Long-term therapy, consisting of oral calcium and vitamin D, is indicated in most cases of hypocalcemia. The goal of long-term treatment is maintenance of serum calcium in the low-normal range. This alleviates hypocalcemic symptoms, while avoiding hypercalciuria, and provides a cushion against treatment-induced hypercalcemia. Oral elemental calcium 1 to 3 g/day in divided doses is usually sufficient. Several pharmacological preparations of calcium are available. Calcium citrate is more soluble than calcium carbonate, particularly in patients taking H 2 antagonists or proton-pump inhibitors and those with achlorhydria.
The principal effect of vitamin D is to increase gut calcium absorption, although it also has an effect on bone resorption. Various forms of vitamin D may be used depending on the specific abnormality of vitamin D synthesis. Vitamin D2 (ergocalciferol—the parent compound) requires hepatic and renal transformation for full activation. For most cases of hypocalcemia, usually hypoparathyroidism, vitamin D3 (cholecalciferol) is sufficient. 25-Hydroxyvitamin D (calcifediol—the product formed by hepatic conversion of vitamin D) may be used in severe liver disease, and 1,25-dihydroxyvitamin D (calcitriol—the active metabolite formed in the kidney) is most appropriate in vitamin D resistance, severe renal impairment, and patients with hypoparathyroidism unresponsive to other forms of vitamin D therapy. Vitamin D requirements may vary based on disease activity, interacting drugs, and dietary calcium intake. Hypercalciuria may occur during treatment. In this situation, a thiazide diuretic can be helpful in reducing urinary calcium excretion.
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