Parathyroid function during acute pancreatitis

Abstract

Abstract The renal handling of calcium and phosphate, which normally reflects parathyroid hormone (PTH) activity, was studied during the first 5 days after admission to hospital in 18 patients with acute pancreatitis. The ionized calcium level in plasma was calculated from the total calcium, albumin, total protein and pH. Hypocalcaemia (Ca < 1·08) was found in 6 patients and was associated with low urine calcium concentrations, hypophosphataemia and lower renal tubular reabsorptions of phosphate. Although these changes were all consistent with an appropriate renal response to increased PTH production in the hypocalcaemic patients, measured levels of PTH were very variable. In one patient who developed tetany, calcium infusion resulted in a rise in plasma calcium and a reversal of renal changes, but had little influence upon PTH levels. We found no evidence that hypomagnesaemia or proteolytic degradation of PTH were factors in the aetiology of hypocalcaemia. The discrepancy between evidence of PTH activity from renal function and immunoassayable levels of PTH in plasma might indicate that the parathyroid response, although present, was inadequate to mobilize enough skeletal calcium to prevent hypocalcaemia; it underlines the need for caution in the interpretation of data from radioimmunoassay techniques when taken in isolation in situations where they have not been fully evaluated.