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)

Sixteen children with refractory diarrhea and three malnourished children who had frequent episodes of acute gastroenteritis but little diarrhea at the time of hospital admission, were studied by peroral upper small intestinal biopsy. Six children were adequately nourished; five children weighed 62 to 79% of expected weight and eight weighed less than 60% of expected weight. Two of the malnourished children had giardiasis. Pathogenic bacteria were found in only one case. Varying degrees of mucosal atrophy with reduction of mean villous height were seen in 18 cases. The concentration of mononuclear inflammatory cells and plasma cells was about half that seen in well-nourished children with severe nongastrointestinal infections. The concentration of mononuclear cells in the lamina propria was about twice that seen in normal adults. The proportions of IgA-producing cells and cells that stained for secretory component were significantly reduced, as compared with normal adult control values. This reduction was most striking in children with malnutrition complicated by giardiasis. Enzyme histochemical studies were performed for leucine aminopeptidase, alkaline phosphatase and acid phosphatase. There was a tendency for considerably reduced acid phosphatase activity in all clinical groups (kwashiorkor, marasmic kwashiorkor and marasmus) of growth-retarded infants.
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PMID:Infantile jejunal mucosa in infection and malnutrition. 10 19

A safety evaluation of Aspergillus fumigatus I21, grown in a cassava carbohydrate and salts medium, was undertaken. Male weanling rats were fed the fungus at 20, 30 and 40% of the diet for 90 days. A control group was given soybean oil meal as the sole source of protein. Weekly determinations of the body weights and feed consumptions were made. A few days prior to termination of the feeding study, a kidney function test was undertaken on the rats. At the end of the feeding period hematology, blood biochemistry, urine analyses and histopathology studies of various tissues were carried out, and organs were weighed. Rats fed A. fumigatus I21 gained less weight than the controls, but kidney weights were increased. Increases in serum alkaline phosphatase and glutamic-oxaloacetic transaminase were not related to dose level. The blood urea nitrogen was increased for the rats fed 40% of the fungus. Rats fed 30 and 40% of the fungus I21 showed a significant drop in albumin. Deficiency in methionine or other essential amino acids through a limited feed consumption may have caused a decrease in albumin synthesis. Rats fed the highest level of the fungus showed increases in neutrophils and monocytes concomitant with decreases in lymphocytes and eosinophils which may be a response to stress. The urine analyses did not reveal any significant differences. The test rats were capable of concentrating urine adequately when deprived of water for 24 hours. No significant differences between the control and experimental groups were found by histopathological examinations.
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PMID:Safety evaluation of Aspergillus fumigatus grown on cassava for use as an animal feed. 33 62

1. 65Zn uptake by blood cells in vitro has been compared with plasma Zn concentration and plasma alkaline phosphatase (EC 3.1.3.1) activity as indicators of an animal's Zn status. 2. Dietary Zn deficiency, low food intake, reduced dietary protein content and endotoxin administration all reduced plasma Zn concentration in the rat. In each case there was a parallel reduction in plasma alkaline phosphatase activity and an increase in 65Zn uptake in vitro by cells of whole blood. 3. A similar relationship between the three measurements existed in sheep with lowered plasma Zn concentrations whether these were caused by dietary deficiency or by post-surgical stress. 4. 65Zn uptake by cells of whole blood did not differentiate dietary Zn deficiency from the other factors which reduce plasma Zn under 'field' conditions. 5. 65Zn uptake by the cells in whole blood in vitro was three to five times less rapid in blood of ruminant origin than in that from non-ruminants. This difference related to the erythrocytes rather than to the leukocytes or the plasma.
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PMID:The assessment of zinc status of an animal from the uptake of 65Zn by the cells of whole blood in vitro. 62 20

Studies of calcium levels in 400 elderly patients in a hospital geriatric unit showed that many patients (42 percent) had hypocalcemia when referred to the unit and that the incidence of hypocalcemia rises proportionately with advancing age; however, in men, the frequency decreases after age 90. Although hypocalcemia is caused by vitamin D deficiency in a number of patients, in most it is caused by malnutrition. The intravenous vitamin D tests is a simple and reliable procedure for differentiating hypocalcemia due to specific vitamin D deficiency from that due to other causes. We suggest that a 15 percent rise in the serum phosphate level after the intravenous administration of 40,000 units of vitamin D3 indicates the presenceof osteomalacia. Little is known about the sequence of development of detectable bone changes and disturbance of serum calcium, phosphate, and alkaline phosphatase levels in the natural course of osteomalacia. Early treatment of osteomalacia is simple and very rewarding. No effort should be spared in detecting it as soon as possible.
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PMID:Detecting the early stages of osteomalacia with the intravenous vitamin D test. 83 Jun 2

The normal values of serum glutamic oxaloacetic transminase, serum glutamic pyruvic transaminase, serum lactic dehydrogenase and serum alkaline phosphatase, total protein, urea, creatine, cholesterol, glucose, magnesium, calcium and inorganic phosphorus were measured monthly over a 12-month period from 10 "pure" Native and 10 Native X British Crossbred pigs. Except for cholesterol, no significant difference was found between the two groups. Similar estimations were made for 5-month and 11-month Village pigs in which the serum alkaline phosphatase, inorganic phosphorus, total protein, urea, creatinine and calcium were significantly lower when compared with the corresponding age group of the pure Native pigs and Crossbred pigs. These lower values are thought to be due to the effects of the malnutrition-parasite complex of Village pigs.
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PMID:Some normal biochemical parameters of pigs in Pupua New Guinea. 93 99

The findings in 20 cases of nutritional rickets treated on an out-patient basis with oral calciferol and calcium gluconate are reported. Attention was paid to their clinical, biochemical and radiological responses. If was noted that presentation at the hospital out-patient department was always delayed until there were obvious and sometimes severe deformities in the children. Biochemical changes noted during the early phase of treatment showed an initial fall in the level of serum calcium and plasma phosohorus and a rise in the serum alkaline phosphatase. About three months after initiating treatment, calcium and phosphorus reverted to normal levels but serum alkaline phosphatase still remained high. Twelve of our cases (60 per cent) suffered from protein calorie malnutrition of the marasmic type and showed an apparent resistance to vitamin D therapy in what may be regarded as normal dosages. Response was however, achieved with substantial increase in the amount of vitamin given. There was a striking sex difference in the ratio of 15 males to five females indicating that males are more likely to develop nutritional rickets than females when subjected to predisposing environmental conditions. Vitamin D resistant type of rickets was not encountered in this study.
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PMID:Rickets in Nigerian children--response to vitamin D. 108 35

Radiologically diagnosed rickets was found to be common in children of the poorer classes in Tehran. It was frequently associated with gastroenteritis or bronchopneumonia and a large proportion of the children were severely underweight for their age. In children below the age of 1 year malnutrition tended to mask the signs of rickets. Convulsions were much less frequent in the malnourished children; the concentration of calcium in the serum was higher and that of alkaline phosphatase was lower than in those who were well nourished. Biochemistry is of little value in the diagnosis of rickets in the presence of malnutrition.
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PMID:Rickets in Tehran. Study of 200 cases. 112 45

Twenty-six 3-week-old genetically obese pigs were fed in two experiments to determine the serum chemistry profile during severe protein malnutrition and repletion. Severe protein deficiency was produced in pigs fed the high-fat, low-protein diet (growth failure, rough hair, low serum total protein and albumin). In Experiment 1, blood was sampled from the anterior vena cava of each pig five times during depletion and three times during repletion to determine serum total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides, total protein, albumin, glucose, Ca, inorganic P, Mg, Na, K, Cl, total bilirubin, urea N, creatinine, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase. In Experiment 2, blood was sampled weekly for 8 weeks for serum total cholesterol, HDL-cholesterol, triglycerides, albumin, glucose, Ca, P, Mg and alkaline phosphatase. HDL-cholesterol was increased (P less than 0.01) and albumin was decreased (P less than 0.01) in protein-deficient pigs in both experiments. Creatinine, total bilirubin, gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase were elevated in protein-deficient pigs compared with controls after 7 weeks of depletion. Inorganic P (P less than 0.01), Ca (P less than 0.01), and Mg (P less than 0.05) concentrations were depressed in protein-depleted pigs compared with controls in both experiments. After 8 weeks of repletion in Experiment 1, all elements except inorganic P were similar in the two groups. Short-term, severe, protein malnutrition affected lipid, electrolyte, and structural mineral metabolism and indices of liver function in the absence of parasites, diarrhea, and infection. The effects were reversed after 8 weeks of repletion. We conclude that the elevated serum cholesterol in protein deficiency is related primarily to an increase in the HDL fraction.
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PMID:Response of blood serum constituents to production of and recovery from a kwashiorkor-like syndrome in the young pig. 135 73

Hypophosphatasia is an inborn error of metabolism that is characterized clinically by defective bone mineralization and biochemically by deficient activity of the tissue-nonspecific isoenzyme of alkaline phosphatase (TNSALP) in serum and in tissues. Clinical severity is extremely variable, ranging from death in utero to pathologic fractures first presenting in adulthood. Severe forms of the disease are inherited in an autosomal recessive fashion; the modes of transmission of mild forms are uncertain. Deficiency of TNSALP activity in this condition suggests that mutations in the TNSALP "candidate" gene are the primary defects. This hypothesis was supported in 1988 by the demonstration, in one inbred infant, that an identical missense mutation in both alleles of the gene encoding TNSALP caused lethal hypophosphatasia. Here we summarize the work leading to that discovery and discuss the recent identification of additional missense mutations in the TNSALP gene associated with the entire clinical spectrum of hypophosphatasia.
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PMID:Missense mutations of the tissue-nonspecific alkaline phosphatase gene in hypophosphatasia. 136 Aug 78

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34


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