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)

Moderately elevated calcemia, increased urine calcium excretion, normal values of phosphate clearance and tubular phosphate resorption, elevated alkaline phosphatase were found in 50 patients with clinically confirmed thyrotoxicosis. With calcium loading, an essential calcium elevation in serum was determined as well as a delayed restoration to the norm of the latter, providing grounds to admit an insufficiency of hypocalcemia leading systems, thyrocalcitonine resp. The characteristic features of the X-ray changes observed are described, especially of osteoporosis. The bone changes were established to be more frequent among females (64% versus 204 among males). They increase in parallel with age advancing, during and severity of the disease. The special X-grams for fine analysis of bone structure according to Meema-Heunk enable the confirmation of intracortical striation in metacarpal bones and phalanges in 56.7 per cent of the examined.
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PMID:[Biochemical and x-ray changes in thyroid osteopathy]. 65 36

A 68-year-old man with a history of organic heart disease and marked weight loss was found to have apathetic thyrotoxicosis and hypercalcemia. Oral propranolol, 20.0 mg four times a day, provoked a gradual fall in serum calcium and alkaline phosphatase. It is concluded that relatively small doses of oral propranolol may be effective in the management of hypercalcemia accompanying thyrotoxicosis and that beta-blocking agents may not only inhibit the enhanced bone resorption caused by thyroid hormones but also block the stimulated osteoblastic activity.
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PMID:Oral propranolol in hypercalcemia associated with apathetic thyrotoxicosis. 66 23

A thyroid hormone analogue, sodium dextro-triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na-DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.
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PMID:Thyroid hormone-like effects without thyrotoxicosis during one year's therapy with NA-DT3 for hypercholesterolemia. 77 45

Fifty eight patients with thyrotoxicosis were examined as well as 9 patients with hypothyroidism and 40 healthy subjects. A tendence towards hypercalcemia and hyperphosphatemia, hypercalciuria, hyperhydroxiprolinuria, elevated alkaline phosphatase were found in hyperthyroidism. In hypothyroidism--hypocalcemia, hypocalciuria, hypohydroxiprolinuria. The changes are associated with the direct effect of thyroid hormones upon bone system (intensified bone metabolism with predominance of destruction). Calciuria and HOP-uria in thyrotoxicosis depend on the severity of the disease. The elevated calcium excretion in thyrotoxicosis speaks for the presence of ostemalacic component. TRP, PEI, mean diametrically opposite in hyper- and hypothyroidism, support the hypothesis of the secondary hypoparathyroidism in thyrotoxicosis and hyperparathyroidism--in the hypothyroidism.
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PMID:[Studies of calcium-phosphorus metabolism in thyrotoxicosis]. 91 16

In this study , serum levels of classical serum markers of bone formation [carboxyterminal propeptide of procollagen type I (S-PICP), bone Gla protein (S-BGP)], and total alkaline phosphatase (S-AP)) were related to the calcium kinetic index of whole skeletal mineralization rate (m) by regression analysis in a variety of metabolic bone diseases. For each disease, the regression coefficient (r) as well as the fraction: standard error of estimate/mean dependent variable (SEE/Y) were determined. In a group of 19 normals, only the regression of S-PICP on m reached significance (r = 0.53, P < 0.02, SEE/Y = 0.44), whereas regressions of S-AP and S-BGP on m were nonsignificant. In a pooled material of high- and low-turnover bone diseases without mineralization defects or spinal fracture [myxedema, thyrotoxicosis, and primary hyperparathyroidism (n = 48)], a highly significant positive regression of S-PICP on m was demonstrable (r = 0.50, SEE/Y = 0.63, P < 0.001). The regression coefficients obtained for S-BGP and S-AP were 0.74 (P < 0.001, SEE/Y = 0.41) and 0.42 (P < 0.01, SEE/Y = 0.55), respectively. When analyzing individual diseases in this group, significant differences among the three markers were detectable. In a group of 52 osteoporotics, S-PICP correlated significantly to m (r = 0.49, P < 0.001, SEE/Y = 0.50). Corresponding r-values for S-BGP and S-AP were 0.21 (NS) and 0.48 (P < 0.001, SEE/Y = 0.61), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of bone formation by biochemical markers in metabolic bone disease: separation between osteoblastic activity at the cell and tissue level. 145 Oct 6

The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (osteoporosis, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum alkaline phosphatase (r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
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PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62

A female newborn whose mother was taking propylthiouracil (PTU) for Graves' disease, presented with transient thyrotoxicosis (serum triiodothyronine 1,710 ng/dl) and signs of acute hepatic injury. Jaundice and choluria were evident on her fourth day of life. Serum total bilirubin reached 14 mg/dl, with a direct fraction of 11 mg/dl. Serum alanine aminotransferase and aspartate aminotransferase showed moderate elevations (110 IU/l and 61.5 IU/l, respectively), as well as the alkaline phosphatase which increased to about twice the upper limit of normal. When incubated with PTU, the patient's cultured peripheral lymphocytes underwent transformation to more than twice the values found in 2 controls, with a stimulation index (SI) of 3.19, compared to SI of 1.45 and 1.15 for the controls, suggesting a hypersensitivity mechanism involved in the hepatic injury. Although about 20 cases of PTU induced hepatic damage were reported in the medical literature, this is, as far as we know, the first description of neonatal liver injury probably caused by placental transfer of this drug.
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PMID:Neonatal hepatitis and lymphocyte sensitization by placental transfer of propylthiouracil. 209 Jun 74

Subacute thyroiditis is generally thought to be a self-limited inflammatory disease of the thyroid gland. This paper describes serial observations on the clinical course of a typical patient with subacute thyroiditis. This patient showed specific features of destructive thyrotoxicosis with increases in the serum levels of acute phase reactants and in the erythrocyte sedimentation rate. She also showed signs of liver dysfunction [slightly increased alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), and leucine aminopeptidase (LAP)], slight anemia, glucose intolerance, increased pancreatic enzymes, splenomegaly, and an increase in peripheral Leu 7 positive (NK/K) cells. These abnormalities all improved with recovery from disease. These findings indicate that in this patient with subacute thyroiditis inflammation is not limited to the thyroid gland but also involves the liver, pancreas and spleen. Thus the subacute thyroiditis in this patient may be a systemic multi-organ disease.
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PMID:Subacute thyroiditis associated with systemic multi-organ disorders. 263 13

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature. 267 Jan 39

Leukocyte alkaline phosphatase (LAP) activity was determined in normal subjects, and in untreated, symptomatic patients with primary hypothyroidism or thyrotoxicosis. The means +/- 1 SD of (n) subjects were, respectively: 61.7 +/- 27.5 (16), 149.9 +/- 56.3 (9) and 96.9 +/- 27.7 (9). The mean LAP values of the hypothyroid and thyrotoxic groups were significantly different from that of the normal group (P less than .01). Values were above the normal range (20 to 120) in seven of the nine hypothyroid patients. LAP values were in the upper half of the normal range in eight of the nine thyrotoxic patients. In the two hypothyroid patients studied at 24-hour intervals, LAP activity was altered markedly within 48 hours of initiation of thyroxine therapy, 25 micrograms daily. In five hypothyroid patients followed for several months after initiating thyroxine replacement, LAP levels were essentially normal within 1 to 2 months. In the thyrotoxic patients, LAP values declined within the first month of medical management, but tended to remain within the normal range.
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PMID:Leukocyte alkaline phosphatase in hypothyroidism and hyperthyroidism. Response to initiation of thyroxine replacement therapy. 272 74


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