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)

We present the results obtained using a 1-84 human parathyroid hormone (PTH) assay in patients with abnormal calcium metabolism. A normal range was established in a series of healthy volunteers. Patients with surgically proven hyperparathyroidism (HPT) showed increased PTH levels which were separate from the normal range. Patients with probable hyperparathyroidism and milder hypercalcaemia showed a raised median PTH level but the range overlapped with normal. Patients with hypercalcaemia of malignancy showed reduced PTH levels and these patients were readily differentiated from those with probable and proven HPT by the use of the assay. In patients with chronic renal failure PTH values ranged from normal to high, the PTH concentration was found to be correlated with plasma alkaline phosphatase, but not with plasma creatinine.
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PMID:The use of an intact molecule parathyroid hormone assay in disorders of calcium metabolism. 306 5

Elevated serum gastrin (SG) has been reported in chronic renal failure (CRF). We studied SG levels in relation to various humoral and gastroduodenal histopathologic findings in 20 controls, 12 uremics under conservative therapy (CT), 27 patients on regular dialysis (RDT) and 8 transplanted patients (Tx). SG and parathyroid hormone (PTH) levels were estimated by radioimmunoassay (RIA), in addition serum BUN, creatinine, Ca++PO4---and alkaline phosphatase (predialysis in RDT) were determined. 20 patients (12 on CT and 8 on RDT) underwent pentagastrin (PG) stimulation test and upper gastrointestinal endoscopy with biopsy of gastric and duodenal mucosa. The mucosal samples were stained for mucopolysaccharides (MPS), nucleic acid (NA) and alkaline phosphatase (AP), and divided into intense, normal or faint staining. Mean SG was 688.71 pg/ml (CT cases), 636.2 pg/ml (RDT cases) and 280.6 pg/ml (Tx cases), all values being significantly higher than controls (118.46 pg/ml). SG level had a linear correlation with serum creatinine in CT patients and predialysis creatinine in RDT patients, but not with other parameters studied (BUN, Ca++,PTH,PO4---AP). The incidence of gastroduodenal erosions (40%) had a significant negative correlation with SG. They were more frequent with normal MPS stain (p = 0.01) and NA staining (p less than 0.001) than faint staining of gastric mucosa biopsy. The acid response to PG stimulation was inversely correlated with SG. We believe that elevated SG is compensatory to a decreased response of the gastroduodenal mucosa to PG. Mere retention of SG does not explain its elevation as its correlation with serum creatinine existed not only in patients on CT, but also in RDT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum gastrin in chronic renal failure: morphological and physiological correlations. 315 79

Progression of chronic renal failure during 35 treatment periods in 27 patients was measured as the rate of change of bimonthly radioisotope GFR for an average of 15 months. Treatments were comprised of: (1) mild protein restriction; (2) more severe protein and phosphorus restriction plus essential amino acids; or (3) the same diet plus ketoacids. Progression was significantly (P less than 0.025) correlated with urinary 17-hydroxycorticosteroid excretion in all three treatment groups; overall r was 0.78 (P less than 0.0001). Multiple regression analysis showed that the following factors were not additional significant determinants of progression: urea N excretion, phosphate excretion, protein excretion, serum calcium times phosphorus product, serum alkaline phosphatase, serum uric acid, serum triglycerides, serum cholesterol, etiology, mean arterial pressure, or enalapril treatment. However, when urinary 17-hydroxycorticosteroid excretion was factored by GFR (with which it was correlated), additional significant regressors appeared: serum triglycerides and polycystic kidney disease, which tended to be associated with more rapid progression, and ketoacid treatment, which tended to be associated with slower progression. Mean 17-hydroxycorticosteroid excretion differed significantly between the three treatment groups, in the order (1) greater than (2) greater than (3) (though not when factored by GFR). Changing from essential amino acids to ketoacids (or vice versa) without change in diet was associated with lower 17-hydroxycorticosteroid excretion on ketoacids (but not when factored by GFR).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progression of chronic renal failure is related to glucocorticoid production. 321 May 47

We measured the serum concentrations of 2 biochemical markers of bone formation, bone Gla-protein (BGP) and bone alkaline phosphatase (BAP), in 164 normal subjects and 164 patients with metabolic bone disorders. The data were reported as Z scores (deviation in SDs from the sex-specific age regression in normal subjects). Both serum BGP and BAP distinguished abnormalities well (mean Z scores for BGP and BAP, respectively) and gave concordant results in patients with hypoparathyroidism (-1.7, -1.4), hyperthyroidism (+1.1, +1.8), primary hyperparathyroidism (+3.6, +2.5), acromegaly (+1.2, +2.8), and postmenopausal osteoporosis (+0.4, +1.9). The 2 markers gave discordant results, however, in patients with glucocorticoid excess (-2.4, +0.9), Paget's disease (+1.8, +41.8), chronic renal failure (+16.3, +0.4), and osteolytic metastases (-1.4, +5.9). These discrepancies may have occurred because serum BGP and BAP concentrations reflect different aspects of osteoblast function or because there are differences in their clearance from the circulation. Consequently, more information is derived about the level of bone formation across the wide range of metabolic bone disorders when both biochemical markers are assayed.
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PMID:Concurrent assays of circulating bone Gla-protein and bone alkaline phosphatase: effects of sex, age, and metabolic bone disease. 325 70

Because of the suggestion that intestinal alkaline phosphatase was elevated in the serum of patients with chronic renal failure, we studied the serum of 42 patients undergoing hemodialysis with elevated enzyme activity. Using a sensitive and specific electroimmunoassay for the intestinal isoenzyme, 26 of 42 serum samples were positive, compared with 3 of 25 samples obtained from hospitalized patients with elevated phosphatase activity. The fractional amount of this isoenzyme was also higher, ranging from 1.5% to 41% of the total serum phosphatase, compared with 0.1%-1.2% in control sera. Kidneys removed during transplantation or postmortem contained a membranous phosphatase with immunologic activity identical to the intestinal isoenzyme in 5 of 6 patients. This enzyme accounted for 8%-21% of the total kidney phosphatase activity. By morphology the immunoreaction was localized to the apical membranes of the collecting tubules. Thus, the kidney is the likely source of the observed increase in serum intestinal-type phosphatase activity noted in patients with chronic renal failure. An elevation in the intestinal isoenzyme rather than the presence of early metabolic bone disease or hepatic disease should be considered in renal failure patients with mildly elevated (up to 50% over normal) total serum alkaline phosphatase.
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PMID:Intestinal alkaline phosphatase in patients with chronic renal failure. 333 99

Biological intra-individual variation in the concentration of 15 biochemical analytes in serum was estimated for 17 patients with chronic renal failure (CRF) and compared with results for apparently healthy individuals. The ratio of the average intra-individual variation in CRF patients to that in normal subjects was 1.5 to 2.0 for sodium, chloride, calcium, and creatinine; 1.2 to 1.5 for hemoglobin, total protein, albumin, globulin, uric acid, cholesterol, and alpha-amylase. The intra-individual CVs for urea, high-density-lipoprotein cholesterol, triglycerides, and alkaline phosphatase did not differ significantly between groups. The intra-individual variation of calcium and the concentration of creatinine in serum correlate significantly (r = 0.661, p less than 0.01). Individual values showed a gaussian distribution for all analytes. There was no time dependence of the intra-individual variation during a three-week interval, except for calcium and cholesterol. The estimated biological component of intra-individual variation and the analytical variation can be used to derive decision-making criteria in monitoring CRF.
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PMID:Intra-individual variation of some analytes in serum of patients with chronic renal failure. 349 51

We report on the results of the clinical trial, where the effects of sucralfate on the serum phosphorus, calcium and alkaline phosphatase in 30 patients with chronic renal failure on intermittent hemodialysis were examined. After 14 days of treatment with sucralfate (1 gram four times daily), we found a significant reduction in serum phosphorus and alkaline phosphatase and an increase in serum calcium. On the basis of its proven hypophosphatemic and ulcer-healing effects, sucralfate can be recommended in treatment of hyperphosphatemia and secondary hyperparathyroidism in chronic renal failure. Serum phosphorus should be checked routinely in patients treated with sucralfate for the peptic ulcer disease.
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PMID:Changes in serum phosphorus, calcium and alkaline phosphatase due to sucralfate. 351 90

Peliosis hepatis is described in a renal transplant recipient and in a patient who was receiving long-term haemodialysis. This uncommon liver lesion has been reported in a number of patients, including 18 renal transplant recipients and two patients with chronic renal failure. However, its cause, clinical features, natural history and clinical significance remain to be determined. We emphasize that, although it is rare, peliosis hepatis should be considered in long-term haemodialysis and renal transplant patients who exhibit hepatomegaly and/or splenomegaly and/or disordered liver function (in particular, elevation of hepatic alkaline phosphatase levels).
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PMID:Peliosis hepatis in a renal transplant recipient and in a haemodialysis patient. 354 May 50

A prospective mammographic study was performed on 151 women to determine the prevalence of breast calcifications in patients with chronic renal failure. Frequency, size, structure, and location of calcific lesions were assessed in 15 patients with compensated renal insufficiency, 22 on hemodialysis, 14 who had renal transplants, and 100 who had normal kidney function. Serum levels of calcium, phosphorus, alkaline phosphatase, and parathyroid hormone were determined for all 151 women. The calcific lesions occurred preponderantly in dialysis patients (arteries, 55%; parenchyma, 68%; and ducts, 36%). Next in order were those with renal transplants (43%, 64%, and 29%, respectively) and those with renal insufficiency (33%, 53%, and 20%, respectively). Patients with renal disease had significantly more calcifications (p less than .001) than the patients with normal kidney function: arteries, 45% vs 8%; parenchyma, 61% vs 27%; and ducts, 29% vs 9%. Frequencies of calcifications correlated with serum levels of parathyroid hormone. None of the calcifications induced by renal disease simulated those seen in carcinoma of the breast.
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PMID:Breast calcifications in renal hyperparathyroidism. 355 17

Renal osteodystrophy is a common and incapacitating complication of chronic renal failure in children. Standard therapy with oral calcium supplements, phosphate binders, and vitamin D preparations is often inadequate to control progressive bone disease. We report the use of parenteral calcitriol therapy in two children, aged 2 and 15 years, respectively, with chronic renal failure. This treatment effectively suppressed secondary hyperparathyroidism in both patients, causing a nearly 50% reduction in circulating parathyroid hormone level and a parallel decline in serum alkaline phosphatase activity. In the younger patient, therapy was associated with healing of subperiosteal bone resorption and accelerated growth velocity. These findings indicate that parenteral administration of calcitriol may be an effective treatment option in some patients with refractory renal osteodystrophy and secondary hyperparathyroidism.
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PMID:Parenteral calcitriol for treatment of severe renal osteodystrophy in children with chronic renal insufficiency. 358 13


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