ECE2016 Guided Posters Pituitary - Clinical (10 abstracts)
1Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital Rikshospitalet, Oslo, Norway; 2Faculty of Medicine, University of Oslo, Oslo, Norway.
Background: Bone turnover is increased in active acromegaly. Despite normalization of bone turnover after treatment, the risk for vertebral fractures remains increased. Gonadal status, but not bone mineral density (BMD) is correlated to vertebral fracture incidence. Trabecular and cortical bone are differentially affected by GH and IGF-1. The trabecular bone score (TBS) is related to bone microarchitecture and provides further information not captured by BMD measurement.
Methods: This longitudinal study included 38 patients with acromegaly consecutively recruited between 2005 and 2015. Dual-energy X-ray absorptiometry (DXA) scans and blood samples for measuring bone turnover (PINP, CTX1) were acquired at baseline and 1 year after transsphenoidal surgery. TBS was analysed at L1-L4 with TBS iNsight software.
Results: Following treatment, the mean TBS decreased by 3.0% (±7.0), from 1.33 (±0.15) to 1.29 (±0.14); P=0.007, whereas BMD L1-L4 increased by 3.2% (±4.9) from 1.20 (±0.19) to 1.24 (±0.20) g/cm2; P<0.001. The changes in BMD and TBS were not correlated (P=0.87).
TBS change in men was 4.5% (±6.7%; P=0.003) and in women 0.3% (±6.8%; P=0.85). There was a trend towards a difference in changes between men vs women (P=0.063).
Mean BMD L1-L4 increased in men +0.050 (±0.051; P<0.001, but not in women +0.016 (±0.061; P=0.36) g/cm2, (P=0.073 for interaction depending on gender).
BMD increased in ultradistal radius and total body (all P<0.01). The increase of BMD was associated with a decrease in PINP and CTX1 (P<0.001) and with lower levels of PINP and CTX1 at follow-up (P<0.02).
Conclusion: Treatment of acromegaly impacts TBS and BMD at L1-L4 in different manners. The reduction of bone turnover markers predicts the increase in BMD. The DXA changes in bone parameters were more pronounced in men. Alterations in trabecular bone architecture may explain the persistent fracture risk despite the increase in BMD after disease control.