Recombinant human erythropoietin(China Resources Angde)

This review focuses on the commonly prescribed medicaments that can be responsible for hypercalcemia, considering the prevalence, the predominant pathophysiological mechanisms, and the optimal medical management of each drug-induced hypercalcemia. Vitamin D supplements and 1α-hydroxylated vitamin D analogues increase intestinal calcium absorption, renal calcium reabsorption as well as bone resorption. In patients with hypoparathyroidism receiving recombinant human PTH, transient hypercalcemia can occur because of overtreatment, usually during acute illness. Thiazide-induced hypercalcemia is mainly explained by enhanced renal proximal calcium reabsorption, changing preexistent asymptomatic normocalcemic or intermittently hypercalcemic hyperparathyroidism into the classic hypercalcemic hyperparathyroidism. Lithium causes hypercalcemia mainly by drug-induced hyperparathyroidism.

Hypoparathyroidism is a rare endocrine disorder characterized by hypocalcaemia and hyperphosphatemia, due to absent or inappropriately low parathyroid hormone levels. For management of chronic hypoparathyroidism, current treatment options involve oral calcium and vitamin D. This standard treatment cannot resolve all problematic aspects of the disease, such as abnormal bone remodeling and reduced quality of life, and is associated with long-term complications, including nephrolithiasis, nephrocalcinosis, renal impairment, cataracts and cerebral calcifications.

In 2015, the FDA (Food and Drug Administration) approved rhPTH (1-84), named Natpara®, a bioengineered recombinant human PTH, for the management of hypoparathyroidism of any etiology, except Autosomal Dominant Hypocalcemia, not well controlled with calcium and active vitamin D. Herein, the authors review its chemistry, pharmacodynamics, pharmacokinetics and clinical efficacy for hypoparathyroidism.

Replacement therapy with rhPTH (1-84) is a fundamental step in the treatment of chronic hypoparathyroidism in cases not well controlled by standard therapy, providing the natural hormone that is lacking for the maintenance of normal calcium levels, and reducing long-term risks associated with conventional therapy. Nevertheless, given the chronic nature of the disease, in the future, further studies will have to be performed to evaluate long-term efficacy and safety of the drug.