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)

In 22 patients who underwent surgery suspected of primary hyperparathyroidism, the surgical findings were compared with the results obtained by pre-operative parathyroid scanning and biochemical screening. Thirteen of 15 parathyroid adenomas were localized by pre-operative scanning, but in five of them a false positive focus was also described. The technique was less useful in primary hyperplasia. Comparable results were reported by other investigators. In both instances the best results were obtained in patients with high parathyroid activity as measured by plasma calcium, plasma alkaline phosphatase and tubular reabsorption of phosphorus (TRP). Parathyroid scintigraphy was especially helpful in the presence of ectopic adenomas and in patients who had undergone previous parathyroid surgery. Unfortunately, the possibility of false positive results makes it unreliable for the diagnosis of primary hyperparathyroidism.
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PMID:Pre-operative localization of hyperfunctioning parathyroid tissue by parathyroid scintigraphy. 94 48

It has been suggested that hypertrophic cardiomyopathy (HCM) may be associated with hyperparathyroidism. We evaluated parathyroid function in 15 patients with HCM and 14 patients with primary dilated cardiomyopathy (DCM), measuring different parameters of calcium metabolism (total serum calcium, ionized calcium, PTH, vitamin D metabolites, alkaline phosphatase, osteocalcin). As a group PTH levels were normal in HCM (intact PTH 3.9 +/- 1.6 pmol/l, midmolecular PTH 59 +/- 13 pmol/l and carboxyterminal PTH 0.6 +/- 0.4 ng/ml), but in 3 patients carboxyterminal PTH levels were persistently higher than normal, while all other parameters of calcium metabolism were normal. We conclude that parathyroid function is normal in patients with HCM, although some of them may have an abnormal secretion and/or metabolism of carboxyterminal PTH fragments, or a circulating substance the interferes with this PTH assay. Parathyroid function in DCM patients was normal, except in a patient who had hyperparathyroidism secondary to vitamin D deficiency.
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PMID:[Parathyroid function in hypertrophic myocardiopathy]. 175 23

In a prospective study the prevalence of sonographically enlarged parathyroid glands in patients on maintenance hemodialysis was investigated and correlated with clinical and laboratory findings of secondary hyperparathyroidism. We examined 97 unselected patients with a 5 MHz probe. In 34% (33/97) a total of 69 parathyroid glands were detected with a statistically significant correlation between the period of dialysis and the incidence of parathyroid enlargement; 47.8% of the glands were hypoechoic, 34.8% moderately echogenic and 17.3% gave echoes similar to the normal thyroid parenchyma. A correlation was found between the finding of enlarged parathyroid glands and blood levels of calcium and alkaline phosphatase. Parathyroid enlargement was found sonographically before, or in the absence of clinical and laboratory findings of secondary hyperparathyroidism. Sonography is therefore a useful technique for early diagnosis of hyperparathyroidism in patients on maintenance dialysis.
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PMID:[Parathyroid sonography in long-term dialysis]. 192 62

We have developed an animal model to study the pathogenesis of secondary hyperparathyroidism by inducing stable uremia in Sprague-Dawley rats by selective microligation of terminal branches of the left renal artery, followed by right nephrectomy. After 4 weeks the animals were killed, the parathyroid glands were removed and weighed, and blood samples were obtained. Of 30 rats, uremia developed in 22 (73%; uremic group) and eight (27%) died or did not become uremic. A sham-operated group of 15 rats served as control (control group). Creatinine levels were 1.8 +/- 0.5 mg/dl in the uremic group versus 0.5 +/- 0.1 mg/dl in the control group (p less than 0.0001). Parathyroid glands were hyperplastic in all rats with uremia and were heavier than parathyroid glands of control animals (70.3 +/- 26 vs 19.1 +/- 8 micrograms; p less than 0.0001). In the group with uremia, parathyroid hormone levels were increased over those of the control group (112.6 +/- 13 vs 28.9 +/- 6.2 pg/ml; p less than 0.0001), whereas osteocalcin levels were similar (36.6 +/- 11 vs 37.5 +/- 1 ng/ml). Serum calcium, phosphate, and alkaline phosphatase levels were similar in both groups. Our model can be used to test hypotheses concerning the treatment of secondary hyperparathyroidism and the relative pathogenetic relevance of vitamin D deficiency and phosphate retention.
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PMID:A new experimental model for secondary hyperparathyroidism. 258 5

Plasma concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 24,25-dihydroxyvitamin D (24,25-(OH)2D) were determined in 17 children with vitamin D deficiency rickets before therapy was started. Thirteen of them also had these tests repeated during treatment. The median 25-OHD concentration was at the lower limit of the reference range before, but increased distinctly within one week of treatment with 1 700-4 000 IU vitamin D per day (17 vs. 37 nmol/l, p less than 0.01). 24,25-(OH)2D was undetectable in twelve of the patients before therapy. Detectable concentrations were in the range of 1.7 to 3.5% of the corresponding 25-OHD levels throughout the study, and the two metabolites were closely correlated (r = 0.84, p less than 0.0005). The median 1,25-(OH)2D concentration was near the average of the reference range before, but increased to well above the upper limit of normal within one week of treatment (121 vs. 368 pmol/l, p less than 0.01). The levels were largely normal after 10 weeks of therapy, as were the plasma concentrations of calcium, phosphate, and alkaline phosphatase. Parathyroid activity, as judged by serum parathyroid hormone or urinary cyclic AMP concentrations, was stimulated in 11 of 12 children studied prior to treatment. It is concluded that there may be no clear-cut differences between normal nad rachitic values of the different vitamin D metabolites under practical clinical conditions. A low 25-OHD level combined with evidence of a stimulated parathyroid activity, and a rise of 1,25-(OH)2D levels to supernormal values following a few days of vitamin D therapy may be diagnostic clues.
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PMID:Plasma concentrations of vitamin D metabolites before and during treatment of vitamin D deficiency rickets in children. 633 Oct 57

High-aluminum dialysate exposure has been incriminated in the pathogenesis of vitamin D-resistant osteomalacia in patients undergoing long-term hemodialysis. Parathyroid-mediated osteitis fibrosa is rare in these patients. Thirteen patients undergoing longterm hemodialysis were transferred from a center (Unit A) where water used to prepare dialysate was high in aluminum (100 to 450 micrograms/liter) to a new center (Unit B) where dialysate was highly purified (aluminum concentration less than 10 micrograms/liter), and changes in calcium metabolism were studied over a 12-month period. After transfer of patients to Unit B, serum aluminum levels fell (p less than 0.01), whereas serum immunoreactive parathyroid hormone levels rose (p less than 0.01) over 10 months. Over this time, predialysis serum calcium levels did not alter significantly, whereas postdialysis serum calcium levels declined slightly (p less than 0.05). Serum phosphate levels did not alter. Serum alkaline phosphatase levels rose progressively in Unit B (p less than 0.001). Discontinuation of dialysate high in aluminum in patients undergoing long-term hemodialysis may facilitate a rise in parathyroid activity.
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PMID:Evidence of increased parathyroid activity on discontinuation of high-aluminum dialysate in patients undergoing hemodialysis. 643 9

Parathyroid crisis occurring in primary hyperparathyroidism is characterized by extremely high circulating levels of parathyroid hormone and acute onset of severe hypercalcemia. We describe a 62-year-old woman with parathyroid crisis probably due to an intratumoral hemorrhage. Renal dysfunction reduced the effectiveness of preoperative management and continued to deteriorate for 5 days after parathyroidectomy. The normalization of serum calcium after parathyroidectomy delayed and it took 6 days. Maintenance of renal function is important for pre- and postoperative courses of the present case. The rapid decrease in serum parathyroid hormone after parathyroidectomy was followed by a rapid and transient (about fivefold) increase in serum alkaline phosphatase with peak value on the 10th postoperative day. This indicated that reversal phase from bone resorption (accelerated by parathyroid hormone) to bone formation lasted about 10 days under the conditions of the present case.
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PMID:The time course of renal function and bone turnover in parathyroid crisis due to intratumoral hemorrhage. 795 Jan 56

Although high-dose intravenous calcitriol has been shown to be effective in suppressing parathyroid hormone (PTH) secretion in dialysis patients with secondary hyperparathyroidism, an increasing number of patients is refractory to treatment. Only a few studies have evaluated the factors that can predict a favorable response to calcitriol, but contrasting results have been reported. This study was performed to evaluate the effect of high-dose intravenous calcitriol on parathyroid function and to investigate the factors that can predict a favorable response to treatment. Thirty-five dialysis patients were selected for intravenous calcitriol treatment (2 microg after dialysis for 12 months) because of increased PTH levels (>325 pg/mL). Before starting the treatment, the set point of calcium and the PTH-ionized calcium (ICa) curve was evaluated in each patient by inducing hypocalcemia and, 1 week later, hypercalcemia to maximally stimulate or inhibit PTH secretion. Parathyroid glands were assessed by high-resolution color Doppler ultrasonography. Throughout the study, calcium carbonate or acetate dosage was modified to maintain serum phosphate less than 5.5 mg/dL. Hypercalcemia was managed by reducing dialysate calcium to 5 mg/dL and, if necessary, calcitriol dose. The therapeutic goal was to reduce PTH levels below 260 pg/mL while maintaining normocalcemia. The patients who achieved the therapeutic goal were considered responders. Taking the data from the 35 patients together, we observed a significant decrease (P < 0.01) in alkaline phosphatase (from 252 +/- 106 IU/L to 194 +/- 81 IU/L) and PTH (from 578 +/- 231 pg/mL to 408 +/- 291 pg/mL), and a significant increase in serum ICa (from 5.1 +/- 0.2 mg/dL to 5.3 +/- 0.2 mg/dL; P < 0.001) after calcitriol therapy. PTH changes after therapy were not correlated to serum ICa changes, serum phosphate levels during treatment, and calcitriol dose. The response to therapy was heterogeneous because PTH levels markedly decreased over the treatment period in 18 responsive patients, whereas they increased or remained unchanged in 14 of 17 nonresponders. In three additional refractory patients, there was a decline in PTH of 20% to 35%, but this decline was associated with hypercalcemia. Pretreatment parathyroid gland size, serum ICa, PTH, maximal PTH induced by hypocalcemia, minimal PTH induced by hypercalcemia, the set point of ICa, and the ICa levels at which maximal PTH secretion and inhibition occurred were higher in the 17 refractory patients than in the 18 responsive patients. However, logistic regression analysis showed that among these parathyroid function parameters, the only significant predictors of a favorable response to calcitriol therapy were the parathyroid gland size and the set point of ICa. Throughout the study, serum phosphate and calcitriol dose were comparable in the two groups. In conclusion, the response to intravenous calcitriol therapy in dialysis patients with secondary hyperparathyroidism is heterogeneous, consisting of patients who are either responsive or refractory to treatment; refractoriness can be predicted by parathyroid volume and calcium set point.
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PMID:Long-term effects of intravenous calcitriol therapy on the control of secondary hyperparathyroidism. 915 8

Parathyroid cells have an intracellular machinery for parathyroid hormone (PTH) secretion that is inversely regulated by the extracellular calcium concentration (Ca2+o). The recently characterized Ca2+o-sensing receptor (CaR) is a G protein-coupled, seven-transmembrane receptor mediating the inhibitory effects of high Ca2+o on PTH secretion. The CaR's precise cell surface localization and the signal transduction pathway(s) mediating its inhibitory effects on PTH secretion have not been characterized fully. Here, we demonstrate that the CaR resides within caveolin-rich membrane domains in bovine parathyroid cells. Chief cells within bovine parathyroid glands exhibit a similar pattern of staining for caveolin-1 and for alkaline phosphatase, a glucosylphosphatidylinositol-anchored protein often enriched in caveolae. Purified caveolin-enriched membrane fractions (CEMF) from bovine parathyroid cells are highly enriched in the CaR and alkaline phosphatase. Other signaling proteins, including Gq/11, eNOS, and several protein kinase C isoforms (i.e. alpha, delta, and zeta), are also present in CEMF. Activation of the CaR by high Ca2+o increases tyrosine phosphorylation of caveolin-1 in CEMF, suggesting that CaR-mediated signal transduction potentially involved in Ca2+o-regulated processes in parathyroid cells occur in caveolae-like domains.
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PMID:The calcium-sensing receptor is localized in caveolin-rich plasma membrane domains of bovine parathyroid cells. 970 6

Selective percutaneous ethanol injection therapy (PEIT) of the parathyroid glands has been shown to be effective in chronic dialysis patients with severe secondary hyperparathyroidism. In this study, we examined whether it was possible to maintain parathyroid function within target range (intact parathyroid hormone [iPTH], 160 to 360 pg/mL) in the long term after successful destruction of hyperplastic tissue. PEIT was performed in 46 patients resistant to calcitriol pulse therapy, and all glands larger than 5 mm in diameter were destroyed by ethanol, guided by power Doppler flow mapping. Serum iPTH levels decreased from 633.3 +/- 359.9 to 226.3 +/- 204.7 pg/mL at 3 weeks and were maintained at 289.9 +/- 222.4 pg/mL at 1 year after PEIT. Total alkaline phosphatase activity decreased from 384.9 +/- 160.1 to 234.0 +/- 110.5 IU/L at 1 year after PEIT. In 19 patients, iPTH levels decreased into relative hypoparathyroidism (iPTH < 160 pg/mL) at 3 weeks after PEIT; however, they recovered at 1 year after PEIT (191.1 +/- 29.6 pg/mL). Parathyroid function was maintained within target range in 80.4% of the patients at 1 year after PEIT with appropriate medical therapy. Surgical parathyroidectomy was not required in any patient. Conversely, in eight other patients with recurrent hyperparathyroidism after subtotal parathyroidectomy, iPTH levels recovered in only 50% of the patients at 1 year after PEIT. Thus, destruction of hyperplastic tissue should be optimized in such patients. Recurrent nerve palsy was observed in only one patient, but was reversible. In conclusion, selective PEIT guided by color Doppler flow mapping is an effective and safe adjunct to medical therapy with a low risk for hypoparathyroidism.
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PMID:Prognosis of parathyroid function after successful percutaneous ethanol injection therapy guided by color Doppler flow mapping in chronic dialysis patients. 1035 97


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