Tarantino Giovanni, Citro Vincenzo, Esposito Pasquale, Giaquinto Sabrina, de Leone Annalisa, Milan Graziella, Tripodi Francesca Saveria, Cirillo Michele, Lobello Roberto
Department of Clinical and Experimental Medicine, Hepatology in Internal Medicine Section, Federico II University Medical School of Naples, Naples, Italy.
BMC Gastroenterol. 2009 Mar 17;9:21. doi: 10.1186/1471-230X-9-21.
Portal hypertension leads to the formation of portosystemic collateral veins in liver cirrhosis. The resulting shunting is responsible for the development of portosystemic encephalopathy. Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity. So, it has become partially obsolete. Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.
One hundred and fifty three consecutive patients with hepatic cirrhosis of various etiologies were recruited to participate in endoscopic and ultrasonography screening for the presence of portosystemic collaterals mostly esophageal varices, but also portal hypertensive gastropathy and large spontaneous shunts.
Based on Child-Pugh classification, the median level of blood ammonia was 45 mcM/L in 64 patients belonging to class A, 66 mcM/L in 66 patients of class B and 108 mcM/L in 23 patients of class C respectively (p < 0.001).The grade of esophageal varices was concordant with venous ammonia levels (rho 0.43, p < 0.001). The best area under the curve was given by ammonia concentrations, i, e., 0.78, when comparing areas of ammonia levels, platelet count and spleen longitudinal diameter at ultrasonography. Ammonia levels predicted hepatic decompensation and ascites presence (Odds Ratio 1.018, p < 0.001).
Identifying cirrhotic patients with high blood ammonia concentrations could be clinically useful, as high levels would lead to suspicion of being in presence of collaterals, in clinical practice of esophageal varices, and pinpoint those patients requiring closer follow-up and endoscopic screening.
门静脉高压导致肝硬化患者形成门体侧支静脉。由此产生的分流是门体性脑病发生的原因。尽管氨在门体性脑病的发生中起一定作用,但尚未发现静脉血氨水平与该疾病的存在或严重程度相关。因此,它已部分过时。认识到需要非侵入性标志物来反映食管静脉曲张的存在,以减少内镜筛查的次数,我们回过头来确定血氨浓度与门体侧支静脉的检测之间是否存在相关性,同时评估脾肿大、脾功能亢进(血小板减少)和肝硬化的严重程度。
连续招募153例不同病因的肝硬化患者,进行内镜和超声检查,以筛查门体侧支循环的存在情况,主要是食管静脉曲张,也包括门静脉高压性胃病和大的自发性分流。
根据Child-Pugh分类,64例A级患者的血氨中位数水平为45 μmol/L,66例B级患者为66 μmol/L,23例C级患者为108 μmol/L(p<0.001)。食管静脉曲张的分级与静脉血氨水平一致(rho 0.43,p<0.001)。在比较血氨水平、血小板计数和超声检查时脾脏纵径的面积时,血氨浓度的曲线下面积最佳,即0.78。血氨水平可预测肝脏失代偿和腹水的存在(优势比1.018,p<0.001)。
识别血氨浓度高的肝硬化患者在临床上可能有用,因为高血氨水平会使人怀疑存在侧支循环,在食管静脉曲张的临床实践中,并确定那些需要密切随访和内镜筛查的患者。