Abstract

IntroductionIn nearly all cases, acromegaly is caused by excess GH from a pituitary adenoma, resulting in elevated circulating levels of GH and, subsequently, IGF-1. Treatment goals are to eliminate morbidity and restore the increased mortality to normal rates. Therapeutic strategies aim to minimize tumor mass and normalize GH and IGF-1 levels. Somatostatin analogues are the medical treatment of choice in acromegaly, as first-line or post-surgical therapy, and have proven efficacy in pituitary tumor volume reduction (TVR).MethodsHere we review the effects of somatostatin analogue therapy on pituitary tumor volume in patients with acromegaly.ResultsTVR with somatostatin analogues may be mediated by direct anti-proliferative effects via activation of somatostatin receptors, or by indirect effects, such as angiogenesis inhibition, and is more pronounced when they are administered as first-line therapy. Various studies of first-line treatment with octreotide LAR have shown significant TVR in ≥73 % of patients. First-line treatment with lanreotide Autogel has shown evidence of TVR, although more studies are needed. In a recent randomized, double-blind, 12-month trial in 358 medical-treatment-naïve acromegaly patients, significant TVR was achieved by 81 % of patients administered pasireotide LAR and 77 % administered octreotide LAR. Pre-operative somatostatin analogue therapy may also induce TVR and improve post-operative disease control compared with surgery alone. TVR is progressive with prolonged treatment, and decreased IGF-1 levels may be its best predictor, followed by age and degree of GH decrease. However, TVR does not always correlate with degree of biochemical control.ConclusionSomatostatin analogues (first- or second-line treatment) are the mainstay of medical therapy and, as first-line medical therapy, are associated with significant pituitary TVR in most patients.

Highlights

  • IntroductionThe goals of treatment in acromegaly are to reduce morbidity and to restore the increased mortality to normal ageand sex-adjusted rates [1]

  • In most cases, acromegaly is caused by excess growth hormone (GH) from a pituitary adenoma, resulting in elevated circulating levels of GH and, subsequently, insulin-like growth factor 1 (IGF-1)

  • Here we review the effects of somatostatin analogue therapy on pituitary tumor volume in patients with acromegaly

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Summary

Introduction

The goals of treatment in acromegaly are to reduce morbidity and to restore the increased mortality to normal ageand sex-adjusted rates [1]. The first-generation somatostatin analogues, octreotide and lanreotide, are currently the medical treatment of choice in acromegaly, as both adjuvant and first-line therapy, and have demonstrated efficacy in controlling GH and IGF-1 levels and in reducing pituitary tumor volume. Long-term (40 months) adjuvant therapy with octreotide LAR has been shown to reduce GH and IGF-1 levels, and reduce tumor volume, in patients with persistent and poorly controlled acromegaly after transsphenoidal surgery, adjuvant radiation, and/or dopamine agonists, but without prior treatment with somatostatin analogues [41]. Data from two recent studies showed a positive correlation between sst receptor expression in pituitary adenomas and both degree of tumor volume reduction and biochemical response with octreotide LAR adjuvant therapy [44, 45] This may help to identify patients most likely to respond to first-generation somatostatin analogues, having failed to achieve adequate control with surgery alone.

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