Faggiano A, Tavares LB, Tauchmanova L, Milone F, Mansueto G, Ramundo V, Del Basso De Caro ML, Lombardi G, De Rosa G, Colao A
Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism in MEN1 patients. [JOURNAL ARTICLE]
Clin Endocrinol (Oxf) 2008 May 14.
Background: In patients with multiple endocrine neoplasia type 1 (MEN1), expression of somatostatin receptor (SST) in parathyroid adenomas and effectiveness of therapy with somatostatin analogues on primary hyperparathyroidism (PHP) have been scarcely investigated.
Objective: To evaluate the effects of depot long acting octreotide (OCT-LAR) in patients with MEN1-related PHP.
Patients: Eight patients with a genetically confirmed MEN1, presenting both PHP and duodeno-pancreatic neuroendocrine tumors (NET), were enrolled.
Design: The initial treatment was OCT-LAR 30 mg every 4 weeks. This therapy was established to stabilize the duodeno-pancreatic NET before to perform parathyroidectomy for PHP. Before OCT-LAR therapy, a SST scintigraphy was performed in all patients. SST subtype 2A immunohistochemistry was performed on parathyroid tumor samples from 3 patients undergone parathyroidectomy after OCT-LAR therapy. Measurements: Serum concentrations of PTH, calcium and phosphorus as well as the 24-h urine calcium-to-creatinine ratio and the renal threshold phosphate concentration were evaluated before and after OCT-LAR.
Results: After OCT-LAR therapy, hypercalcemia and hypercalciuria normalized in 75% and 62.5% of patients, respectively, and serum phosphorus and renal threshold phosphate significantly increased. Serum PTH concentrations significantly decreased in all patients and normalized in two of them. SST subtype 2A immunostaining was found in all parathyroid adenomas investigated, while SST scintigraphy showed a positive parathyroid tumor uptake in 3 of 8 patients (37.5%).
Conclusion: Six months of OCT-LAR therapy controlled hypercalcaemia and hypercalciuria in two thirds of patients with MEN1-related PHP. Direct OCT-LAR effects mediated by binding to SST expression on parathyroid tumor cells are likely the main mechanism to explain the activity of this compound on calcium and phosphorus abnormalities in MEN1 PHP.
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