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.

scholarly journals Successful Treatment for Hypercalcemia due to Cosecretion of Parathyroid Hormone-Related Protein and 1,25-Dihydroxyvitamin D3 in Non-Small-Cell Lung Cancer: A Case Report and Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Takunori Ogawa ◽  
Jun Miyata ◽  
Koichi Fukunaga ◽  
Akihiko Kawana ◽  
Takashi Inoue
Keyword(s):  
Lung Cancer ◽  
Case Report ◽  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Successful Treatment ◽  
Related Protein ◽  
Hypercalcemia Of Malignancy ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Parathyroid Hormone Related Protein

Hypercalcemia of malignancy frequently manifests as paraneoplastic syndrome in patients with solid tumors. A 71-year-old man was diagnosed with stage IIIB lung squamous cell carcinoma. Laboratory examination revealed high serum calcium concentration with elevated serum parathyroid hormone-related protein (PTHrP) and 1,25-dihydroxyvitamin D3 levels. As the patient did not respond to the initial treatment with calcitonin, extracellular fluid infusion, and chemotherapy, systemic prednisolone was administered additionally. Thus, the levels of serum calcium normalized and PTHrP and 1,25-dihydroxyvitamin D3 decreased simultaneously. To our knowledge, this is the first case report on the successful treatment of hypercalcemia of malignancy caused by PTHrP and 1,25-dihydroxyvitamin D3 cosecretion in a patient with lung cancer.

Unusual behaviour of an unusual tumour: calcitriol-induced hypercalcaemia in metastatic oesophageal neuroendocrine carcinoma

2020 ◽  
Vol 13 (8) ◽  
pp. e235209
Author(s):  
Filip Ionescu ◽  
Ioana Petrescu ◽  
Maria Marin
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Neuroendocrine Carcinoma ◽  
Solid Tumours ◽  
Related Protein ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Parathyroid Hormone Related Protein ◽  
Solid Malignancies ◽  
Osteolytic Metastases

Hypercalcaemia in malignancy is most commonly caused by paraneoplastic secretion of parathyroid hormone-related protein or osteolytic metastases. Very rarely (<1% of cases), the mechanism behind increased serum calcium is increased production of calcitriol (1,25-dihydroxyvitamin D) and even rarer is the occurrence of this phenomenon in solid malignancies, with few such instances reported in the literature. We present a case of a neuroendocrine malignancy originating in the oesophagus associated with calcitriol-induced hypercalcaemia, a phenomenon that has not been previously described. We review the pathophysiology of calcitriol-induced hypercalcaemia and previously reported cases of solid tumours with this presentation.

scholarly journals Serum 1,25-Dihydroxyvitamin D as a Biomarker of the Absence of Hypercalciuria in Postsurgical Hypoparathyroidism

2016 ◽  
Vol 102 (1) ◽  
pp. 259-266 ◽  
Author(s):  
Luis García-Pascual ◽  
María José Barahona ◽  
Verónica Perea ◽  
Rafael Simó
Keyword(s):  
Serum Calcium ◽  
Characteristic Curve ◽  
Linear Regression Analysis ◽  
Predictive Biomarkers ◽  
Multiple Linear Regression Analysis ◽  
Calcium Excretion ◽  
Cross Sectional ◽  
Oral Calcium ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Abstract Context: Hypercalciuria is an adverse event of postsurgical hypoparathyroidism treatment that can lead to renal complications. The collection of 24-hour urine to detect hypercalciuria is often considered unreliable. Objective: The purpose of this study was to find useful predictive biomarkers of hypercalciuria in patients with permanent postsurgical hypoparathyroidism receiving treatment with oral calcium and calcitriol supplements. Design and Setting: The investigation was designed as a prospective cross-sectional study. An outpatient hospital clinic served as the study setting. Patients: Fifty-four consecutive observations were made of 34 stable outpatients with postsurgical hypoparathyroidism taking oral calcium and calcitriol supplements, and 17 adult controls without hypoparathyroidism. Intervention: There were no interventions. Main Outcome Measure: Hypercalciuria was defined as 24-hour urine calcium &gt;300 mg. Results: Patients without hypercalciuria (n = 21) vs those with hypercalciuria (n = 33) had lower levels of serum 1,25-dihydroxyvitamin D (33.5 ± 11.9 pg/mL vs 45.8 ± 9.5 pg/mL; P &lt; 0.001), similar albumin-corrected serum calcium (8.3 ± 0.5 vs 8.6 ± 0.5 mg/dL; P = nonsignificant), and serum parathyroid hormone (12.5 ± 5.7 vs 10.7 ± 6.8 pg/mL; P = nonsignificant). Multiple linear regression analysis showed an independent relationship between 1,25-dihydroxyvitamin D and urinary calcium excretion (B = 6.2 ± 1.423; P &lt; 0.001). A cutoff value of 33.5 pg/mL for serum 1,25-dihydroxyvitamin D to predict the absence of hypercalciuria had 100% sensitivity and 63.6% specificity, and the area under the receiver operating characteristic curve was 0.797. No patients with serum 1,25-dihydroxyvitamin D levels of &lt;33.5 pg/mL presented with hypercalciuria, regardless of the level of albumin-corrected serum calcium. Conclusions: Routine measurement of serum 1,25-dihydroxyvitamin D may be useful as a biomarker to predict the absence of hypercalciuria in patients with permanent postsurgical hypoparathyroidism who are receiving treatment with oral calcium and calcitriol supplements.

Severe metabolic acidosis and disturbances of calcium metabolism induced by acetazolamide in patients on haemodialysis

1990 ◽  
Vol 78 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Sergio De Marchi ◽  
Emanuela Cecchin
Keyword(s):  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Normal Control ◽  
Serum Calcium ◽  
Normal Subjects ◽  
Inorganic Phosphorus ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

1. To investigate mechanisms of extrarenal buffering in uraemic acidosis, we studied the effects of the carbonic anhydrase inhibitor, acetazolamide, in normal subjects and in patients with end-stage kidney disease on maintenance haemodialysis with virtually no urine output. 2. Acetazolamide (500 mg) was administered daily for 7 days, after pretreatment for 1 month with 1,25-dihydroxyvitamin D (n = 12) or placebo (n = 12); only placebo was administered to a third group (n = 12) of haemodialysis patients. In addition, acetazolamide was administered to normal control subjects (n = 12). 3. Treatment with acetazolamide resulted in a more marked metabolic acidosis in haemodialysis patients than in normal control subjects and the effect in haemodialysis patients was attenuated by prior treatment with 1,25-dihydroxyvitamin D. 4. The administration of acetazolamide to haemodialysis patients led to an increase in serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase and parathyroid hormone, and a reduction in serum calcium, whereas acetazolamide had no effect on these variables in normal subjects. In contrast, in the haemodialysis patients previously treated with 1,25-dihydroxyvitamin D, acetazolamide increased serum inorganic phosphorus, bone isoenzyme of alkaline phosphatase, parathyroid hormone and serum calcium. 5. We hypothesize that the metabolic acidosis induced by acetazolamide in haemodialysis patients may result from interference with the mechanisms of extrarenal buffering. 6. As parathyroid hormone, 1,25-dihydroxyvitamin D and carbonic anhydrase are thought to be involved in bone buffering, we suggest that the marked acidosis seen in haemodialysis patients treated with acetazolamide may be due to impaired parathyroid hormone-mediated bone buffering.

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.

scholarly journals Effects of the Potassium-Binding Polymer Patiromer on Markers of Mineral Metabolism

2018 ◽  
Vol 14 (1) ◽  
pp. 103-110 ◽  
Author(s):  
David A. Bushinsky ◽  
David M. Spiegel ◽  
Jinwei Yuan ◽  
Suzette Warren ◽  
Jeanene Fogli ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Serum Potassium ◽  
Mineral Metabolism ◽  
Serum Phosphate ◽  
Intact Parathyroid Hormone ◽  
Once Daily ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Potassium Binding

Background and objectivesPatiromer is a sodium-free, nonabsorbed, potassium-binding polymer that uses calcium as the counter-exchange ion and is approved for treatment of hyperkalemia. The 4-week TOURMALINE study in patients with hyperkalemia previously demonstrated that patiromer administered once daily reduces serum potassium similarly when given with or without food. We report a prespecified exploratory efficacy analysis as well as a post hoc efficacy and safety analysis of the TOURMALINE study on circulating markers of mineral metabolism.Design, setting, participants, & measurementsAdults with hyperkalemia (potassium >5.0 mEq/L) were randomized to once-daily patiromer 8.4 g without/with food for 4 weeks, with doses adjusted to achieve and maintain serum potassium 3.8–5.0 mEq/L. Baseline and week 4 serum and 24-hour urine markers of mineral metabolism are reported for all patients combined (evaluable for efficacy, n=112; evaluable for safety, n=113). P values were calculated using a paired t test for change from baseline, unless otherwise specified.ResultsMean (SD) baseline eGFR was 41±26 ml/min per 1.73 m2. Mean (SD) changes from baseline to week 4 were 0.0±0.5 mg/dl (P=0.78; n=100) for albumin-corrected serum calcium, −0.2±0.2 mg/dl (P<0.001; n=100) for serum magnesium, and −0.1±0.7 mg/dl (P=0.47; n=100) for serum phosphate. Median (quartile 1, quartile 3) changes in 24-hour creatinine-normalized urine calcium and phosphate from baseline to week 4 were 2.5 (−11.5, 23.7) mg/24 h (P=0.10; n=69) and −43.0 (−162.6, 35.7) mg/24 h (P=0.004; n=95), respectively. Median (quartile 1, quartile 3) changes in intact parathyroid hormone and 1,25-dihydroxyvitamin D from baseline to week 4 were −13 (−31, 4) pg/ml (P<0.001; n=97) and −2 (−9, 3) pg/ml (P=0.05; n=96), respectively. There were no changes in fibroblast growth factor-23 or 25-hydroxyvitamin D. In patients (n=16) with baseline serum phosphate >4.8 mg/dL, the mean (SD) changes in serum and 24-hour creatinine-normalized urine phosphate from baseline to Week 4 were −0.6±0.8 mg/dl (n=13) and −149.1±162.6 mg/24hr (n=9), respectively.ConclusionsPatiromer lowered urine phosphate in all patients, and lowered both serum and urine phosphate in a small subset of patients with hyperphosphatemia. Intact parathyroid hormone and 1,25-dihydroxyvitamin D decreased, with no change in serum calcium.

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