Parameters of Vitamin D Metabolism in Patients with Hypoparathyroidism

Only a few studies evaluating the metabolism of vitamin D in patients with hypoparathyroidism (HypoPT) have been performed thus far, and, in particular, they mainly investigated the process of vitamin D activation (specifically, 1 alpha-hydroxylation). This study, therefore, aimed to evaluate the extended spectrum of vitamin D metabolites in patients with HypoPT compared to healthy individuals. We examined 38 adult patients with chronic HypoPT in comparison to 38 healthy adults. The assessment included biochemical parameters (total calcium, albumin, phosphorus, creatinine, and magnesium), parathyroid hormone (PTH), and vitamin D metabolites (25(OH)D-3, 25(OH)D-2, 1,25(OH)(2)D-3, 3-epi-25(OH)D-3, and 24,25(OH)(2)D-3) in serum. Our data show that an adequate level of 25(OH)D-3 (median 35.3 (29.6; 42.0) ng/mL) is achieved with standard doses of cholecalciferol (median 2000 (2000; 2500) IU per day) in HypoPT patients. They also presented with supraphysiological levels of 1,25(OH)(2)D-3 (median 71 (47; 96) vs. 40 (34; 59) pg/mL, p < 0.001) and the increased production of inactive metabolite (median 24,25(OH)(2)D-3 3.8 (3.0; 5.1) vs. 1.9 (1.3; 2.7) ng/mL, p < 0.001; median 25(OH)D-3/24,25(OH)(2)D-3 ratio 8.9 (7.6; 11.1) vs. 13.5 (11.1; 17.0), p < 0.001) as compared to the control group. This might be a consequence of the therapy received (treatment with activated vitamin D) and the pathophysiology of the disease (lack of PTH). The abnormality of vitamin D metabolism does not seem to interfere with the achievement of hypoparathyroidism compensation.

Automated summary

This study evaluated the extended spectrum of vitamin D metabolites in patients with HypoPT compared to healthy individuals. The results showed that patients with HypoPT achieved an adequate level of 25(OH)D-3 with standard doses of cholecalciferol, but they had supraphysiological levels of 1,25(OH)(2)D-3 and increased production of inactive metabolite. The abnormality of vitamin D metabolism does not seem to interfere with the achievement of hypoparathyroidism compensation.