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Comparison between Six-Year Therapy with Long-Acting Somatostatin Analogs and Successful Surgery in Acromegaly: Effects on Cardiovascular Risk Factors

Institute of Endocrine Sciences (C.L.R., V.V., P.B.-P., E.O., F.D., C.G., E.F., A.L., A.S., M.A.) and Occupational, Clinical and Environmental Epidemiology Research Center (A.B.), Fondazione Instituto di Ricovero e Cura a Carattere Scientifico Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, and Department of Endocrinology, Ospedale S. Giuseppe-Fatebenefratelli, AfaR (M.A.), University of Milan, 20122 Milan, Italy

Address all correspondence and requests for reprints to: Cristina L. Ronchi, Institute of Endocrine Sciences, Fondazione Instituto di Ricovero e Cura a Carattere Scientifico, Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via F. Sforza 35, 20122 Milan, Italy. E-mail: cristina.ronchi{at}unimi.it.

Context: The effects of chronic therapy with long-acting somatostatin analogs (SSTa) on metabolic and cardiovascular parameters have been partially elucidated in acromegalic patients.

Objective: The objective of this study was to compare the long-term effects of SSTa treatment and successful surgery on GH/IGF-I secretion and cardiovascular risk parameters in acromegaly.

Design, Patients, and Intervention: This was a retrospective study of 36 acromegalic patients treated with SSTa and evaluated after a median of 66 months and of 33 sex-, age-, and body mass index-matched cured patients evaluated after a similar period of remission, all from the Institute of Endocrine Sciences (Milan, Italy).

Main Outcome Measures: The main outcome measures were fasting and post-oral load glucose homeostasis, hemoglobin A_1c, insulin sensitivity and secretion by several indexes, lipid profile, and blood pressure.

Results: Fasting and areas under the glucose response curve rose in patients controlled (n = 29) and not controlled (n = 7) by SSTa, becoming higher than those in cured subjects. A 1% hemoglobin A_1c increase was observed in all nondiabetic SSTa patients, but not in cured subjects. Basal insulin secretion and resistance, evaluated by homeostasis model assessment, decreased in all SSTa patients, whereas oral glucose tolerance test-derived insulin secretion and resistance, evaluated by insulinogenic index and oral glucose tolerance test-derived insulin secretion, improved only in SSTa-treated controlled patients. Triglycerides did not change during SSTa, whereas high-density lipoprotein cholesterol increased in SSTa-treated controlled patients. At the last visit, the contemporary presence of at least three cardiovascular risk factors was more frequent in patients treated with SSTa than in cured subjects.

Conclusions: SSTa therapy induces long-lasting disease control and improvement of insulin sensitivity and high-density lipoprotein cholesterol levels in responsive patients. The progressive glucose homeostasis alterations, observed independently from the degree of cure, suggest the need for glucose homeostasis and peripheral vascular complications monitoring during chronic SSTa treatment.

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