Abstract
Introduction/backgroundVitamin D deficiency further increases circulating parathyroid hormone (PTH) levels in patients with primary hyperparathyroidism (pHPT), with potential detrimental effects on bone mass.MethodsThis was an observational clinical study in consecutive conservatively treated postmenopausal women (n=40) with pHPT and coexistent 25-hydroxyvitamin D deficiency (25OHD ≤50 nmol/l (≤20 ng/ml)). Patients who showed an increase in serum 25OHD above the threshold of vitamin D deficiency (>50 nmol/l; n=28) using treatment with various commonly prescribed vitamin D preparations were, for the purposes of statistical analyses, allocated to the treatment group. Patients who were retrospectively identified as having received no treatment with vitamin D and/or remained vitamin D deficient were considered as non-responders/controls (n=12). Adjusted calcium (adjCa), PTH and 25OHD concentrations were monitored in all subjects up to 54 months (mean observation period of 18±2 months).ResultsProlonged increased vitamin D intake, regardless of the source (serum 25OHD, increase from 32.2±1.7 nmol/l at baseline to 136.4±11.6 nmol/l, P<0.0001), significantly reduced serum PTH (13.3±1.1 vs 10.5±1.0 pmol/l, P=0.0001), with no adverse effects on adjCa levels (2.60±0.03 vs 2.60±0.02 mmol/l, P=0.77) and renal function tests (P>0.73). In contrast, serum PTH remained unchanged (15.8±2.6 vs 16.3±1.9 pmol/l, P=0.64) in patients who remained vitamin D deficient, with a significant difference between groups in changes of PTH (P=0.0003). Intrapartial correlation analyses showed an independent negative correlation of changes in 25OHD with PTH levels (r ic=−0.41, P=0.014).ConclusionsProlonged treatment with vitamin D in various commonly prescribed preparations appeared to be safe and significantly reduced PTH levels by 21%.
Highlights
Primary hyperparathyroidism in postmenopausal women is frequently associated with vitamin D deficiency [1, 2], which in turn is an additional stimulus for further increases in circulating parathyroid hormone (PTH) levels [3, 4, 5]
Circulating PTH levels decreased in 89% (25/28) of the patients who were treated with vitamin D, with a mean decrease in circulating PTH of 21% (Fig. 2)
The prevalence of vitamin D deficiency is high in postmenopausal women with primary hyperparathyroidism (pHPT) [20], with potential detrimental effects on bone mass [6]
Summary
Primary hyperparathyroidism (pHPT) in postmenopausal women is frequently associated with vitamin D deficiency [1, 2], which in turn is an additional stimulus for further increases in circulating parathyroid hormone (PTH) levels [3, 4, 5]. Recent studies indicate that treatment of vitamin D deficiency may have the potential to reduce circulating PTH levels in patients with pHPT, without adverse effects on serum-adjusted calcium (adjCa) levels [3, 4, 5]. In the general population, beneficial effects of vitamin D replacement on bone mass and risk of fractures have been reported [6], as well as various additional factors that could argue for replacement with vitamin D. These include non-skeletal effects such as improved neuromuscular function and protection from hypertension, heart failure and resistance to infection [7]. There is an increased risk of severe and potentially life-threatening hypocalcaemia in patients with combined pHPT and vitamin D deficiency following parathyroidectomy [10], whereas correcting vitamin D deficiency has been shown to reduce both the incidence of post-operative hypocalcaemia and the length of stay in hospital [11]
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