Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
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The rate of perinatal encephalopathy and the nature of its outcomes in relation to the syndrome of the acute period of the disease were studied in 102 children. Also examined were the cytochemical parameters of blood leukocytes, alkaline phosphatase of neutrophils, acid phosphatase of lymphocytes, succinate and alpha-glycerophosphate dehydrogenase of lymphocytes in prematurely born infants on the 8th-15th and the 30th-45th days of life. It has been ascertained that in addition to the comatose and convulsive syndromes the prognosis of the disease is the least favourable in the syndrome of total inhibition of the CNS in the acute period. Furthermore, the findings of the conducted study open the possibility of preliminary individual prognosis of the disease on the basis of the cytochemical picture at the end of the acute period.
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PMID:[Development of children with a history of perinatal encephalopathy]. 342 43

Hepatic metabolism is the primary process of elimination of propafenone. It therefore is important to understand the effect of altered liver function on the disposition and elimination kinetics of this drug. Patients with abnormal liver function probably will require treatment with propafenone for cardiac arrhythmias; an understanding of the relationship between liver function and the pharmacokinetics of propafenone will provide a rational basis for optimal dosage adjustments in these individuals. Our results demonstrate that both systemic clearance and bioavailability of propafenone are sensitive to variability in liver function. The bioavailability of propafenone is inversely related to the clearance of indocyanine green (ICG), whereas a direct relationship exists between systemic clearance of propafenone and ICG clearance. Comparisons of clinical parameters with the propafenone data yielded interesting results. An overall clinical grading of severity of liver disease based on the presence or absence of portal hypertension (i.e., varices and/or splenomegaly), prior encephalopathy, and ascites did not correlate well with propafenone results. However, albumin, total bilirubin, serum glutamic oxaloacetic transaminase (SGOT) concentrations and prothrombin time values correlated strongly with the overall results. No definite relationships with subjects' age; weight; and hemoglobin, alkaline phosphatase, lactic acid dehydrogenose, cholesterol, blood urea nitrogen, or creatinine levels were detected. These results demonstrate that moderate to severe liver disease significantly affects the absorption and disposition of propafenone. In patients with cirrhosis, and presumably other forms of hepatic dysfunction, careful adjustments of propafenone doses are needed to optimize therapy.
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PMID:Influence of hepatic dysfunction on the pharmacokinetics of propafenone. 369 82

To investigate the natural history of compensated cirrhosis, 293 consecutive patients without previous major complications (ascites, jaundice, encephalopathy or gastrointestinal hemorrhage) were studied in terms of morbidity (probability of developing decompensated cirrhosis during follow-up) and survival. Patients were diagnosed by liver histology between 1968 and 1980. Median follow-up was 63 months. Decompensation of cirrhosis was considered when a patient first developed one of the major complications of the disease. Ten years after diagnosis, the probability of developing decompensated cirrhosis and the survival probability rate were 58 and 47%, respectively. A multivariate survival analysis (Cox's regression model) using clinical, biochemical and histological data obtained at diagnosis disclosed seven factors that predicted prognosis: serum bilirubin; serum gamma-globulin concentration; hepatic stigmata; prothrombin time; sex; age, and alkaline phosphatase. According to the contribution of each one of these factors to the final model, a prognostic index was constructed that allows calculation of the estimated survival probability. The predicting value of this index was validated by a split sample testing technique.
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PMID:Compensated cirrhosis: natural history and prognostic factors. 380 91

A healthy twenty-month-old boy ingested a maximal dose of valproate from which about 750 mg/kg were absorbed. Cerebral coma, which lasted for twenty hrs, was followed by an undisturbed period of approximately sixteen hrs. Death from cardiorespiratory failure due to severe bronchopneumonia occurred 46.5 hrs after the ingestion of the drug. The serum valproic acid concentration reached a peak of 1061 micrograms/ml within three hours, and fifteen minutes before death it had fallen to 187 micrograms/ml. The half-life of 16.6 hrs was within the range usually found. Metabolic acidosis, hypernatraemia and hyperosmolarity could be corrected, unlike the hypocalcaemia, which developed later. Bilirubin, GOT, GPT, gamma-GT, alkaline phosphatase, blood glucose, diastase, urea, creatinine, haemoglobin as well as PT and PTT and the platelet count were all normal. Leucopenia with 1,600 per microliter developed only during the bronchopneumonial stage. The histo-pathological findings were acute hypoxic damage of the myocardium, kidneys and certain neurones of vulnerable areas of the brain (neuronal microvesiculation and tigrolysis) in addition to a severe cerebral oedema in the final stage. A morphological substrate of an acute valproate encephalopathy was not demonstrable. The liver showed no necrosis or cholostasis. The vertebral marrow was inconspicuous. All the results indicate that liver function was not impaired in spite of the initial maximal concentration of valproic acid. In all probability the patient might have survived the acute valproate intoxication had it not been for the bronchopneumonia.
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PMID:Acute valproate intoxication with fatal outcome in an infant. 393 45

Oral administration of manganese chloride (25 mg/kg b. w. daily) to monkeys for a period of 18 months produced congestion and marked increase in weight of testis. Histopathologic examination revealed interstitial oedema and degeneration of seminiferous tubules. Activities of succinic dehydrogenase, glucose-6-phosphate dehydrogenase and acid phosphatase were significantly inhibited whereas NADH-diaphorase and alkaline phosphatase activities showed only slight inhibition in seminiferous tubules of treated monkeys. It was concluded that chronic exposure to manganese does not produce sever degenerative changes in the testis earlier than metal induced encephalopathy in primates.
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PMID:Manganese induced testicular changes in monkeys. 624 33

The prognostic significance of a battery of clinical, laboratory, and histological indicators was assessed in relation to mortality risk in a 1-year study of 253 patients with alcoholic liver disease, of whom 51 died within such time. The relative risk associated with each abnormality was calculated. A number of abnormalities was found to be statistically associated with a higher risk of death. Among the clinical abnormalities, these were: collateral circulation, edema, ascites, encephalopathy, spider nevi, anorexia, and weakness. Among the laboratory tests, these were: albumin, bilirubin, hemoglobin, abnormal prothrombin time, and alkaline phosphatase. Two hundred and sixteen of these patients had liver biopsies in which the quantifiable abnormalities were scored. Among the histological findings, the alterations significantly related to mortality were necrosis, Mallory, and inflammation, while the presence of cirrhosis per se did not influence the mortality risk. The relative risk factors for mortality associated with the histological alterations were lower than those derived from clinical or laboratory measurements. The advantage of using only clinical and laboratory items to derive a global, quantitative expression of severity is discussed. The relative mortality risks provided a means of calculating a "unit of severity" for each clinical and laboratory abnormality. A combined clinical and laboratory index (CCLI) results when these mortality-risk units are added. Such a combined index had a quasi-linear relationship with the risk of mortality for the complete population. This method compared well with severity scores derived from computerized, linear step-wise discriminant function (SDF) analysis and from a logistic regression (LR) analysis. The factors chosen to have independent prognostic significance by the SDF analysis were: encephalopathy, albumin, prothrombin time, and hemoglobin, while only encephalopathy, albumin, and hemoglobin were chosen by the LR analysis. Within a range of values, LR can provide a good discrimination in relation to mortality, similar to that observed for the CCLI in its complete range. However, there are some advantages to the CCLI method vs. the LR or SDF analyses. The CCLI is less susceptible to being unduly influenced by a nonspecific effect of treatment on the items chosen than the SDF and LR analyses, as the CCLI contains a large number of factors. Obtaining a single-severity score such as the CCLI is of value in: (a) assessing the effectiveness of treatment modalities; (b) analyzing the success of randomization; (c) separating cohorts of different severity, and (d) comparing new liver tests, histological abnormalities, or specific biological events with the severity of alcoholic liver disease.
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PMID:Assessment of prognostic factors in alcoholic liver disease: toward a global quantitative expression of severity. 662 18

Effectiveness of surgically induced acute hepatic failure in pig and most suitable time to apply artificial support in hepatic coma are evaluated in this work. Five male pigs weighing about 30-35 kg are employed. Latero-lateral porto-caval shunt was performed; the vascular disconnection of liver was obtained by ligature of blood vessels. Ligature was also placed on main biliary way after cholecistectomy. Blood samples were obtained (at 0, 1, 2, 6, 12, 18, 24 hours) to essay serum bilirubin, alkaline phosphatase and GOT-GPT levels as index of cholestasis and necrosis. Porto-caval encephalopathy was evaluated by means of serum ammonium levels, aminoacid pattern and E.E.G. Serum aminoacid pattern was carefully determined; its changes were found similar in man during coma. All pigs died 24-36 hours after surgery with liver ischemic and necrosis. Clinical and laboratory data obtained in experimental conditions were found similar to picture of acute hepatic failure in man, confirming validity of our model.
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PMID:[Acute experimental hepatic insufficiency in pigs. Validity of a model with biohumoral and electroencephalographic monitoring]. 667 5

Nine patients on long-term hemodialysis with dialysis encephalopathy were studied, with sex matched control subjects for eight of the patients. Each patient with dialysis encephalopathy and control subject were contemporaries in a similar dialysis environment. Rib and other fractures were found in excess in the patients with dialysis encephalopathy (p less than 0.005 and p less than 0.01). These patients had less radiographic hyperparathyroid bone disease, and no more osteopenia as measured by metacarpal thickness than did their control counterparts. Severe osteomalacia was documented by bone biopsy in four of te patients. In a retrospective review of clinical, biochemical and pharmacologic differences, the patients with dialysis encephalopathy were significantly older at the start of dialysis (45.6 years versus 38.6 years, p less than 0.02) and had higher mean concentrations of blood urea nitrogen (BUN) and lower serum hemoglobin in the first year of dialysis than the control subjects. Blood pressure weight, creatinine, calcium, phosphate, alkaline phosphatase and a number of transfusions did not differ significantly. There was no difference in prescribed vitamin D and elemental aluminum in phosphate binders. This study demonstrates that patients with dialysis encephalopathy had more rib fractures without more parathyroid or osteopenic bone disease than did the control subjects and suggests that the etiology of dialysis encephalopathy and osteomalacia is multifactorial.
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PMID:Dialysis encephalopathy and osteomalacic bone disease: a case-controlled study. 703 24

The hemodialysis unit at Columbia, South Carolina, opened in April, 1974. By June of 1977, 7 patients had died from dialysis encephalopathy, and 16 of the 51 surviving patients showed speech disorders, fits, and myoclonic jerks. Pathologic fractures were seen in 22 patients. Bone histomorphometry showed severe osteomalacia with minimal, if any, osteitis fibrosa, and serum alkaline phosphatase activity was normal. The mean serum aluminum concentration in 33 random patients was elevated at 83.5 microgram/liter (control group, 13.9 microgram/liter, P less than 0.001). The mean bone aluminum concentration in 4 patients who died from this syndrome was 307 ppm of bone ash (normal, less than 10 ppm). Dialysis fluid aluminum was high at 140 microgram/liter. Purification of the dialysis fluid with a water softener, reverse osmosis and a deionizer and abandoning extra-strength Basaljel resulted in a notable clinical and EEG improvement. None of 81 new patients who started hemodialysis between July of 1977 and July of 1979 after the change in treatment have developed any such symptoms. A syndrome of hemodialysis encephalopathy accompanied by pathologic osteomalacic fractures is described. Recovery is possible. The syndrome was eradicated after purification of the dialysis fluid.
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PMID:Hemodialysis encephalopathy with osteomalacic fractures and muscle weakness. 721 57

The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
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PMID:Encephalopathy in infants and children with chronic renal disease. 729 12


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