthalein at 30 minutes. Multiple acquired portosystemic shunts were revealed by laparotomy and/or portography. Non-inflammatory fibrosis was present to different degrees in all the dogs' livers, and on the basis of its predominant location these were classified as having central perivenous fibrosis, diffuse pericellular fibrosis or periportal fibrosis. The response to symptomatic treatment and anti-fibrotic therapy with glucocorticosteroids or colchicine was variable. Seven dogs died or were euthanased shortly after diagnosis, but one dog survived two-and-a-half years, and three dogs were still alive more than four years after the initial diagnosis.
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PMID:Idiopathic hepatic fibrosis in 15 dogs. 821 1


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