Effects of medical therapies for acromegaly on glucose metabolism

Abstract

Objective: Abnormalities of glucose metabolism are common findings of acromegaly. However, robust evidence on whether therapy with somatostatin analogs (SSAs) or pegvisomant (PEG) differently affects glucose metabolism is lacking. The purpose of this study was to evaluate the effects of therapy with SSAs, PEG, or their combination on glucose metabolism in a large series of acromegalic patients. Design: This was a historical-prospective study. Among 50 consecutive acromegalic patients under SSA therapy, acromegaly in 19 patients was controlled. PEG used in combination with SSA therapy allowed the control of acromegaly in the remaining 31 patients and was then continued as monotherapy in 18 patients. Methods: The following parameters were evaluated at the diagnosis of acromegaly and during different treatments: fasting plasma glucose (FPG) and insulin concentrations, insulin sensitivity (QUICK-I), homeostasis model assessment of insulin resistance (HOMA2-IR), and plasma glucose and insulin concentrations during the oral glucose tolerance test (OGTT). Comparison was made using analysis for paired data. Results: Insulin resistance improved when acromegaly was controlled with therapy with SSAs, PEG, or SSACPEG. However, FPG concentrations were higher during SSA therapy (alone or combined with PEG) than at the diagnosis of acromegaly, even when corrected for disease activity, whereas they were reduced during PEG therapy. Mean glucose concentrations during the OGTT were higher in patients receiving SSA therapy than in those receiving PEG therapy. In addition, the prevalence of diabetes or impaired glucose tolerance was higher during SSA therapy than at diagnosis or during PEG therapy and was not influenced by disease control. Conclusions: Medical therapies for acromegaly reduce insulin resistance and increase insulin sensitivity; on the contrary, glucose indexes may be differently affected by SSA or PEG therapy.

60 YEARS OF NEUROENDOCRINOLOGY: Acromegaly

“…In contrast to SSA, PEG decreases fasting plasma glucose (Urbani et al 2013) and improves glucose tolerance (Colao et al 2006) and insulin sensitivity (Schreiber et al 2007). Switching from SSA to PEG significantly improves diabetes control in diabetic ACM cases .…”

Mechanisms of development of carbohydrate metabolism disturbances in acromegalic patients depending on treatment

“…Исследование механизмов развития НУО при акромегалии в зави-симости от терапии показало, что как после хирур-гического, так и на фоне медикаментозного лечения акромегалии происходит снижение инсулиноре-зистности печени (HOMA-IR) и инсулинзависимых тканей в целом (Matsuda). Данные результаты согла-суются с результатами других исследований и свиде-тельствуют о снижении инсулинорезистентности печени и периферических инсулинзависимых тка-ней на фоне хирургического и медикаментозного лечения акромегалии [7,10,11].…”

“…[2,[4][5][6] и специфические для акромегалии (длительность и *e-mail: trigolosova_ira@mail.ru © Коллектив авторов, 2015 активность заболевания, проводимое лечение и т.п.) [2,7,8]. Основной метод лечения акромегалии -хирургический, который, по данным современных исследований [9,10], является не только наиболее эффективным, но и оказывает положительное влия-ние на состояние углеводного обмена.…”

“…ПРОБЛЕМЫ ЭНДОКРИНОЛОГИИ, 1,2015 тропного гормона (СТГ), снижая его секрецию, с другой -подавляют секрецию инсулина, что само по себе может вести к нарушению углеводного об-мена (НУО) [7,11].…”

Profile of pegvisomant in the management of acromegaly: an evidence based review of its place in therapy

“…2) SSA treatment has a divergent effect on glucose metabolism: a positive one lowering GH/IGF-I levels, decreasing insulin resistance and a negative effect suppressing insulin secretion. 35,36 A recent meta-analysis showed that SSA have a minor impact on glucose homeostasis in acromegaly, 36 although some controversy persists, 37 and 3) PEG has positive effects on glucose metabolism in acromegaly. [38][39][40][41][42] PEG does not exert any direct effect on pancreatic β-cell function and unlike SSA it does not suppress insulin secretion.…”