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)

A 5-year-old boy was found to have severe rickets in association with hyperpigmented, linear, verrucous, epidermal tumors, typical of the epidermal nevus syndrome. Normocalcemia (9.6 mg/dl), hypophosphatemia (2.0 mg/dl), elevated serum alkaline phosphatase concentration (313 IU), decreased renal tubular reabsorption of phosphorus (35%), radiologic evidence of rickets, and lack of response to usual therapeutic doses of vitamin D suggested hypophosphatemic vitamin D-resistant rickets. Therapy with vitamin D in doses to 750,000 IU and oral phosphate, 2.0 gm/day, failed to induce healing of the rickets. A subtotal parathyroidectomy performed when the patient was 9 years old was also without effect. When he was 12 years old several fibroangiomas on the face and left lower limb were excised. Within three months all biochemical abnormalities resolved and radiologic evidence of healing was observed. A portion of excised tissue was homogenized and injection of the supernate into a 6-week-old puppy induced excessive phosphaturia. The data suggest that the rickets was induced by a phosphaturic substance extractable from the tumors.
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PMID:Vitamin D-resistant rickets associated with epidermal nevus syndrome: demonstration of a phosphaturic substance in the dermal lesions. 19 29

Biochemical evidence for hypoparathyroidism and roentgenographic evidence for hyperparathyroidism were present in a 7-year-old girl with seizures and tetany. She was hypocalcemic (4.7 mg/dl), hyperphosphatemic (11 mg/dl), and normomagnesemic, with elevated parathyroid hormone level (2,603 pg/dl and 3,693 pg/dl in immunoassays utilizing two different antisera). Somatic features of pseudohypoparathyroidism were absent. Increased serum alkaline phosphatase activity (335 IU/liter) with evidence of subperiosteal bone resorption suggested parathyroid hormone activity on bone. Intramuscular administration of parathyroid extract caused a rise in serum calcium level (9.6 mg/dl) and a fall in serum phosphorus level (7.9 mg/dl). The serum calcium, phosphorus, and alkaline phosphatase activity became normal during vitamin D therapy. Parathyroid hormone values and bone roentgenograms became normal. With serum calcium and phosphorus levels normal, ethylenediaminetetraacetic acid infusion was followed by an increase in plasma parathyroid hormone level but not in urinary cyclic adenosine monophosphate (AMP) or phosphaturia; in contrast, parathyroid extract induced cyclic AMP excretion and phosphaturia. These results suggest that endogenous parathyroid hormone in this patient affects bone resorption but not renal handling of phosphate. We infer that this represents a defective endogenous parathyroid hormone.
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PMID:Hypo-hyperparathyroidism: evidence for a defective parathyroid hormone. 19 77

In six infants aged between 5 and 8 months with vitamin D deficient rickets, we have studied blood levels of calcium (Ca), phosphorus (P), alkaline phosphatase, immunoreactive parathyroid hormone (PTH) and calcitonin (CT), as well as urinary excretion of Ca, P, hydroxyproline and cyclic AMP, both under basal conditions and during a 4h infusion of 20 mg/kg 10% Ca gluconate in normal saline. Under basal conditions all the infants had high alkaline phosphatase (range: 470--770 U.I./1); PTH (range: 620--1200 pg Eq/ml) and CT (range: 440--750 pg/ml) but two infants had hypocalcaemia and four had normocalcaemia and hypophosphataemia. The urinary Ca excretion was low whereas the urinary P, hydroxyproline and cyclic AMP excretions were high. During Ca infusion the total serum Ca and CT levels increased, while alkaline phosphatase and PTH fell. After the end of the infusion, CT levels fell perceptibly; phosphaturia, hydroxyprolinuria and cyclic AMP decreased on the day of the infusion.
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PMID:Parathyroid hormone and calcitonin levels in vitamin D deficient rickets. 21 86

Thirteen phosphorus balances were performed in four thalassemic children aged 6 to 10 years. No correlation was found between phosphorus intake and serum level or between phosphorus intake and net absorption. There was a positive correlation among daily phosphorus intake, net absorption, and 24-hour urinary excretion. The 24-hour urinary excretion level was higher than net absorption, indicating that these children have normal phosphorus absorption but abnormally high renal phosphaturia, which leads to a deficiency of phosphorus. A strongly positive correlation was found between values for hemoglobin and serum alkaline phosphatase. In the thalassemic patients with hemoglobin levels larger than or equal to 7.5 gm/100 ml, the serum alkaline phosphatase values were larger than or equal to 15 King-Armstrong units, suggesting normal osteoblast function.
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PMID:Phosphaturia in thalassemia. 99 19

The influence was studied of the type of immunosuppression on calciuria, phosphaturia, and on the levels of parathyroid hormone (PTH), calcitonin (CT), 25-hydroxycholecalciferol (25/OH/D), total calcium, magnesium, and alkaline phosphatase activity in 24 patients after renal transplantation. Twelve of these patients received cyclosporin with prednisone (group CyA) and other 12 were treated with azathioprine and prednisone (group Aza). Independently of the type of immunosuppression used, in both groups a significantly higher concentration of PTH, CT, 25/OH/D and greater activity of alkaline phosphatase were demonstrated in relation to healthy controls. In both studied groups the patients had also a significantly reduced calciuria and phosphatemia than controls. In group Aza the patients had a significantly lower phosphaturia and significantly higher magnesemia than in group CyA. The results of these investigations suggest a certain influence of the type of immunosuppression on the intensity of calcium-phosphate metabolism in renal graft recipients.
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PMID:[Selected parameters of calcium and phosphate metabolism in patients after kidney transplantation and administration of azathioprine or cyclosporin A]. 221 34

A study was undertaken in 46 subjects; 21 patients diagnosed as having HRL and 25 volunteers patients. Biochemical and hormonal analyses were performed in the study population, including determination of Ca, P, Mg, Cr in blood and urine, phosphate tubular resorption (PTR), maximum tubular phosphate resorption (MTPR), fasting calcium secretion (FCS), alkaline phosphatase (AP), hydroxyprolinuria (HPR), osteocalcin (BGP), parathormone (PTH), cAMP, and 1-25(OH)2D. The stone formers showed lower calcemia values (p less than or equal to 0.005d), higher phosphaturia, and magnesiuria (p less than or equal to 0.0005), higher FCS (P less than or equal to 0.005) and higher values for PTH (p less than or equal to 0.01) and cAMP (p less than or equal to 0.0025). No significant differences were observed for the other parameters evaluated. Classification of the patient group into 2 subgroups (renal SbR and absorptive SbA) according to FCS values greater or lower that 0.16 mg/dl, the SbR patient group revealed a higher PTH and 1-25(OH)2D values (p less than or equal to 0.05). There appears to be no increase of bone resorption since AP, HPR, and BGP values in our patients fell within normal ranges. The 1-25(OH)2D levels were also normal and, with respect to the control group, were only elevated for the SbR patient group, whose PTH levels were also observed to be elevated. These increments appear to be related and may result in intermediate forms between renal and absorptive hypercalciuria.
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PMID:[Parathormone, cyclic AMP, 1,25 dihydroxyvitamin D and osteocalcin in hypercalciuric renal lithiasis]. 254 53

In order to ascertain the blood levels and the biologic responses obtained after administration of two noninjectable forms of salmon calcitonin (SCT) (i.e., a nasal spray and a suppository), two doses of 200 IU each were administered at 3 hour intervals nasally to 8 normal subjects, and rectally to 9 normal subjects. Five untreated subjects served as controls. All were given a standardized diet for 2 days before the test. Plasma salmon-calcitonin, ionized calcium, phosphate, sodium, proteins, creatinine, and alkaline phosphatase were measured repeatedly after the administration of the drug. Modifications in fractionated urinary calcium, phosphate, sodium, and creatinine excretions (and hydroxyproline for the 8 subjects treated by the nasal spray) were compared with the values measured on the previous day. Plasma concentrations of SCT were found to increase sharply with both routes of administration, the peaks being high and short after rectal administration, low but more sustained after nasal application. Despite these differences, almost similar biologic effects could be demonstrated: transient hypocalcemia, increased calciuria, phosphaturia, and natriuria. Urinary hydroxyproline excretion decreased. Plasma sodium did not increase, whereas it did in the controls. In conclusion, nasal sprays and suppositories of SCT appear to exert the known biologic effects of SCT, and might be favored for long-term treatment in diseases representing indications for calcitonin therapy.
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PMID:The effect of rectal and nasal administration of salmon calcitonin in normal subjects. 312 Nov 49

Studies were conducted in a patient with idiopathic hypophosphatemic osteomalacia to delineate the roles of parathyroid hormone (PTH), vitamin D and renal tubular function. A 43-year-old woman presented with progressive skeletal pains resulting in severe incapacity. Workup revealed: hypophosphatemia with a low tubular maximal phosphate reabsorption per glomerular filtrate (TmP/GFR) of 1.05 mg/dl, normocalcemia, hypocalciuria, elevated alkaline phosphatase and glycinuria. PTH and urinary cyclic AMP (UcAMP) were normal, while calcitriol was low. Renal tubular acidosis or other transport defects were not present and no tumor was found. Biopsy was diagnostic for osteomalacia, and the patient responded to 1-alpha OHD3 and phosphate therapy. Hyperparathyroidism was ruled out by 1) normocalcemia persisting after 1-alpha OHD3 and calcium loading and 2) normal PTH and UcAMP challenged by phosphate supplements. Combined calcium and 1-alpha OHD3 administration resulted in hypercalciuria, decreased UcAMP and increased, but not corrected, TmP/GFR. These findings suggest that the osteomalacia was due to hypophosphatemia caused by a renal leak. PTH is only contributory to the phosphaturia. Low calcitriol level contributes to the osteomalacia directly and indirectly through impaired mineral absorption and, therefore, is also responsible for the hypocalciuria.
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PMID:Metabolic studies in a patient with idiopathic hypophosphatemic osteomalacia. 334 50

Twenty-one patients with histologically proved osteomalacia from various causes were investigated for biochemical and radiological evidence of osteomalacia and secondary hyperparathyroidism. Among the 15 who maintained a normal serum calcium, seven had a raised phosphate excretion index, seven had a raised serum alkaline phosphatase, and six had phalangeal erosions. On the other hand, six patients had a subnormal serum calcium; of these, none showed a raised phosphate excretion index, one had a raised serum alkaline phosphatase, and one had erosions. The phosphate excretion index and the alkaline phosphatase were strongly correlated (r = +0.84). It is concluded that this absence of manifest secondary hyperparathyroidism in some patients with osteomalacia is due to failure of an increase in the release of parathyroid hormone. Measurement of phosphaturia does not appear to be a useful means of detecting osteomalacia. Subsequently, the 24-hour (stable) strontium space measurement was found to be the most sensitive single biochemical screening test for osteomalacia.
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PMID:Secondary hyperparathyroidism in osteomalacia. 541 49

Chronic mercuric chloride intoxication in an aged horse given 0.8 mg Hg/kg/day for 14 weeks was manifest by signs of progressive respiratory difficulty and renal disease. The effects were not self-limiting after mercury was withdrawn, and the animal was destroyed six weeks later. Renal function changes included heavy glycosuria, modest proteinuria, phosphaturia, reduced urine osmolality, gradually increasing urine production, reduced glomerular filtration rate, and terminally, azotemia. The condition bore similarities to the Fanconi syndrome in man. Urinary gamma-glutamyl transpeptidase, alkaline phosphatase and amino-aspartate transferase activities were inconsistent indicators of tubular damage in random samples at this dose rate. The pathologic response was characterized by extensive granulomatous infiltration throughout the lungs, in particular, and to a lesser extent in the kidneys, liver and bone marrow. The renal changes included this marked interstitial reaction and proximal tubular degeneration. Mercury levels were negligible in the lungs and highest in the renal cortex. The granulomatous reaction was not encountered in previous mercury toxicity studies in horses and may indicate an individual sensitivity to the agent.
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PMID:Some effects of chronic mercuric chloride intoxication on renal function in a horse. 621 26


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