Endocrine Abstracts

Introduction: VitD deficiency, the pandemics of which we currently observe, may result in secondary hyperparathyroidism even if not accompanied by hypocalcaemia.

Aim: To assess VitD levels as a cause of secondary hyperparathyroidism.

Material and methods: 257 healthy volunteers with normal kidney function (GFR< 60 ml/min) (28.4% males), median age 57 years, were included. In each participant, serum calcium, phosphates, creatinine, PTH and total VitD levels, as well as urinary calcium in urine morning sample, were measured. Daily calcium intake was estimated with a dietary questionnaire. Statistical analysis was performed with Statistica 12 Software.

Results: Median VitD level in the investigated group was 21.22 ng/ml; PTH – 41.17 pg/ml, serum calcium – 2.39 mmol/l, serum phosphates – 1.12 mmol/l, serum creatinine – 68 μmol/l, and urinary calcium – 2.69 mmol/l. Median daily calcium intake was 689 mg. There was statistically significant negative correlation between VitD and PTH levels (r=−0.19, P=0.0018), independent of serum creatinine. This relationship was particularly significant for measurements performed during autumn/winter (r=−0.34, P<0.0001), while losing its significance in study subjects subgroup investigated during spring/summer (r=−0.06, P=0.5153). Kruskal-Wallis ANOVA analysis showed a statistically significant difference in PTH levels in relation to VitD deficiency severity (predefined ranges: <10; 10–19.9; 20–29.9 and ≥30 ng/ml) (P=0.0078). A significantly higher PTH level was observed in subjects with severe VitD deficiency (<10 ng/ml) when compared to subgroups with VitD levels of 20–29.9 ng/ml (P=0.0147) and ≥30 ng/ml (P=0.0401). A significant negative correlation was found also between serum PTH and serum calcium (r=−0.13, P=0.0447).

Conclusions: Lack of significant negative correlation between serum PTH and VitD, seen during spring and summer confirms that appropriate sunlight exposure is sufficient to correct VitD deficiency. Significant increase in PTH levels is seen mostly in subjects with particularly low VitD levels, which may be an argument for redefining the recommended normal range of VitD.