Primary hyperparathyroidism (PHPT) is a systemic disease. Although it affects explicitly the kidney, ureter, bladder complex, and bone, it invariably affects all human organ systems, including the pancreas, gallbladder, and even the cardiovascular system. The systemic effects of PHPT are mediated by persistently elevated serum calcium and parathyroid hormone (PTH) and low serum phosphate. Parathyroid hormone (PTH) and vitamin D are vital in calcium and phosphate homeostasis. Low calcium and high phosphate are potent stimuli for PTH secretion. At the same time, an optimum magnesium level is required for PTH secretion and action. In PHPT, there is an autonomous secretion of PTH, which results in persistently elevated serum calcium and low phosphate. It has a documented long-term effect leading to low bone mass, increased incidence of fractures, recurrent renal stone disease, pancreatitis, and even cardio-vascular impairment [1]. In the Western literature, the incidence of symptomatic PHPT ranges from 10% to 20% [2], but in developing countries like India, the incidence is as high as 95% [3]. Contrary to this, in recent times, the incidence of asymptomatic PHPT in India has been increasing [4].