Guidelines on prevention and treatment of vitamin D deficiency

The Italian Society for Osteoporosis, Mineral Metabolism and Bone Diseases (SIOMMMS) has elaborated the following guidelines about the definition, prevention and treatment of inadequate vitamin D status. The highlights are presented here.     

中国高血压指南二十年

自1999年以来,我国先后颁布四版高血压指南,对高血压的认识,也从早期关注血管病变,转到器官保护及心血管综合征概念的确立,无不体现着步步深化和日益提高的过程。本文通过回顾四部指南的更新过程,对高血压防治理念的变迁做一综述。     

The effect of a combined oral calcium and vitamin D supplement for treating mild to moderate vitamin D deficiency in postmenopausal women

Objective

To evaluate the efficacy of a combined calcium and vitamin D (Ca-D3) supplement for vitamin D deficiency in a small group of postmenopausal women.

Methods

A prospective open label 3 month-study.

Participants

23 postmenopausal women (mean age 61.2 yrs) with vitamin D deficiency were given a combined oral Ca-D3 supplement called “Osteoblast”. The supplement comprises 500 mg elemental calcium and 500 IU of cholecalciferol. The dosing regimen comprised a loading dose of 1000 IU of cholecalciferol per day for one month (two tablets) and thereafter a maintenance dose of 500 IU of cholecalciferol per day for 2 months (one tablet).

Outcome measure

Serum was collected for calcium, 25 hydroxyvitamin D3 (25OHD3), and PTH measurements, as well as early morning 2-hour urine calcium/creatinine excretion index (Uca/creat). Specimens were collected at baseline and after 3 months of therapy. Data are reported as mean ± 1 standard error and 95% confidence intervals.

Results

Data was available for the 21 subjects who completed the study. Two subjects (9%) withdrew because of gastrointestinal intolerance. There were 3 subjects with moderate (12.5–24 nmol/L) and 18 with mild (25–49 nmol/L) vitamin D deficiency. Ten subjects (48%) had secondary hyperparathyroidism. Following the oral Ca-D3 combination, serum 25OHD3 levels normalised in all subjects with 18 (86%) subjects achieving values of greater than 70 nmol/L. Serum 25OHD3 levels increased from 36 (31–41) to 91 (79–102) nmol/L (p = 0.0001), increasing by an average of 152% over the 3-month period. There was a corresponding 38% decrease in serum PTH concentrations at 3 months (5.1 + 0.6 pmol/L), compared with baseline (8.0 + 1 pmol/L) (p = 0.001). No subject developed hypercalcemia, but an elevated Uca/creat excretion index occurred in one subjects.

Conclusions

A combined oral Ca-D3 product (Osteoblast) is effective for treating vitamin D deficiency and is adequately tolerated.     

Parathyroid function in human vitamin D deficiency and vitamin D deficiency in primary hyperparathyroidism

Serum immunoreactive parathyroid hormone (iPTH) concentrations were measured in patients with chronic simple vitamin D deficiency, and these values were related to the bone disease and the prevailing serum calcium and phosphorus values. The osteodystrophy in these patients mimics azotemic osteodystrophy, and there is a similar variability of serum calcium and phosphorus, including syndromes of “pseudohypoparathyroidism” and “hypercalcemic secondary hyperparathyroidism.” Observations were made on the reactivity of PTH secretion to calcium infusion and on the involution of secondary hyperparathyroidism after correction of vitamin D deficiency in these patients. It is proposed speculatively that vitamin D may act directly on the parathyroid glands, conceivably through the formation of calcium-binding protein, and that chronic lack of this effect could contribute to parathyroid hyperplasia and inappropriate development of hypercalcemia.     

Primary hyperparathyroidism and vitamin D deficiency

Primary hyperparathyroidism (PHPT) and vitamin D (VD) deficiency are frequent conditions due to the widespread application of assays for calcium and VD. PHPT presentation is dominated by diversity in its expression and the current predominance of asymptomatic forms. VD, which plays a major role in calcium and phosphate homeostasis, is also involved in many physiological processes in this disease, such as lipid and glucose metabolism, and in the signalling pathways and functioning of many cell types. The bone and cardiometabolic complications described in PHPT are exacerbated by vitamin D deficiency, the prevalence of which varies according to many parameters (environment, skin pigmentation, associated chronic diseases, liver and kidney function, assay kit used, etc.). In response to this observation, experts in field from medical societies validated the indication for systematic assay of VD occurring with PHPT and the need for replacement in case of deficiency. Several epidemiological studies have confirmed that replacement with natural vitamin D is well tolerated and safe in subjects with PHPT and VD deficiency. This supplementation reduces hyperparathormonemia, does not have symptomatic effects on calciuria, and especially improves the bone and functional condition of patients.     

Severe primary hyperparathyroidism and vitamin D deficiency

Primary hyperparathyrodism is a common disease, often asymptomatic. A young post-partum woman was hospitalized for functional impotence of the upper right limb and poor health status. Laboratory tests revealed severe primary hyperparathyroidism (osteitis fibrosa cystica and nephrolithiasis) associated with vitamin D deficiency. Technetium 99m and thallium parathyroid scintigraphy showed increased uptake under the left thyroid lobe. After surgical resection of a parathyroid adenoma, serum calcium fell markedly and parathyroid levels declined but remained above normal. Calcium and 25(OH)-vitamin D supplementation led to normal calcium and vitamin D levels in three Months, with marked improvement in the bone lesions visualized on the six-Month x-rays. Based on this observation, we describe the many radiological aspects of bone involvement in long-standing hyperparathyroidism aggravated by vitamin D deficiency. Early diagnosis of hyperparathyroidism is crucial.     

Vitamin D deficiency and disorders of vitamin D metabolism.

The disorders of vitamin D metabolism are inherited metabolic abnormalities involving mutations of the vitamin D receptor or enzymes involved in the metabolism of vitamin D to its biologically active form 1,25-dihydroxyvitamin D. Although these mutations are rare, studies in affected patients and animal models have helped to identify critical actions of vitamin D and the mechanism by which it exerts its effects. Vitamin D deficiency, however, is an increasingly recognized problem among the elderly and in the general population. Screening for vitamin D deficiency only in those patients with known risk factors will result in a large proportion of unrecognized affected patients.