Department of Pneumology and Intensive Care Medicine, University Hospital Aachen, Aachen, Germany.
Department of Cardiology, Angiology and Intensive Care Medicine, University Hospital Aachen, Aachen, Germany.
Respir Res. 2018 Sep 20;19(1):183. doi: 10.1186/s12931-018-0889-6.
Fibroblast growth factor 23 (FGF23) regulates phosphate metabolism by increasing renal phosphate excretion and decreasing 1.25-dihydroxyvitamin D synthesis. Reports about hypophosphatemia in patients with chronic obstructive pulmonary disease (COPD) suggest altered phosphate metabolism. Therefore, we hypothesized that disturbances in phosphate-regulatory hormones such as FGF23 and parathyroid hormone (PTH) are present in COPD patients.
We investigated 40 COPD patients (63.5 ± 9.9 years, 27 male), each matched with two age- and sex-matched controls without any primary lung disease. COPD patients underwent lung function testing in advance. All patients had a glomerular filtration rate (GFR) > 60 mL/min/1.73m. We measured concentrations of intact FGF23 (iFGF23) and c-terminal FGF23 (c-term FGF23), phosphate, parathyroid hormone (PTH) and C-reactive protein (CRP) levels in COPD patients and controls.
Phosphate (1.0 ± 02 vs. 1.1 ± 0.2 mmol/L; p = 0.027), PTH (54.2 ± 29.4 vs. 68.7 ± 31.8 pg/mL; p = 0.002) and iFGF23 (46.3 ± 29.0 vs. 57.5 ± 33.5 pg/mL; p = 0.026 ) levels were significantly lower in COPD patients compared with controls. There was a significant negative correlation between c-term FGF23 and total lung capacity (r = - 0.4; p = 0.01), and between c-term FGF23 and CRP in COPD patients (r = 0.48; p = 0.002). iFGF23 and c-term FGF23 were positively correlated with phosphate and PTH in the control group.
We confirmed lower average serum phosphate levels in COPD patients compared with controls. However, our data do not suggest a causative role for FGF23 or PTH in COPD because levels of both phosphate-lowering hormones appear to be adaptively decreased as well. Therefore, further investigations are needed to identify the pathogenesis of low phosphate levels in patients with COPD and the relationship between phosphate-regulatory hormones and disease progression.
成纤维细胞生长因子 23（FGF23）通过增加肾脏磷酸盐排泄和减少 1,25-二羟维生素 D 合成来调节磷酸盐代谢。有关慢性阻塞性肺疾病（COPD）患者低磷酸盐血症的报告表明磷酸盐代谢发生改变。因此，我们假设 COPD 患者存在磷酸盐调节激素（如 FGF23 和甲状旁腺激素（PTH））的紊乱。
我们调查了 40 名 COPD 患者（63.5±9.9 岁，27 名男性），每位患者均与两名年龄和性别匹配的无原发性肺部疾病的对照相匹配。COPD 患者在进行肺功能测试之前接受了检查。所有患者的肾小球滤过率（GFR）>60 mL/min/1.73m。我们测量了 COPD 患者和对照组中完整 FGF23（iFGF23）和 C 端 FGF23（c-term FGF23）、磷酸盐、甲状旁腺激素（PTH）和 C 反应蛋白（CRP）的浓度。
与对照组相比，磷酸盐（1.0±0.2 与 1.1±0.2 mmol/L；p=0.027）、PTH（54.2±29.4 与 68.7±31.8 pg/mL；p=0.002）和 iFGF23（46.3±29.0 与 57.5±33.5 pg/mL；p=0.026）水平明显较低。在 COPD 患者中，c-term FGF23 与总肺容量呈显著负相关（r=-0.4；p=0.01），与 CRP 呈显著正相关（r=0.48；p=0.002）。在对照组中，iFGF23 和 c-term FGF23 与磷酸盐和 PTH 呈正相关。
我们证实 COPD 患者的平均血清磷酸盐水平低于对照组。然而，我们的数据并不表明 FGF23 或 PTH 在 COPD 中起因果作用，因为这两种降低磷酸盐的激素水平似乎也适应性降低。因此，需要进一步研究以确定 COPD 患者低磷酸盐血症的发病机制以及磷酸盐调节激素与疾病进展之间的关系。
