Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was conducted of the chemical effects on the human kidney induced by the chronic ingestion of uranium in drinking water. Subjects were divided into two groups: The low-exposure group, whose drinking water was obtained from a municipal water system and contained < 1 microgram uranium/L, and the high-exposure group, whose drinking water was obtained from private drilled wells and contained uranium levels that varied from 2 to 781 micrograms/L. Years of residence varied from 1 to 33 years in the low-exposure group and from 3 to 59 years in the high-exposure group. The indicators of kidney function measured in this study included glucose, creatinine, protein, and beta 2-microglobulin (BMG). The markers for cell toxicity studied were alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), lactate dehydrogenase (LDH), and N-acetyl-beta-D-glucosaminidase (NAG). Urinary glucose was found to be significantly different and positively correlated with uranium intake for males, females, and pooled data. Increases in ALP and BMG were also observed to be correlated with uranium intake for pooled data. In contrast, the indicators for glomerular injury, creatinine and protein, were not significantly different between the two groups nor was their urinary excretion correlated to uranium intake. These results suggest that at the intakes observed in this study (0.004 microgram/kg to 9 micrograms/kg body wt), the chronic ingestion of uranium in drinking water affects kidney function and that the proximal tubule, rather than the glomerulus, is the site for this interference.
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PMID:Chronic ingestion of uranium in drinking water: a study of kidney bioeffects in humans. 962 21

Parathormone has been shown to increase the secretion and production of lysosomal enzymes including tartrate-resistant acid phosphatase. All our 68 patients with proven primary hyperparathyroidism had signs of hyperparathyroid bone disease. Tartrate-resistant acid phosphatase and bone alkaline phosphatase activities are raised as a result of enhanced bone remodelling. Serum beta 2-microglobulin concentration in patients with primary hyperparathyroidism was normal 1.6 (1.4-1.8) mg/l versus 1.8 (1.7-2.2) mg/l in 51 control subjects. In hyperparathyroid patients, serum beta 2-microglobulin concentration does not correlate with plasma tartrate-resistant acid phosphatase activity which is known to be a sensitive biological marker of bone remodelling (r = 0.088). Our findings indicate that serum beta 2-microglobulin does not behave as a biological marker of remodelling in patients with enhanced remodelling in primary hyperparathyroidism.
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PMID:Beta 2-microglobulin does not behave as a biological marker of bone remodeling in patients with primary hyperparathyroidism. 987 25

The effect of positive acceleration on plasma levels of calcitonin gene related peptide (CGRP), and endothelin as well as renal function in pilots were observed in this study. 20 pilots were exposed to +2.5 Gz 10 s and +3.0 Gz 10 s with an interval of 5 min without anti-G suits. Samples of plasma and serum were taken 2Omin before and after exposure. Plasma levels of CGRP and endothelin after the exposure were significantly increased (P<0.01), but alkaline phosphatase(AKP), blood levels of beta 2-microglobulin(beta 2-MG), Ca2+ in serum showed no significant change (P>0.05) as compared with those before exposure. There was a correlation between CGRP and endothlin (r=0.772, P<0.01). It is concluded that positive acceleration(+2.5, +3.0Gz) could increase plasma levels of CGRP and endothlin but did not affect renal function.
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PMID:Effect of +Gz on plasma levels of calcitonin gene related peptide, endothelin and renal function in pilots. 1154 Dec 77

Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.
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PMID:[Renal osteodystrophy (I)]. 1208 22

Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.
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PMID:[Renal osteodystrophy(II)]. 1208 54

A male newborn infant was recognized having Fanconi-Bickel syndrome (FBS) in the neonatal period. The presenting clinical findings were hyperglycemia and polyuria detected during an episode of acute enteritis. Physical examination was normal, biochemical analyses were suggestive of FBS: glycosuria, proteinuria, phosphaturia, generalized aminoaciduria, and increased levels of urinary beta 2-microglobulin, serum glucose and serum alkaline phosphatase. The molecular genetic analysis showed homozygosity for mutations within the gene of the glucose transporter 2 (Glut 2), 1213 C>T. The patient demonstrated improved clinical and metabolic status following institution of diet with frequent small meals and galactose-free-milk as well as pharmacological treatment with phosphate and vitamin alpha-OH-D3. In conclusion, infants showing hyperglycemia and polyuria may be considered having FBS also in the neonatal period. Early institution of adequate caloric intake and replacement of electrolytes and vitamin D may avoid or reduce metabolic complications.
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PMID:The Fanconi-Bickel syndrome: a case of neonatal onset. 1511 30


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