Vitamin-D Intoxication During Treatment of Hypoparathyroidism

Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

“…However, the therapeutic use of Vitamin D is restricted as a consequence of its toxicity in humans, causing hypercalcemia [20,21]. Therefore, to avoid toxic effects, we tested structurally modified "non-hypercalcemic" analogues for their potency in upregulating estrogen activity.…”

The Relevance of 25‐hydroxycalciferol Measurements in the Treatment of Hypoparathyroidism*

“…@ denotes patients who were hypocalcaemic on one or more occasions. 1968a, Hossain, 1970) who, while previously well controlled on a given dose of vitamin D became hypo-or hypercalcaemic for no apparent reason. We believe that serial measurements of 25-OHC may help avoid some of these seemingly capricious events.…”

Clinical Manifestations of Hypoparathyroidism

“…116 However, standard therapy with calcium supplementation and vitamin D or its activated metabolites can cause renal calcification both in the form of nephrocalcinosis and nephrolithiasis. 117 Maintaining a serum calcium level sufficient to prevent symptoms without causing elevated urine calcium excretion is difficult because in the absence of PTH, urinary calcium loss is higher at any given serum calcium concentration than would otherwise be the case. 35,118 Estimates of the prevalence of nephrolithiasis range from 2 to 15% with a hazard ratio four-fold higher than the general population.…”