Zullo A, Rinaldi V, Hassan C, Folino S, Winn S, Pinto G, Attili A F
Department of Clinical Medicine, Gastroenterology II, University of Rome La Sapienza, Italy.
Ital J Gastroenterol Hepatol. 1998 Aug;30(4):405-9.
The role of Helicobacter pylori as a cause of hyperammonaemia in cirrhotics has still not been fully clarified. This study was aimed at evaluating the effect of acute Helicobacter pylori urease inhibition by oral acetohydroxamic acid administration on blood ammonia levels in cirrhotic patients.
Twenty-nine cirrhotics (14 males, 15 females; mean age: 63 years; Child-Pugh class: 14 A, 9 B, and 6 C) undergoing upper gastrointestinal endoscopy were enrolled in the study. The presence of Helicobacter pylori infection was assessed by rapid urease test and histology. A semi-quantitative grading of bacterial density was also performed at histology. All patients received oral acetohydroxamic acid 750 mg, and blood samples for assessment of ammonia levels were taken before and at 15, 30, 60 and 90 minutes after administration.
Helicobacter pylori infection was detected in 20 patients, while 9 patients were uninfected. Acetohydroxamic acid administration led to a significant reduction in blood ammonia levels at 15 and 30 minutes (mean +/- SD, 113 +/- 44 vs 101 +/- 43 and 93 +/- 38 micrograms/dl, respectively; p = 0.002) only in patients with Helicobacter pylori infection. Moreover, the reduction was statistically significant only in Child-Pugh B/C class patients and in those with moderate/marked Helicobacter pylori density in gastric mucosa. Basal ammonia levels did not differ between Helicobacter pylori positive and negative patients, nor in patients with mild and moderate/marked Helicobacter pylori density in gastric mucosa, while Child-Pugh class B/C cirrhotics had higher basal ammonia levels than class A cirrhotics, in both Helicobacter pylori positive and negative groups.
Our data showed that Helicobacter pylori urease inhibition by acetohydroxamic acid administration significantly reduces blood ammonia levels in patients with more advanced liver cirrhosis and in those with a high bacterial density in gastric mucosa.
幽门螺杆菌作为肝硬化患者高氨血症病因的作用仍未完全阐明。本研究旨在评估口服乙酰氧肟酸对急性幽门螺杆菌脲酶的抑制作用对肝硬化患者血氨水平的影响。
29例接受上消化道内镜检查的肝硬化患者(14例男性,15例女性;平均年龄:63岁;Child-Pugh分级:14例A类,9例B类,6例C类)纳入本研究。通过快速尿素酶试验和组织学评估幽门螺杆菌感染情况。组织学检查还对细菌密度进行了半定量分级。所有患者口服750mg乙酰氧肟酸,给药前及给药后15、30、60和90分钟采集血样以评估氨水平。
20例患者检测到幽门螺杆菌感染,9例未感染。仅在幽门螺杆菌感染患者中,口服乙酰氧肟酸导致给药后15和30分钟血氨水平显著降低(平均±标准差,分别为113±44与101±43和93±38μg/dl;p = 0.002)。此外,仅在Child-Pugh B/C级患者以及胃黏膜中幽门螺杆菌密度为中度/重度的患者中,这种降低具有统计学意义。幽门螺杆菌阳性和阴性患者的基础氨水平无差异,胃黏膜中幽门螺杆菌密度为轻度和中度/重度的患者之间也无差异,而在幽门螺杆菌阳性和阴性组中,Child-Pugh B/C级肝硬化患者的基础氨水平均高于A类患者。
我们的数据表明,口服乙酰氧肟酸抑制幽门螺杆菌脲酶可显著降低晚期肝硬化患者以及胃黏膜细菌密度高的患者的血氨水平。