Wang T F, Hwang S J, Lee E Y, Tsai Y T, Lin H C, Li C P, Cheng H M, Liu H J, Wang S S, Lee S D
Department of Medicine, Veterans General Hospital-Taipei, Taiwan, Republic of China.
J Gastroenterol Hepatol. 1997 Jun;12(6):445-9. doi: 10.1111/j.1440-1746.1997.tb00464.x.
Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58 +/- 8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Forty-one (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (> 4 mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6 +/- 0.6 vs 2.9 +/- 0.7 gm/dL, respectively; P < 0.05), a longer prothrombin time (13 +/- 6 vs 16 +/- 6 s, respectively; P < 0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P < 0.05) and more patients with ascites (8 vs 50%, respectively; P < 0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9 +/- 4.5 vs 17.1 +/- 4.1 mmHg, respectively; P < 0.01) and a lower systemic vascular resistance (SVR; 1144 +/- 332 vs 1010 +/- 318 dyn.s/cm5, respectively; P < 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5 were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.
胆囊壁增厚在肝硬化患者中很常见，但其确切病因尚未完全明确。我们针对胆囊壁增厚情况，评估了肝硬化患者的临床、生化和血流动力学数据。排除患有胆结石、急慢性胆囊炎、心力衰竭、血清肌酐水平大于2mg/dL和/或血清丙氨酸氨基转移酶水平大于400U/L的患者后，77例肝硬化患者（75例男性，2例女性；平均年龄58±8岁）被纳入研究。收集了每位患者的临床、生化、超声和血流动力学数据。77例肝硬化患者中有41例（53%）存在胆囊壁增厚（>4mm）。与胆囊壁正常的患者相比，胆囊壁增厚的患者血清白蛋白水平显著更低（分别为3.6±0.6与2.9±0.7g/dL；P<0.05），凝血酶原时间更长（分别为13±6与16±6秒；P<0.05），Child-Pugh C级患者更多（分别为6%与37%；P<0.05），腹水患者更多（分别为8%与50%；P<0.05）。此外，与胆囊壁正常的患者相比，胆囊壁增厚的患者肝静脉压力梯度更高（分别为13.9±4.5与17.1±4.1mmHg；P<0.01），全身血管阻力更低（SVR；分别为1144±332与1010±318dyn.s/cm5；P<0.05）。通过多因素分析，腹水的存在和SVR低于900dyn.s/cm5与胆囊壁增厚独立相关，而肝静脉压力梯度大于10mmHg仅有边缘性显著关联。腹水的存在、SVR降低和门静脉高压与肝硬化患者胆囊壁增厚的发生有关，表明胆囊壁增厚的发展可能是多因素的。
