胎盘生长因子水平既不能反映晚期慢性肝病患者门静脉高压的严重程度，也不能反映门静脉高压性胃病的严重程度。
Placental growth factor levels neither reflect severity of portal hypertension nor portal-hypertensive gastropathy in patients with advanced chronic liver disease.
机构信息
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria; Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Vienna, Austria; Hospital Hietzing, Vienna, Austria.
出版信息
Dig Liver Dis. 2021 Mar;53(3):345-352. doi: 10.1016/j.dld.2020.09.006. Epub 2020 Oct 6.
BACKGROUND & AIMS: Experimental data indicates that placental growth factor (PLGF) is involved in the pathophysiology of portal hypertension (PH) due to advanced chronic liver disease (ACLD). We investigated serum levels of PLGF and its "scavenger", the receptor soluble fms-like tyrosine kinase-1 (sFLT1, or sVEGFR1), in ACLD patients with different severity of PH and portal-hypertensive gastropathy (PHG).
METHODS
PLGF and sVEGFR1 were measured in ACLD patients with hepatic venous pressure gradient (HVPG) ≥6 mmHg (n = 241) and endoscopic evaluation of PHG (n = 216). Patients with pre-/posthepatic PH, TIPS, liver transplantation and hepatocellular carcinoma were excluded.
RESULTS
Thirty-two (13%) patients had HVPG 6-9 mmHg, 128 (53%) 10-19 mmHg and 81 (34%) ≥20 mmHg; 141 (59%) had decompensated ACLD (dACLD). PLGF (median 17.2 vs. 20.8 vs. 22.4 pg/mL; p = 0.002), sVEGFR1 (median 96.0 vs. 104.8 vs. 119.3 pg/mL; p < 0.001) levels increased across HVPG strata, while PLGF/sVEGFR1 ratios remained similar (0.19 vs. 0.20 vs. 0.18 pg/mL; p = 0.140). The correlation between PLGF and HVPG was weak (Rho = 0.190,95%CI 0.06-0.31; p = 0.003), and the PLGF/sVEGFR1 ratio did not correlate with HVPG (p = 0.331). The area-under-the-receiver operating characteristics (AUROC) for PLGF to detect clinically significant PH (CSPH;i.e. HVPG ≥ 10 mmHg) yielded only 0.688 (0.60-0.78; p < 0.001). When compared to ACLD patients without PHG, PLGF levels (20 without vs. 21.4 with mild vs. 17.1 pg/mL with severe PHG, respectively; p = 0.005) and PLGF/sVEGFR1 ratios (0.20 vs. 0.19 vs. 0.17; p = 0.076) did not increase with mild and severe PHG.
CONCLUSION
While PLGF levels tended to increase with severity of PH, the PLGF/sVEGFR1 ratio remained stable across HVPG strata. Neither PLGF nor the PLGF/sVEGFR1 ratio had diagnostic value for prediction of CSPH. The severity of PHG was also not associated with stepwise increases in PLGF levels or PLGF/sVEGFR1 ratio.
背景与目的
实验数据表明，胎盘生长因子（PLGF）在由于慢性肝病进展（ACLD）导致的门脉高压症（PH）的病理生理学中发挥作用。我们研究了不同严重程度的 PH 和门脉高压性胃病（PHG）的 ACLD 患者的血清 PLGF 及其“清道夫”受体可溶性 fms 样酪氨酸激酶-1（sFLT1，或 sVEGFR1）水平。
方法
我们在 HVPG≥6mmHg（n=241）和内镜评估 PHG（n=216）的 ACLD 患者中测量了 PLGF 和 sVEGFR1。排除了肝前/后 PH、TIPS、肝移植和肝细胞癌患者。
结果
32 例（13%）患者 HVPG 为 6-9mmHg，128 例（53%）为 10-19mmHg，81 例（34%）≥20mmHg；141 例（59%）为失代偿性 ACLD（dACLD）。PLGF（中位数 17.2pg/mL vs. 20.8pg/mL vs. 22.4pg/mL；p=0.002）、sVEGFR1（中位数 96.0pg/mL vs. 104.8pg/mL vs. 119.3pg/mL；p<0.001）水平随 HVPG 分层而升高，而 PLGF/sVEGFR1 比值保持相似（0.19pg/mL vs. 0.20pg/mL vs. 0.18pg/mL；p=0.140）。PLGF 与 HVPG 之间的相关性较弱（Rho=0.190，95%CI 0.06-0.31；p=0.003），并且 PLGF/sVEGFR1 比值与 HVPG 不相关（p=0.331）。PLGF 检测临床显著 PH（即 HVPG≥10mmHg；CSPH）的受试者工作特征曲线下面积（AUROC）仅为 0.688（0.60-0.78；p<0.001）。与无 PHG 的 ACLD 患者相比，PLGF 水平（20 例无 PHG 与 21.4 例轻度 PHG 与 17.1pg/mL 重度 PHG 相比，分别为 20pg/mL vs. 21.4pg/mL vs. 17.1pg/mL；p=0.005）和 PLGF/sVEGFR1 比值（0.20 vs. 0.19 vs. 0.17；p=0.076）在轻度和重度 PHG 中并未升高。
结论
虽然 PLGF 水平随 PH 的严重程度呈上升趋势，但 PLGF/sVEGFR1 比值在 HVPG 分层中保持稳定。PLGF 或 PLGF/sVEGFR1 比值均无预测 CSPH 的诊断价值。PHG 的严重程度也与 PLGF 水平或 PLGF/sVEGFR1 比值的逐步升高无关。
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