Clinical practice is therefore very variable as to how vitamin D deficiency can be corrected and dependent on the local availability of the two forms of vitamin D. We recognize that monotherapy with cholecalciferol would be the ideal preparation, and when available it should be used in preference to ergocalciferol. However, due to the lack of cholecalciferol at our institution we use the following regimen and have found this to be effective although there are no trial data.

• For all patients with vitamin D deficiency we start by initially giving large doses of oral ergocalciferol (2.5 mg/100 000 U) either as a one-off dose or weekly for up to four doses depending on baseline levels of 25(OH)D. Those patients with very low levels (e.g. <20 nmol/l with raised PTH levels) are given four doses.

   

• For patients with osteoporosis we add at the same time two tablets per day of a calcium and cholecalciferol preparation (e.g. Adcal D3® or Calcichew D₃® forte, which have cholecalciferol 10 µg/400 IU and calcium 500 mg per tablet), used for adjunctive treatment for osteoporosis, which general practitioners are able to prescribe, and patients can obtain from community pharmacists.

   

• For patients without osteoporosis we add at the same time two to six tablets per day of generic calcium and ergocalciferol (ergocalciferol 10 µg/400 IU and calcium 92 mg per tablet). This preparation can also be prescribed by general practitioners and allows for larger doses of ergocalciferol without too much calcium.

   

• We aim to increase 25(OH)D levels to at least >50 nmol/l and preferably >80 nmol/l, as well as to ensure PTH suppression within normal range in patients with secondary hyperparathyroidism.

   

Vitamin D intoxication is extremely rare and does not seem to occur when levels of 25(OH)D are <150 ng/ml (374 nmol/l) [6]. Vieth et al. [56] demonstrated a lack of toxicity following supplementation with cholecalciferol 700 µg (28 000 IU) per week for >6 months. Similarly, Heaney et al. [57] showed that 20 weeks supplementation at 125 µg and 250 µg (5000 and 10 000 IU, respectively) of cholecalciferol per day did not cause hypercalcaemia in any subject.

Calcitriol [1,25(OH)₂D] may have a role in patients with chronic kidney disease where renal hydroxylation is poor. It is possible that increasing circulating levels of 1,25(OH)₂D may act in an endocrine manner to immunomodulate. This is suggested by the inverse relationship of both 25(OH)D and 1,25(OH)₂D with RA disease activity [24] and the only intervention study of vitamin D used calcitriol [25]. However, calcitriol is unregulated by the body and can cause hypercalcaemia, hypercalciuria and subsequent risk of renal stones that limits use. There is the future potential for vitamin D analogues that are tissue selective with more non-classical actions and less propensity to mobilize calcium stores, which may limit this hypercalcaemic effect.

^{Extracted from}

Clinical aspects of vitamin D in the management of rheumatoid arthritis

P. Leventis¹ and S. Patel Rheumatology 2008 47(11):1617-1621