TY - JOUR
T1 - Coexistence of bone and vascular disturbances in patients with endogenous glucocorticoid excess
AU - Yano, Chieko
AU - Yokomoto-Umakoshi, Maki
AU - Fujita, Masamichi
AU - Umakoshi, Hironobu
AU - Yano, Seiichi
AU - Iwahashi, Norifusa
AU - Katsuhara, Shunsuke
AU - Kaneko, Hiroki
AU - Ogata, Masatoshi
AU - Fukumoto, Tazuru
AU - Terada, Eriko
AU - Matsuda, Yayoi
AU - Sakamoto, Ryuichi
AU - Ogawa, Yoshihiro
N1 - Funding Information:
This work was supported in part by the grants from “ JSPS KAKENHI ” ( JP20K16525 and 21J40043 to M. Y-U., 22H04993 to Y.O., and 22K08627 to H.U.), “ The JSBMR Rising Stars Grant ” (to M. Y-U.), “ JAPAN Osteoporosis Foundation ” (to M. Y-U.), “ Takeda Science Foundation ” (to H.U.), “ Kaibara Morikazu Medical Science Promotion Foundation ” (to H.U. and M. Y-U.), “ Japan Foundation for Applied Enzymology ” (to H.U. and M. Y-U.), “ The Uehara Memorial Foundation ” (to H.U.), and “ Secom Science and Technology Foundation ” (to Y.O.).
Funding Information:
This work was supported in part by the grants from “JSPS KAKENHI” (JP20K16525 and 21J40043 to M. Y-U., 22H04993 to Y.O., and 22K08627 to H.U.), “The JSBMR Rising Stars Grant” (to M. Y-U.), “JAPAN Osteoporosis Foundation” (to M. Y-U.), “Takeda Science Foundation” (to H.U.), “Kaibara Morikazu Medical Science Promotion Foundation” (to H.U. and M. Y-U.), “Japan Foundation for Applied Enzymology” (to H.U. and M. Y-U.), “The Uehara Memorial Foundation” (to H.U.), and “Secom Science and Technology Foundation” (to Y.O.).
Publisher Copyright:
© 2022
PY - 2022/12
Y1 - 2022/12
N2 - Purpose: Bone and vascular diseases are considered to share pathogenic mechanisms. Excess glucocorticoids, key regulators of cardiovascular and metabolic homeostasis, may promote both diseases simultaneously. We used endogenous Cushing's syndrome (CS) to investigate whether glucocorticoid excess underlies coexisting bone and vascular diseases. Methods: We included 194 patients with adrenal tumors (ATs): autonomous cortisol secretion (ACS, n = 97) and non-functional AT (n = 97). ACS was further classified into overt CS (n = 17) and subclinical CS (SCS, n = 80). Arterial stiffness was defined as a brachial-ankle pulse wave velocity (baPWV) ≥ 1800 cm/s. Results: Patients with ACS had higher coexistence rates of vertebral fracture and arterial stiffness (23 % vs. 2 %; p < 0.001) and vertebral fracture and abdominal aortic calcification (22 % vs. 1 %; p < 0.001) than those with non-functional AT. In patients with ACS, baPWV was negatively correlated with trabecular bone score (TBS, r = −0.33; p = 0.002), but not with bone mineral density, and vertebral fracture was associated with arterial stiffness in the logistic regression analysis. In the multivariate analysis of variance, the degree of cortisol excess (defined as CS, SCS, and non-functional AT) determined the correlation between TBS and baPWV (partial η2 = 0.07; p < 0.001). In the analysis of covariance, patients with coexisting vertebral fracture and arterial stiffness had higher levels of serum cortisol after the 1-mg dexamethasone suppression test than those without. Conclusion: In endogenous glucocorticoid excess, bone and vascular diseases frequently coexisted, and deteriorated bone quality, not bone loss, was related to arterial stiffness. Thus, glucocorticoid excess may perturb the bone-vascular axis.
AB - Purpose: Bone and vascular diseases are considered to share pathogenic mechanisms. Excess glucocorticoids, key regulators of cardiovascular and metabolic homeostasis, may promote both diseases simultaneously. We used endogenous Cushing's syndrome (CS) to investigate whether glucocorticoid excess underlies coexisting bone and vascular diseases. Methods: We included 194 patients with adrenal tumors (ATs): autonomous cortisol secretion (ACS, n = 97) and non-functional AT (n = 97). ACS was further classified into overt CS (n = 17) and subclinical CS (SCS, n = 80). Arterial stiffness was defined as a brachial-ankle pulse wave velocity (baPWV) ≥ 1800 cm/s. Results: Patients with ACS had higher coexistence rates of vertebral fracture and arterial stiffness (23 % vs. 2 %; p < 0.001) and vertebral fracture and abdominal aortic calcification (22 % vs. 1 %; p < 0.001) than those with non-functional AT. In patients with ACS, baPWV was negatively correlated with trabecular bone score (TBS, r = −0.33; p = 0.002), but not with bone mineral density, and vertebral fracture was associated with arterial stiffness in the logistic regression analysis. In the multivariate analysis of variance, the degree of cortisol excess (defined as CS, SCS, and non-functional AT) determined the correlation between TBS and baPWV (partial η2 = 0.07; p < 0.001). In the analysis of covariance, patients with coexisting vertebral fracture and arterial stiffness had higher levels of serum cortisol after the 1-mg dexamethasone suppression test than those without. Conclusion: In endogenous glucocorticoid excess, bone and vascular diseases frequently coexisted, and deteriorated bone quality, not bone loss, was related to arterial stiffness. Thus, glucocorticoid excess may perturb the bone-vascular axis.
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U2 - 10.1016/j.bonr.2022.101610
DO - 10.1016/j.bonr.2022.101610
M3 - Article
AN - SCOPUS:85135873754
SN - 2352-1872
VL - 17
JO - Bone Reports
JF - Bone Reports
M1 - 101610
ER -
