Quantitative Ultrasound of the Heel and Some Parameters of Bone Turnover in Patients with Acromegaly

Abstract

Acromegaly caused by growth hormone (GH) hypersecretion is characterized by enhanced skeletal growth and soft tissue enlargement. Insulin-like growth factor-1 (IGF-1) is the main peripheral mediator of GH action and it has a crucial role in the maintenance of a normal bone mass. However, in some patients with acromegaly, secondary osteoporosis is observed, despite the strong anabolic effect of GH and IGF-1 in bones. It is thought to be due to hypogonadism. The bone changes are accompanied by increased turnover. The aim of this study was to assess bone properties by ultrasound and turnover in patients with acromegaly. The study was carried out in 26 patients (13 men, 13 women): 14 with active acromegaly and 12 cured by surgery who had non-active disease. Speed of sound (SOS), broadband ultrasound attenuation (BUA) and their combination Stiffness Index (SI) by quantitative ultrasound (QUS) of the heel, hormonal status, serum osteocalcin (OC) concentration and the urinary excretion of pyridinoline collagen crosslinks (PYR) were all studied. Controls were 20 age- and sex-matched healthy persons. We observed statistically significantly lower QUS values in patients with active disease than in those whose disease was cured. The differences were more pronounced in men. QUS values were lower in the entire group of patients compared with the controls; however, the differences were not statistically significant. Serum OC concentrations and urinary PYR excretion were higher in active disease. Statistically significant inverse correlations between serum GH levels and SOS (r = -0.58, p = 0.002); BUA (r = -0.66; p = 0.0001); T-score (r = -0,65, p = 0.0001) and Z-score (r = -0.66, p = 0.0001) were found only in male patients. No correlations between IGF-1, duration of the disease, OC, PYR and other data studied were observed. In conclusion, we have shown decreased QUS parameters suggesting impaired bone properties and quality in terms of density and elasticity in men, but not in women, with active acromegaly. This finding suggests osteoporosis with increased bone turnover. The above-mentioned changes might be caused by the action of GH on trabecular bone and its metabolism, since no hypogonadism in male patients was shown. Moreover, the influence of acromegaly on heel geometry and soft tissue swelling should also be considered.

Seven-year follow-up in a case of primary hyperparathyroidism using quantitative ultrasound and dual X-ray absorptiometry

“…It was validated in various hormonal disorders such as menopause, primary hyperparathyroidism, acromegaly or metabolic bone diseases [2,[5][6][7]. Moreover, QUS is suitable both for monitoring of the antiresorptive therapy and for the prediction of fracture occurrences.…”

Pituitary disorders and osteoporosis

“…GH and its main peripheral mediator insulin-like growth factor-1 (IGF-1) stimulate proliferation, differentiation, and extracellular matrix production in osteoblastic cells. GH and IGF-1 also promote osteoclast recruitment and bone resorption activity [27][28][29][30]. In prepubertal period anabolic action of GH is responsible for longitudinal bone growth, whereas during the adolescence and early adulthood it induces skeletal maturation until the achievement of peak bone mass.…”

“…In some studies BMD was reported to be increased or within the reference ranges, while in other papers it was decreased [17,26,[34][35][36][37]. Conflicting data on bone mineral density might be related to gonadal status, different skeletal sites being measured, various techniques employed, subject's gender, age, and activity of the disease [28,36,38]. Hypogonadal patients with acromegaly are at higher risk of osteoporosis, particularly at sites composed predominantly of trabecular bone, which has more intimate contact with the circulation and is influenced by sex steroids to a greater extent [34,39,40].…”

“…It is well known that in patients with acromegaly bone turnover is increased [28,29,35]. A specific marker of bone formation, osteocalcin, is elevated in subjects with active disease [28,29,35,40,43].…”

“…A specific marker of bone formation, osteocalcin, is elevated in subjects with active disease [28,29,35,40,43]. Indicators of bone resorption such as urinary hydroxyproline/creatinine, urinary type I collagen cross-linked N-telopeptide, and serum C-terminal collagen type I cross-links are in higher concentrations than in controls [28,29,35,40,43]. Additionally, serum calcium and phosphate values and 24-hour urinary calcium are elevated in patients with active disease [27,29,34,35,41].…”