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Urine Calcium (urine + calcium)
Selected AbstractsGenetic Contribution to Bone Metabolism, Calcium Excretion, and Vitamin D and Parathyroid Hormone RegulationJOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2001D. Hunter Abstract A classical twin study was performed to assess the relative contribution of genetic and environmental factors to bone metabolism, calcium homeostasis, and the hormones regulating them. It was examined further whether the genetic effect is menopause dependent. The subjects were 2136 adult twins (98.3% female): 384 monozygotic (MZ) and 684 dizygotic (DZ) twin pairs. The intraclass correlations were calculated, and maximum likelihood model fitting was used to estimate genetic and environmental variance components. The intraclass correlations for all of the variables assessed were higher in MZ twin pairs. The heritabilities (95% CIs) obtained from model fitting for hormones regulating bone metabolism and calcium homeostasis were parathyroid hormone (PTH), 60% (54,65%); 25-hydroxyvitamin D [25(OH)D]; 43% (28,57%), 1,25-hydroxyvitamin D [1,25(OH)], 65% (53,74%); and vitamin D binding protein 62% (56,66%). The heritabilities (95% CIs) for markers of bone formation also were assessed; bone-specific alkaline phosphatase (BSAP), 74% (67,80%), and osteocalcin, 29% (14,44%); marker of bone resorption deoxypyridinoline (DPD), 58% (52,64%); and measure of calcium homeostasis 24 h urine calcium, creatinine (Cr), 52% (41,61%). The magnitude of genetic influence differed with menopause for most variables. This study provides evidence for the importance of genetic factors in determining bone resorption and formation, calcium excretion, and the hormones regulating these processes. It shows for the first time a clear genetic effect on bone resorption in premenopausal women and the regulation of PTH, vitamin D metabolism, and calcium excretion. The genes controlling bone hormones and markers are likely to be useful therapeutic and diagnostic targets. [source] Increased serum phosphate levels and calcium fluxes are seen in smaller individuals after a single dose of sodium phosphate colon cleansing solution: a pharmacokinetic analysisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2009E. D. EHRENPREIS Summary Background, Sodium phosphate containing colonoscopy preparations may cause electrolyte disturbances and calcium-phosphate nephropathy. Decreased body weight is an unexplored risk factor for complications with sodium phosphate ingestion. Aim, To perform a pharmacokinetic analysis of a single dose of Fleet Phospho-Soda in smaller and larger individuals. Methods, Seven subjects weighing <55 kg (Group I) and six weighing >100 kg (Group II) consumed 45 mL Fleet Phospho-Soda. Serum electrolytes were measured. Hydration was closely maintained by monitoring weight, fluid intake and total body water. Results, Marked increases in serum phosphate were seen in Group I compared to Group II. For example, mean serum phosphate at 120 min was 7.8 ± 0.5 mg/dL in Group I and 5.1 ± 0.8 mg/dL in Group II (P < 0.001). Normalized area under the phosphate vs. time curve for Group I was 1120 ± 190 mg/dL*min and 685 ± 136 mg/dL*min for Group II (P < 0.001). Twelve-hour urine calcium was lower in Group I (16.4 ± 7.6 mg) than in Group II (39.2 ± 7.8 mg, P < 0.001). Conclusions, Increased serum phosphate occurs in smaller individuals after ingestion of sodium phosphate preparations, even with strict attention to fluid intake. Smaller body weight poses a potential risk for calcium-phosphate nephropathy. [source] Mechanism of Formation of Human Calcium Oxalate Renal Stones on Randall's PlaqueTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 10 2007Andrew P. Evan Abstract Although calcium oxalate (CaOx) renal stones are known to grow attached to renal papillae, and specifically to regions of papillae that contain Randall's plaque (interstitial apatite deposits), the mechanisms of stone overgrowth on plaque are not known. To investigate the problem, we have obtained biopsy specimens from two stone patients that included an attached stone along with its tissue base and have studied the ultrastructural features of the attachment point using light and transmission electron microscopy, Fourier transform infrared spectroscopy (,-FTIR), and immunohistochemical analysis. The epithelium is disrupted at the attachment site. The denuded plaque that borders on the urinary space attracts an envelope of ribbon-like laminates of crystal and organic matrix arising from urine ions and molecules. Into the matrix of this ribbon grow amorphous apatite crystals that merge with and give way to the usual small apatite crystals imbedded in stone matrix; eventually CaOx crystals admix with apatite and become the predominant solid phase. Over time, urine calcium and oxalate ions gradually overgrow on the large crystals forming the attached stone. Anat Rec, 290:1315-1323, 2007. © 2007 Wiley-Liss, Inc. [source] Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism (PHP) in multiple endocrine neoplasia type 1 (MEN1) patientsCLINICAL ENDOCRINOLOGY, Issue 5 2008Antongiulio Faggiano Summary Background, In patients with multiple endocrine neoplasia type 1 (MEN1), expression of somatostatin receptor (SST) in parathyroid adenomas and effectiveness of therapy with somatostatin analogues on primary hyperparathyroidism (PHP) have been scarcely investigated. Objective, To evaluate the effects of depot long acting octreotide (OCT-LAR) in patients with MEN1-related PHP. Patients, Eight patients with a genetically confirmed MEN1, presenting both PHP and duodeno-pancreatic neuroendocrine tumours (NET), were enrolled. Design, The initial treatment was OCT-LAR 30 mg every 4 weeks. This therapy was established to stabilize the duodeno-pancreatic NET before to perform parathyroidectomy for PHP. Before OCT-LAR therapy, a SST scintigraphy was performed in all patients. SST subtype 2A immunohistochemistry was performed on parathyroid tumour samples from three patients undergone parathyroidectomy after OCT-LAR therapy. Measurements, Serum concentrations of PTH, calcium and phosphorus as well as the 24-h urine calcium : creatinine ratio and the renal threshold phosphate concentration were evaluated before and after OCT-LAR. Results, After OCT-LAR therapy, hypercalcaemia and hypercalciuria normalized in 75% and 62·5% of patients, respectively, and serum phosphorus and renal threshold phosphate significantly increased. Serum PTH concentrations significantly decreased in all patients and normalized in two of them. SST subtype 2A immunostaining was found in all parathyroid adenomas investigated, while SST scintigraphy showed a positive parathyroid tumour uptake in three of eight patients (37·5%). Conclusion, Six months of OCT-LAR therapy controlled hypercalcaemia and hypercalciuria in two-thirds of patients with MEN1-related PHP. Direct OCT-LAR effects mediated by binding to SST expression on parathyroid tumour cells are likely the main mechanism to explain the activity of this compound on calcium and phosphorus abnormalities in MEN1 PHP. [source] |