scholarly journals Risedronate, a Highly Effective Oral Agent in the Treatment of Patients with Severe Paget’s Disease1

1998 ◽  
Vol 83 (6) ◽  
pp. 1906-1910
Author(s):  
Frederick R. Singer ◽  
Thomas L. Clemens ◽  
Rachelle A. Eusebio ◽  
Pirow J. Bekker
Keyword(s):  
Serum Alkaline Phosphatase ◽  
Urinary Calcium ◽  
Oral Agent ◽  
Normal Range ◽  
Intact Pth ◽  
Urinary Hydroxyproline ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Percent Decrease ◽  
Phosphorus Levels

Thirteen patients with severe Paget’s disease of bone [mean serum alkaline phosphatase (SAP) level 17 times the upper limit of normal] were treated with 30 mg oral risedronate daily for 8 weeks. Patients were followed for 16 weeks without treatment. The change from baseline SAP was the primary end point. Those patients whose SAP levels did not reach the normal range were retreated with 30 mg for another 8 weeks. There was a mean percent decrease in SAP of 77% after the first course of risedronate treatment and 87% after the second course of treatment. All patients who completed the study had a decrease in SAP of at least 77% from the baseline. The urinary hydroxyproline/creatinine level was decreased by 64% and 79%, respectively, during the first and second treatment courses. There were transient asymptomatic decreases in serum calcium and phosphorus levels. The urinary calcium/creatinine ratio also decreased in these patients. Serum intact PTH and 1,25-dihydroxyvitamin D levels increased transiently during risedronate treatment. Oral risedronate was well tolerated by the patients. Only one patient discontinued treatment because of an adverse event (diarrhea) thought to be related to risedronate therapy.

Regulation of 1,25 (OH)2D synthesis in hypoparathyroidism and pseudohypoparathyroidism

1988 ◽  
Vol 255 (5) ◽  
pp. E730-E736
Author(s):  
N. A. Breslau ◽  
R. S. Weinstock
Keyword(s):  
Serum Phosphorus ◽  
Phosphorus Concentration ◽  
Parathyroid Hormone Receptor ◽  
Cyclic Monophosphate ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Complex Patients ◽  
Phosphorus Deprivation ◽  
Parathyroid Extract ◽  
Phosphorus Levels

We examined the regulation of 1,25-dihydroxyvitamin D [1,25(OH)2D] synthesis in patients with hypoparathyroidism (n = 5) and pseudohypoparathyroidism (n = 5) by administration of parathyroid extract (PTE) and N6,O2-dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP) and by phosphorus deprivation with antacids. In response to PTE, patients with hypoparathyroidism increased serum 1,25(OH)2D from 17 +/- 5 to 30 +/- 5 (SD) pg/ml (P less than 0.01). An approximate doubling of the 1,25(OH)2D concentration also occurred following dbcAMP infusion or phosphorus deprivation (serum phosphorus 4.4 +/- 0.5 to 2.6 +/- 1.1, P less than 0.01). Serum phosphorus and 1,25(OH)2D concentrations were inversely correlated (r = -0.73, P less than 0.001). Patients with pseudohypoparathyroidism had negligible responses to PTE with respect to urinary adenosine 3', 5'-cyclic monophosphate excretion, serum phosphorus concentration, or 1,25(OH)2D synthesis. They did show a rise in serum 1,25(OH)2D from 17 +/- 4 to 44 +/- 5 pg/ml (P less than 0.001) in response to dbcAMP infusion. During phosphorus deprivation, serum phosphorus decreased from 4.1 +/- 0.8 to 3.2 +/- 1.2 mg/dl (P less than 0.05), but there was no change in serum 1,25(OH)2D concentration or any correlation between serum phosphorus and 1,25(OH)2D levels. Although reduction in mean serum phosphorus levels was generally not as great in patients with pseudohypoparathyroidism, one such patient attained serum phosphorus of 1.2 mg/dl and still did not increase serum 1,25(OH)2D concentration. In addition to an abnormal parathyroid hormone receptor-adenylate cyclase complex, patients with pseudohypoparathyroidism appear to have an abnormal renal 1 alpha-hydroxylase, which does not respond appropriately to phosphate deprivation.

Estrogens and progestogens conserve bone in rats deficient in calcitonin and parathyroid hormone

1989 ◽  
Vol 257 (6) ◽  
pp. E903-E908
Author(s):  
A. Goulding ◽  
E. Gold
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Ovariectomized Rats ◽  
Lower Plasma ◽  
Urinary Hydroxyproline ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Thyroxine Replacement ◽  
Total Body ◽  
D Values

To examine the abilities of estrogens and progestogens to slow bone resorption and conserve bone in ovariectomized rats deficient in calcitonin (CT) or parathyroid hormone (PTH), nine groups of animals with 45Ca-labeled bones were studied for 12 wk. Rats were thyroidectomized (TX), parathyroidectomized (PTX), or given sham neck operations (Sham) and treated orally with either estrogen, 300 micrograms 17 beta-estradiol.kg body wt-1.wk-1; progestogen, 500 micrograms norethisterone acetate.kg body wt-1.wk-1; or placebo (Plac). The TX rats had parathyroid autografts and thyroxine replacement. In all surgical groups, estradiol (E2) and norethindrone (Nor) slowed urinary 45Ca excretion and conserved bone (P less than 0.001). However E2 lowered urinary hydroxyproline more than Nor. Total body Ca values (mg +/- SD) were Sham + Plac, 3,079 +/- 201; Sham + E2, 3,886 +/- 335; Sham + Nor, 3,567 +/- 459; TX + Plac, 3,123 +/- 159; TX + E2, 3,869 +/- 235; TX + Nor, 3,540 +/- 422; PTX + Sham, 3,067 +/- 249; PTX + E2, 3,775 +/- 414; PTX + Nor, 3,635 +/- 467. Importantly, E2 and Nor conserved bone as effectively in TX and PTX groups as in Sham rats, although the PTX rats had slower bone resorption and lower plasma 1,25-dihydroxyvitamin D values (P less than 0.001) than groups with intact parathyroids. We conclude that the effects of estrogens and progestogens to slow bone resorption and conserve bone are independent of CT and PTH. These findings appear relevant to the pathogenesis and treatment of postmenopausal osteoporosis.

scholarly journals Vitamin D Repletion in Patients with Primary Hyperparathyroidism and Coexistent Vitamin D Insufficiency

2005 ◽  
Vol 90 (4) ◽  
pp. 2122-2126 ◽  
Author(s):  
Andrew Grey ◽  
Jenny Lucas ◽  
Anne Horne ◽  
Greg Gamble ◽  
James S. Davidson ◽  
...  
Keyword(s):  
Vitamin D ◽  
Primary Hyperparathyroidism ◽  
Serum Calcium ◽  
Serum Alkaline Phosphatase ◽  
Vitamin D Insufficiency ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Total Serum ◽  
Calcium Excretion ◽  
Intact Pth

Abstract Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium <12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] <20 μg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 μg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P < 0.01) and 26% at 12 months (P < 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = −0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion.

scholarly journals Dipyridamole decreases renal phosphate leak and augments serum phosphorus in patients with low renal phosphate threshold.

1998 ◽  
Vol 9 (7) ◽  
pp. 1264-1269 ◽  
Author(s):  
D Prié ◽  
F B Blanchet ◽  
M Essig ◽  
J P Jourdain ◽  
G Friedlander
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Chronic Treatment ◽  
Serum Phosphorus ◽  
Calcium Excretion ◽  
Normal Range ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Renal Phosphate Reabsorption ◽  
A Prospective Study

It has been shown that an acute infusion of dipyridamole increased renal phosphate reabsorption in rats and humans. A prospective study was performed to determine whether chronic treatment by dipyridamole given orally could decrease renal phosphate leak and increase serum phosphorus in patients with idiopathic low renal phosphate threshold (TmPO4/GFR < 0.77 mM). Sixty-four patients with low TmPO4/GFR were included and treated with dipyridamole (75 mg, 4 times daily) for more than 12 mo. Serum phosphorus, TmPO4/GFR, parathyroid hormone, serum calcium, and 1,25-dihydroxyvitamin D were measured sequentially before treatment, and after 3, 6 to 9, and 12 mo of treatment. Under chronic treatment with dipyridamole, TmPO4/GFR and serum phosphorus significantly increased in 80% of patients within 3 mo, with maximal values reached within 9 mo. This improvement persisted after 12 mo of treatment. In 28 patients, 1,25-dihydroxyvitamin D concentrations were above the normal range (> 42 pg/ml) and normalized in parallel with the increase of serum phosphorus. The 24-h calcium excretion (which was initially increased in patients with high vitamin D concentrations) and urolithiasis decreased under treatment. Ionized serum calcium and parathyroid hormone remained unchanged. After 2 yr, treatment was discontinued in three patients; serum phosphorus and TmPO4/GFR decreased within 1 mo after discontinuation. Dipyridamole at a dose of 75 mg 4 times daily increases low TmPO4/GFR and improves hypophosphatemia in patients with renal phosphate losses and can be used to treat these patients.

Possible link between vitamin D and hyperoxaluria in patients with renal stone disease

1993 ◽  
Vol 84 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Sandro Giannini ◽  
Martino Nobile ◽  
Rocco Castrignano ◽  
Tecla Pati ◽  
Andrea Tasca ◽  
...  
Keyword(s):  
Vitamin D ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Urinary Oxalate ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Stone Formers ◽  
Group 2 ◽  
Urinary Oxalate Excretion ◽  
Group 1

1. Vitamin D seems to play an essential role in the pathogenesis of idiopathic hypercalciuria at least in part via intestinal hyperabsorption of calcium. Hyper-absorption of calcium, in turn, might enhance the intestinal uptake of free oxalate, thus leading to hyperoxaluria. To verify this hypothesis we studied 75 calcium-stone-formers subdivided as follows: group 1 (15 patients) with isolated hyperoxaluria; group 2 (25 patients) with hyperoxaluria and hypercalciuria; group 3 (22 patients) with isolated hypercalciuria; group 4 (12 patients) with no metabolic abnormalities. 2. As expected, urinary calcium excretion differed in the various groups (P < 0.001), being highest in groups 2 and 3; urinary oxalate excretion, by definition highest in groups 1 and 2, was even more pronounced in group 2 than in group 1 (P < 0.05). Although in the normal range, the serum 1,25-dihydroxyvitamin D concentration was higher (P < 0.001) in the two hypercalciuric groups (2 and 3), showing peak levels in group 2. 3. When the data from the 75 stone-formers were pooled, there was a positive correlation between the serum concentration of 1,25-dihydroxyvitamin D and urinary calcium excretion (P < 0.001) and urinary oxalate excretion (P < 0.003), the latter relationship also being present when only the two hypercalciuric groups (groups 2 and 3) were considered together (P < 0.05). 4. Our data seem to confirm a relevant role for the vitamin D system in the pathogenesis of calcium nephrolithiasis due to increased intestinal calcium absorption, but also because this in turn induces a greater intestinal absorption of oxalate, thus leading to the occurrence or exacerbation of hyperoxaluria.

Effect of Parathyroid Hormone on Vitamin D Metabolism in Osteopetrosis

PEDIATRICS ◽  
1981 ◽  
Vol 68 (1) ◽  
pp. 109-112
Author(s):  
Dagfinn Aarskog ◽  
Lage Aksnes ◽  
Trond Markestad
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Serum Levels ◽  
Target Cells ◽  
Normal Range ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Basal Serum ◽  
Parathyroid Extract

Indices of vitamin D metabolism were studied before and after infusion of bovine parathyroid hormone extract in three children with osteopetrosis. Basal serum concentrations of calcium, alkaline phosphatase, and 25-hydroxyvitamin D tended to be low. Serum immunoreactive parathyroid hormone levels were in the upper normal range in two patients. A marked increase in urinary cyclic adenosine 3': 5'-monophosphate(cAMP) in all patients was solely due to an increase in the nephrogenous cAMP. The basal concentration of 1,25-dihydroxyvitamin D was clearly more than the upper limit of normal range in all three patients and increased after parathyroid extract infusion in one patient. The basal serum levels of 24,25-dihydroxyvitamin D were within normal limits and tended to decrease after parathyroid extract infusion in two of the patients. Parathyroid hormone and 1,25-dihydroxyvitamin D act in concert to increase calcium resorption from bone, and the increased serum levels of both these factors may reflect lack, or unresponsiveness, of target cells in bone.

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