Introduction: In chronic kidney disease (CKD) patients, serum concentration of type I collagen N-telopeptide (S-NTX) increases as renal function declines because of perturbed bone metabolism by renal dysfunction itself and impaired urinary excretion of NTX. Glucocorticoid (GC), which is often used for the treatment of kidney disease, may enhance bone resorption. We studied the bone resorption state in GC-treated CKD patients and the effects of bisphosphonate on S-NTX.
Methods: We measured S-NTX and creatinine clearance (Ccr) in 48 non-diabetic patients with declining renal function who had never received GC, vitamin D, calcium or bisphosphonate (reference group). Bone markers including S-NTX and BSAP (bone specific alkaline-phosphatase) in 144 patients receiving GC (prednisone equivalent of > or =2.5 mg/day) for more than 6 months (GC-treated group) were measured. We compared the GC-treated group to the reference group in a cross-sectional study. In a longitudinal study, we further followed 55 patients from the GC-treated group, whose Ccr was more than 60 mL/min (CKD stage 1 or 2) for 1 year after 2.5 mg/day of risedronate was commenced.
Results: In the reference group, S-NTX was correlated with Ccr (S-NTX = 456.6/Ccr + 4.5, r = 0.797, P < 0.0001). S-NTX values in the GC-treated group were higher than those found in the reference group at any Ccr. We defined the resorption index (RI) as a ratio of measured S-NTX to estimated NTX given by the correlation curve. Whereas BSAP did not change significantly, S-NTX decreased significantly by risedronate treatment. RI decreased from 1.59 (baseline) to 1.54, 1.25 (P < 0.01, versus baseline) and 1.23 (P < 0.01) at 1, 3 and 6 months after the start of therapy, respectively, which means that S-NTX values approached the correlation curve. Percent changes of S-NTX at 3 months were larger in patients with higher pretreatment S-NTX.
Conclusion: Higher S-NTX in the GC-treated group suggests that bone resorption is enhanced by GC. In CKD patients with mild renal dysfunction, S-NTX is a practical and useful marker for monitoring bone resorption during GC treatment.
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http://dx.doi.org/10.1016/j.bone.2006.04.022 | DOI Listing |
J Clin Endocrinol Metab
November 2024
Division of Rheumatology, Department of Internal Medicine, Toho University School of Medicine.
J Transl Med
November 2024
Department of Orthopedics, Affiliated Hospital of Nanjing University of Chinese Medicine, 155 Hanzhong Road, Nanjing, Jiangsu Province, 210029, China.
Glucocorticoids (GCs) are key inducers of osteonecrosis, yet not all patients treated with GCs develop glucocorticoid-associated osteonecrosis (GAON). The factors mediating this relationship are unclear. Studies have shown that gut microbiota and their metabolites influence bone metabolism, but their role in GAON is unclear.
View Article and Find Full Text PDFCancer Diagn Progn
September 2024
Department of Gastroenterological Surgery, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan.
Background/aim: Despite the remarkable developments in chemotherapy for gastric cancer (GC), rapid tumor growth is sometimes experienced during chemotherapy. This study investigated the association of tumor growth rate (TGR) during second-line chemotherapy with the prognosis of patients with GC.
Patients And Methods: We retrospectively reviewed 29 patients with GC treated with nab-paclitaxel plus ramucirumab as second-line chemotherapy between 2017 and 2019 at Osaka Metropolitan University.
J Cell Physiol
September 2024
Department of Pharmacology, Instituto de Ciencias Biomedicas, Universidade de São Paulo, São Paulo, Brazil.
Chronic and excessive glucocorticoid (GC) exposure can cause Cushing's syndrome, resulting in fat accumulation in selected body areas. Particularly in the brown adipose tissue (BAT), GC acts negatively, resulting in whitening of the tissue. We hypothesized that dysregulation of microRNAs by GC could be an additional mechanism to explain its negative actions in BAT.
View Article and Find Full Text PDFBone
October 2024
Department of Anatomy, Physiology and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada. Electronic address:
Glucocorticoids (GCs) are the leading cause of secondary osteoporosis. The emerging perspective, derived primarily from 2D histological study of trabecular bone, is that GC-induced bone loss arises through the uncoupling of bone formation and resorption at the level of the basic multicellular unit (BMU), which carries out bone remodeling. Here we explore the impact of GCs on cortical bone remodeling in the rabbit model.
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