Fibroblast growth factor 23 (FGF23) has been reported to be involved in cardiovascular disease. The aim of this study was to investigate the association between FGF23 and the presence of coronary artery disease (CAD), as well as the number of stenotic vessels. A total of 254 eligible participants (167 men and 87 postmenopausal women) were enrolled in this study. Coronary angiography was used for diagnosis of CAD. Serum intact FGF23 levels were determined by a two-sided sandwich enzyme-linked immunosorbent assay. The median serum FGF23 levels of the entire study population were 39.9 (33.1-47.5) pg/mL. Serum FGF23 levels were higher in subjects with one-vessel disease than those without CAD (P < 0.05), which further increased significantly in the subjects with multi-vessel disease (P < 0.05). Serum FGF23 levels increased with cumulative number of stenotic vessels (P for trend < 0.001). Multiple stepwise regression analysis revealed estimated glomerular filtration rate (standardized β = -0.298; P < 0.001) and body mass index (standardized β = 0.132; P = 0.049) were independent factors correlated with FGF23. Multivariate logistic regression analysis showed that FGF23 was positively and independently associated with the presence of CAD (odds ratio = 1.058, 95% confidence interval = 1.025-1.092; P = 0.001). Additionally, FGF23 was also correlated with multi-vessel disease significantly (odds ratio = 1.034, 95% confidence interval = 1.007-1.062; P = 0.013). In conclusion, serum FGF23 levels exhibit positive and independent association with the presence of CAD and increase with the cumulative number of stenotic vessels.
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http://dx.doi.org/10.1111/1440-1681.12467 | DOI Listing |
Sao Paulo Med J
January 2025
Associate Professor, Department of Nephrology, Ankara Bilkent City Hospital, Ankara, Turkey.
Background: Insulin resistance often occurs in patients with chronic kidney disease (CKD) owing to mineral and bone metabolism disorders. Fibroblast growth factor (FGF)-23 and soluble klotho (s-KL) play crucial roles in linking CKD with mineral and bone metabolism.
Objective: This study aimed to examine the relationship between insulin resistance and FGF-23 and s-KL in patients with non-diabetic pre-dialysis patients with CKD.
Eur J Prev Cardiol
January 2025
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Rd, Chaoyang District, Beijing 100029, China.
Aims: Fibroblast growth factor 23 (FGF23) has been implicated in the occurrence of atrial fibrillation (AF), but its prognostic value in AF patients remains unclear.
Methods And Results: A total of 35 197 AF patients with available follow-up data (3.56, 0.
J Clin Endocrinol Metab
January 2025
Department of Endocrinology, Key Laboratory of Endocrinology, State Key Laboratory of Complex Severe and Rare Diseases, Dongcheng District, National Commission of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.
Context: Phosphate homeostasis was compromised in tumor-induced osteomalacia (TIO) due to increased fibroblast growth factor 23 (FGF23) secretion. Nevertheless, the glucose metabolic profile in TIO patients has not been investigated.
Objectives: This work aimed to clarify the glucose metabolic profiles in TIO patients and explore their interaction with impaired phosphate homeostasis.
JCEM Case Rep
February 2025
First Department of Internal Medicine, Wakayama Medical University, Wakayama City, Wakayama 641-8509, Japan.
Tumor-induced osteomalacia is characterized by hypophosphatemia and fragility fractures caused by fibroblast growth factor 23 (FGF23)-producing tumors. We report a case of tumor-induced osteomalacia in which the tumor location could be determined by gallium 68 (Ga)-DOTATOC positron emission tomography (PET)/computed tomography (CT). A 74-year-old woman had recurrent fractures and bone pain.
View Article and Find Full Text PDFBone Rep
March 2025
Department of Joint and Trauma Surgery, The Third Affiliated Hospital, Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou 510630, China.
Phosphaturic mesenchymal tumor (PMT) is a rare benign mesenchymal tumor characterized by excessive secretion of fibroblast growth factor 23 (FGF23), leading to phosphate loss and systemic osteomalacia. Despite recent progress in PMT research, no consensus on diagnosis and treatment guidelines has been established. This case series describes the clinical and pathological features of six pathologically confirmed PMT patients treated at the Third Affiliated Hospital of Sun Yat-sen University from 2010 to 2024, aiming to provide new insights for the management of this condition.
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