High calcium intake leads to

Ans. a. Milk-Alkali syndrome The milk-alkali syndrome is due to excessive ingestion of calcium and absorbable antacids such as milk or calcium carbonate. It is much less frequent since proton-pump inhibitors and other treatments became available for peptic ulcer disease. For a time, the increased use of calcium carbonate in the management of secondary hyperparathyroidism led to reappearance of the syndrome. The chronic form of the disease, termed Burnett's syndrome, is associated with irreversible renal damage. The acute syndromes reverse if the excess calcium and absorbable alkali are stopped.' Milk-Alkali Syndrome The milk-alkali syndrome is due to excessive ingestion of calcium and absorbable antacids such as milk or calcium carbonateQ. It is much less frequent since proton-pump inhibitors and other treatments became available for peptic ulcer disease. For a time, the increased use of calcium carbonate in the management of secondary hyperparathyroidism led to reappearance of the syndrome. Several clinical presentations-acute, subacute, and chronic-have been described, all of which feature hypercalcemia, alkalosis, and renal failureQ. The chronic form of the disease, termed Burnett's syndrome, is associated with irreversible renal damageQ. The acute syndromes reverse if the excess calcium and absorbable alkali are stoppedQ. Individual susceptibility is dependent on the fractional calcium absorption as a function of calcium intake. Some individuals absorb a high fraction of calcium, even with intakes >2 g of elemental calcium per day, instead of reducing calcium absorption with high intake, as occurs in most normal individuals. Development of hypercalcemia causes increased sodium excretion and some depletion of total-body water. These phenomena and perhaps some suppression of endogenous PTH secretion due to mild hypercalcemia lead to increased bicarbonate resorption and to alkalosis in the face of continued calcium carbonate ingestion Alkalosis per se selectively enhances calcium resorption in the distal nephron, thus aggravating the hypercalcemia. The cycle of mild hypercalcemia -4 bicarbonate retention alkalosis renal calcium retention -4 severe hypercalcemia perpetuates and aggravates hypercalcemia and alkalosis as long as calcium and absorbable alkali are ingestedQ.