# Acromegaly treatment and bone: a bidirectional relationship

## TL;DR

This paper reviews how acromegaly affects bone health and how treatments for the disease may influence bone metabolism.

## Contribution

The paper provides a review of how GH/IGF-I-lowering drugs affect bone metabolism and vertebral fractures in acromegaly.

## Key findings

- Excess GH and IGF-I increase the risk of fragility vertebral fractures in acromegaly patients.
- Somatostatin receptor ligands may reduce the incidence of vertebral fractures.
- The direct effects of these drugs on bone metabolism remain unclear.

## Abstract

Acromegaly is a rare disease caused by the elevated and autonomous secretion of growth hormone (GH) from a pituitary somatotroph tumor or neuroendocrine tumors, and the subsequent hypersecretion of insulin-like growth factor I (IGF-I) in peripheral tissues. Excess GH and IGF-I cause several chronic and systemic complications that impact mortality, morbidity, and quality of life in patients with acromegaly. Excess GH and IGF-I play a crucial role in bone remodeling by increasing osteoclastogenesis and impairing osteoblastogenesis. Several studies have demonstrated an increased prevalence and incidence of fragility vertebral fractures (VFs) in patients with acromegaly. Long-term exposure to high levels of GH and IGF-I is recognized as a risk factor for fragility fractures in patients with acromegaly. Recent studies have shown that first- and second-generation somatostatin receptor ligands (SRLs) can reduce the incidence of vertebral fractures (i-VFs). However, a direct effect of these molecules on bone metabolism has not yet been reported. Aims: This review summarizes the results of studies investigating the frequency of i-VFs according to different GH/IGF-I-lowering drugs and the potential effects of these treatments on bone metabolism, as well as preclinical data on potential molecular pathways that interact between GH/IGF-I-lowering drugs and bone metabolism.