Korula J, Ralls P
Department of Medicine (Hepatology) and Radiology, University of Southern California School of Medicine, Los Angeles.
Gastroenterology. 1991 Sep;101(3):800-5. doi: 10.1016/0016-5085(91)90542-s.
The effect of obliterating esophageal varices by endoscopic sclerotherapy on portal pressure was prospectively studied in 11 cirrhotic patients with variceal hemorrhage. Portal venous pressure gradient, determined as the difference between transhepatic portal and hepatic vein pressure, increased by a mean of 31.1% +/- 14.5% in 8 (73%) and decreased by a mean of 30.1% +/- 11.7% in 3 (27%) patients, with no statistically significant change overall (P = 0.1). These changes in portal venous pressure gradient occurred despite an improvement in the laboratory and clinical parameters of hepatic function. Deep abdominal sonography with color flow imaging at variceal obliteration showed patent paraumbilical veins in 6 (55%) patients, 3 of whom had decreases in portal venous pressure gradient (29%, 19%, 42.5%) at variceal obliteration. In 5 (45%) patients without patent paraumbilical veins, a statistically significant increase in portal venous pressure gradient between initial endoscopic variceal sclerotherapy and variceal obliteration was noted (P = 0.008). Rebleeding (single episode in all 4 patients, before obliteration in 3 patients) occurred in those with an increase in portal venous pressure gradient; all patients with portal venous pressure gradient decreases were nonbleeders. No correlation between changes in portal venous pressure gradient and time to variceal obliteration, number of sclerotherapy treatments, or rebleeding episodes was observed. Thus, an increase in portal venous pressure gradient was noted in the majority of patients at variceal obliteration. Although the portal venous pressure gradient decrease may be explained by a patent paraumbilical vein, the mechanism of portal venous pressure gradient increase is not clear. It is speculated that this portal venous pressure gradient increase may be caused by an increase in collateral resistance or flow or a combination of both, resulting from obliteration of esophageal varices by endoscopic sclerotherapy.
对11例伴有静脉曲张出血的肝硬化患者进行前瞻性研究，观察内镜硬化疗法消除食管静脉曲张对门静脉压力的影响。门静脉压力梯度通过经肝门静脉压与肝静脉压之差来确定，8例（73%）患者平均升高31.1%±14.5%，3例（27%）患者平均降低30.1%±11.7%，总体无统计学显著变化（P = 0.1）。尽管肝功能的实验室和临床参数有所改善，但门静脉压力梯度仍发生了这些变化。在静脉曲张消除时进行的彩色多普勒腹部超声检查显示，6例（55%）患者的脐旁静脉通畅，其中3例在静脉曲张消除时门静脉压力梯度降低（分别为29%、19%、42.5%）。在5例（45%）脐旁静脉不通畅的患者中，观察到从最初的内镜下静脉曲张硬化疗法到静脉曲张消除期间门静脉压力梯度有统计学显著升高（P = 0.008）。门静脉压力梯度升高的患者发生了再出血（4例患者均为单次出血，3例在静脉曲张消除前出血）；门静脉压力梯度降低的所有患者均未出血。未观察到门静脉压力梯度变化与静脉曲张消除时间、硬化疗法治疗次数或再出血发作之间存在相关性。因此，大多数患者在静脉曲张消除时门静脉压力梯度升高。虽然门静脉压力梯度降低可能由通畅的脐旁静脉解释，但门静脉压力梯度升高的机制尚不清楚。推测这种门静脉压力梯度升高可能是由于内镜硬化疗法消除食管静脉曲张导致侧支阻力或血流量增加或两者共同作用所致。
