Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 16 P283

Endocrine tumours

Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism in MEN-1 patients

Antongiulio Faggiano1, Lidice Tavares1, Francesco Milone1, Gelsomina Mansueto2, Valeria Ramundo1, Maria Laura Del Basso De Caro2, Gaetano Lombardi1, Gaetano De Rosa2 & Annamaria Colao1

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1Federico Ii University, Departments of Molecular and Clinical Endocrinology and Oncology, Naples, Italy; 2Federico Ii University, Biomorphological and Functional Sciences, Naples, Italy.


Background: Expression of somatostatin receptor (SST) and therapy with somatostatin analogues have been scarcely investigated in parathyroid tumors.

Objective: To evaluate the effects of depot long acting octreotide (OCT-LAR) on primary hyperparathyroidism in patients affected with multiple endocrine neoplasia type 1 (MEN-1).

Subjects and methods: Eight patients with a genetically confirmed MEN-1 were enrolled. All patients presented with primary hyperparathyroidism together with duodeno-pancreatic neuroendocrine tumors. A SST scintigraphy was performed in all patients before therapy with OCT-LAR. OCT-LAR 30 mg was administered every 4 weeks in all patients. Effects of OCT-LAR therapy on serum PTH, serum and urinary calcium and phosphorus were evaluated for 6 months.

Results: OCT-LAR normalized hypercalcemia and hypercalciuria in 75% and 62.5% of patients, respectively, while serum PTH levels were significantly decreased but still above the normal range. At SST scintigraphy, a positive parathyroid tumor uptake was found in 37.5% of MEN1 patients. The decrease of both serum PTH and serum and urinary calcium levels after therapy with OCT-LAR occurred regardless from the SST scintigraphy results.

Conclusions: OCT-LAR controlled hypercalcemia and hypercalciuria associated with hyperparathyroidism in two thirds of patients with MEN1-related parathyroid adenomas. However, these effects seem to be dissociated by the suppression of PTH levels.

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