Extracellular cyclic AMP levels in osteomalacia.

Abstract

Abstract. Plasma and urinary cyclic AMP were measured in a 62-year-old man with severe osteomalacia due to a gluten-induced enteropathy. Before therapy, plasma cyclic AMP was normal and both urinary and nephrogenous cyclic AMP were markedly increased. A calcium infusion acutely diminished the elevated iPTH and urinary cyclic AMP levels. Following a bolus infusion of PTE, there was no phosphaturia despite a somewhat exaggerated increase in cyclic AMP excretion. With appropriate therapy, serum calcium, phosphorus, alkaline phosphatase, iPTH and 25-OHD3 and urinary and nephrogenous cyclic AMP gradually returned to normal. The response to PTE infusion after normalization of serum electrolytes, iPTH, and 25-OHD3 levels was similar to that seen before therapy. These results demonstrate that non-azotaemic malabsorptive osteomalacia is associated with elevations in urinary and nephrogenous cyclic AMP which gradually fall to normal with therapy. In contrast to studies in the vitamin D deficient rat, the maximal urinary cyclic AMP response to PTE is not diminished in the human with malabsorptive osteomalacia. The lack of a phosphaturic response to PTE depite a normal increase in urinary cyclic AMP excretion, as seen in our patient, is similar to that described in some patients with pseudohypoparathyroidism, suggesting that the response is not specific for the latter disorder. Finally, the data suggest that endogenous PTH does not modulate its renal receptors, at least in terms of cyclic AMP generation.