Basics of Management of Calcium and Bone Disorders

Calcium homeostasis is maintained by three hormones (parathyroid hormone (PTH), 1,25-dihydroxyvitamin D3, and calcitonin. PTH acts on the kidneys to increase calcium reabsorption and secretion of Vitamin D3 by activating 25 (OH) Vit D3 to 1,25-dihydroxyvitamin D3, and on bones it stimulates osteoclasts leading to bone reabsorption and release of free calcium. Vitamin D3 stimulates calcium absorption from the gut. Calcitonin on the other side do the opposite to PTH and Vitamin D3, it is released from the thyroid parafollicular cells and acts on the bones to deposit calcium in case of hypercalcaemia, Calcitonin increases urinary calcium excretion and inhibits absorption in the intestines. Hypomagnesemia will reduce parathyroid hormone leading to calcium deficiency, common scenario with Proton pump inhibitor. FGF23 causes renal phosphate wasting and low 1,25(OH)2D3 in normal kidney function but its effect is lost in advanced kidney disease. Elevated FGF23 from bones occurs in X-linked hypophosphatemia rickets, hypophosphatemia rickets type 1, and tumour-induced osteomalacia due to FGF23-producing tumours.