The impact of vitamin D status and parameters of calcium metabolism in patients with primary hyperparathyroidism

Abstract

Vitamin D repletion in PHP seems safe. Considering the documented adverse influence of vitamin D deficiency in PHP, particularly on skeletal manifestations and on the postoperative course, vitamin D repletion is warranted.

Low 25‐Hydroxyvitamin D in Primary Hyperparathyroidism: Enhanced Conversion Into 1,25‐Hydroxyvitamin D May Not Be “True” Deficiency

“…(1,2,6,(15)(16)(17)20,21) In contrast, an isolated study has documented a lack of exaggerated rise in already existent hypercalcemia upon vitamin D supplementation. (12) However, in this study, 25OHD remained subnormal probably because of inadequate supplementation. The rise in serum calcium in our study, and in others, may be attributed to a further exaggerated rise in 1,25 (OH)D and a lack of suppression or a paradoxical rise of elevated PTH.…”

“…The presence of low serum 25OHD in subjects with PHP is wellestablished. (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) However, concurrently elevated serum 1,25 (OH)D concentrations in subjects with PHP have rarely been reported in the past 30 years. (15)(16)(17) This study also found normalization of mean concentrations of serum calcium, 25OHD, and 1,25(OH)D following a decline in circulating serum PTH levels after surgery.…”

“…The major role of PTH may be attributed to its well-established, multiple direct physiologic effects on calcium metabolism, including enhanced gastrointestinal absorption and bone resorption, as well as inhibited renal excretion. (12,13) However, PTH induced a rise in 1,25 (OH)D via accelerated conversion of 25OHD; this may also be a minor contributor to hypercalcemia because calcium absorption by the gut and the kidneys is facilitated by 1,25(OH)D. The minor contribution of 1,25(OH)D to hypercalcemia was also evident by (23)(24)(25) However, a consequent exaggerated rise in serum PTH with induction of a recurrence of hypercalcemia may confirm the major role of PTH in hypercalcemia. Therefore, low serum 25OHD in subjects with PHP alone (group1) was caused by enhanced conversion into 1,25(OH)D induced by elevated circulating PTH, a well-established physiologic effect of PTH and not a "true" vitamin D deficiency.…”

“…The 1,25(OH)D/25OHD ratio is an accepted index of expression of 1,25(OH)D generation from 25OHD. ( 3,9,12,14 ) PTH and both vitamin D levels were determined by a commercial laboratory (Mayo Clinic, Rochester, MN, USA) using well‐established immunoassays with interassay and intra‐assay coefficients of variation ranging from 12% to 15%. The usual blood tests for calcium, phosphorus, liver enzymes, albumin, serum urea nitrogen, creatinine, electrolytes, glucose, etc., were assessed by the local hospital laboratory using a chemical analyzer.…”

“…S ubnormal serum 25OHD concentrations are reported to occur frequently in individuals with primary hyperparathyroidism (PHP) and are attributed to concurrent vitamin D deficiency. (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) It is plausible that the prevalence of vitamin D deficiency is overestimated and exaggerated because low serum 25OHD levels may be explained by its enhanced conversion into 1,25-hydroxyvitamin D [1,25(OH)…”