Calcium homeostasis in patients with acute pancreatitis.

Abstract

Calcium homeostasis was studied serially in six patients admitted to the surgical intensive care unit because of acute pancreatitis. All developed ionized hypocalcemia. Serial assays of serum parathyroid hormone (PTH) revealed a prompt response to this hypocalcemia (1143 +/- 239 versus 574 +/- 24 pg/ml, P less than 0.05). Serum 1,25-dihydroxyvitamin D (1,25(OH)2D) levels rose from 26 +/- 8 to 104 +/- 17 pg/ml (P less than 0.01) in the expected time frame subsequent to the PTH peak, confirming the biologic significance of the PTH increases observed. Despite these significant elevations of PTH and 1,25(OH)2D, the expected prompt return of ionized calcium concentrations to normal levels was not seen. Also, urinary cyclic adenosine monophosphate production was not stimulated. These results suggest an acute functional resistance of bone to physiologic levels of PTH stimulation during the acute phase of pancreatitis. Fluid sequestration and hypovolemia are marked at this time. We suggest that pancreatitic hypocalcemia may occur when oligemic bone cannot respond normally to PTH and 1,25(OH)2D stimulation. As such, it may represent an end organ failure syndrome associated with shock and poor tissue perfusion.