Plasma Chromogranin-A in Primary Hyperparathyroidism*

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Abstract
We sought an explanation for prior findings of high plasma chromogranin-A (Chr-A) in primary hyperparathyroidism. Chr-A was measured in plasma samples from 55 controls and 73 patients with primary hyperparathyroidism caused by adenoma (n = 14), sporadic or familial hyperplasia (n = 10), or familial multiple endocrine neoplasia type 1 (FMEN1; n = 49). Serum or plasma samples were also tested for calcium, PTH, gastrin, pancreatic polypeptide, CGα, and PRL. Plasma Chr-A was 34 ± 10 in parathyroid adenoma, 55 ± 33 in parathyroid hyperplasia without FMENl, 63 ± 88 in FMENl, and 25 ± 8 in controls (mean ± SD; nanograms per ml; FMENl or parathyroid hyperplasia vs. control, P < 0.05). Plasma Chr-A did not correlate with other hormonal variables in controls. Plasma Chr-A correlated with log serum gastrin (r = 0.43; P = 0.003) and plasma PTH (r = 0.52; P < 0.05) only in FMENl. In FMENl, plasma Chr-A was highest in subjects with Zollinger-Ellison syndrome (ZES, 120 ± 127; no ZES, 30 ± 33 (P < 0.0001). Parathyroidectomy did not decrease plasma Chr-A in patients with parathyroid adenoma or parathyroid hyperplasia. For FMENl patients with available pre- and postparathyroidectomy samples, Chr-A decreased postoperatively in four of five patients with ZES compared to none of six patients without ZES (P < 0.05). Elevated plasma Chr-A is not a general feature of primary hyperparathyroidism. Elevated plasma Chr-A in primary hyperparathyroidism was restricted principally to patients who also had ZES. Primary hyperparathyroidism may influence the level of Chr-A by an effect of hypercalcemia or elevated PTH on Chr-A secretion from pancreatic islet tissue.