Abstract

Acromegaly is the clinical consequence of chronic exposure of the tissues to excess GH and IGF‐I. It is almost exclusively the result of a GH‐secreting pituitary adenoma. In addition to the somatic features, uncontrolled acromegaly is associated with a number of complications and excess mortality. Management is aimed at control of the tumour; normalization of GH and IGF‐I secretion and relief of symptoms. Initial management of GH‐secreting pituitary adenoma is widely accepted as endonasal trans‐sphenoidal surgery, with second‐line therapy where disease is uncontrolled in most cases being somatostatin analogue therapy. With the combination of surgery and somatostatin analogue therapy, control is achieved in around 75% of patients; however, this leaves a significant proportion of patients requiring multimodality therapy to achieve remission. Within the UK, the health system has finite resources, and decisions for management require consideration of efficacy and cost‐effectiveness. To add to the complexity, subtle differences exist in availability of high‐cost medications used in the treatment of patients with acromegaly across the devolved nations of the UK. In this article, we discuss options for the management of persistent acromegaly following initial surgery and somatostatin analogue therapy, and explore earlier use of dopaminergics and conservative management.

Highlights

  • Is the clinical consequence of chronic exposure of the tissues to excessive growth hormone (GH) and IGF-I

  • Pasireotide is a second-generation somatostatin analogues (SSA) that displays high-affinity binding to human SSTR1, 2, 3 and 5, with 30-40 fold higher affinity for SSTR1 and SSTR5, though slightly lower affinity for SSTR2, compared with octreotide and lanreotide.[45]

  • The initial phase II clinical study comparing subcutaneous pasireotide and octreotide suggested pasireotide to have the greater efficacy in controlling GH and IGF-I levels.[46]

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Summary

Introduction

Is the clinical consequence of chronic exposure of the tissues to excessive growth hormone (GH) and IGF-I.

Results
Conclusion
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