The urinary excretion of cyclic adenosine monophosphate (AMP) and cyclic guanosine monophosphate (GMP) was examined in normal controls, 16 patients with hyperparathyroidism and six with hypoparathyroidism. The diurnal pattern of excretion of both nucleotides was not altered by either exercise or altered parathyroid function. Whereas calcitonin increased cyclic AMP excretion in a patient with Paget's disease, no effects on either nucleotide were observed in a parathyroidectomized patient. Calcium infusions produced variable effects on cyclic AMP and cyclic GMP excretion. Cyclic AMP excretion was elevated in 14 of 15 patients with hyperparathyroidism, and normal renal function; it decreased in all patients after removal of hyperplastic or adenomatous parathyroid glands. Three patients with carcinoma and hypercalcemia excreted normal amounts of cyclic AMP, those with hyperparathyroidism excreted increased amounts, and low levels were excreted by six hypoparathyroid patients and by one with hypercalcemic sarcoidosis. The 24-hour urinary output of cyclic AMP may be useful in differentiating hypercalcemia of various causes. SINCE the discovery of adenosine 3′,5′-monophosphate1 (cyclic AMP) by Sutherland and Rall, the concept that the nucleotide is the “second messenger” for many hormone-induced responses has evolved.1 2 3 Studies from many laboratories have supported this hypothesis and provided information describing numerous factors that regulate the metabolism of the nucleotide. Relatively few reports, however, have dealt with the application of cyclic AMP metabolism to clinical medicine. Chase et al.4 stated that patients with pseudohypoparathyroidism had decreased urinary excretion of cyclic AMP and, unlike normal subjects, failed to increase their excretion after administration of parathyroid hormone. During the course of the studies reported.
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