Journal of Practical Hepatology ›› 2021, Vol. 24 ›› Issue (6): 923-926.doi: 10.3969/j.issn.1672-5069.2021.06.039

• Cholelithiasis • Previous Articles     Next Articles

Gallbladder mucosal tissue helicobacter pylori infection and its toxic gene levels in patients with gallbladder calculous cholecystitis

Xiong Maocheng, Lei Yanmei, Li Liangmin, et al   

  1. Department of Nuclear Medicine, Affiliated Hospital, Chengdu University of Traditional Chinese Medicine, Chengdu 610000, Sichuan Province, China
  • Received:2021-05-08 Published:2021-11-15

Abstract: Objective The aim of this study was to probe gallbladder mucosal tissue helicobacter pylori (Hp) infection and its toxic gene cytotoxin-associated gene A (CagA) and cholecystokinin-A receptor (CCK-AR) mRNA in patients with gallbladder calculous cholecystitis. Methods 98 patients with calculous cholecystitis were enrolled in our hospital between January 2019 and December 2020, and all patients underwent surgical removal of gallbladder. The Hp DNA in gallbladder mucosa was detected by polymerase chain reaction amplification, and the CagA and CCK-AR mRNA levels were measured by real-time fluorescent quantitative polymerase chain reaction. The activity of gallbladder mucosal phospholipase A2 (PLA2) was detected by hydrochloric titration. Results The transmission electron microscopy showed simple hyperplasia of gallbladder mucosal epithelium in 33 cases, intestinal metaplasia in 45 cases, and dysplasia in 20 cases; the gallbladder mucosa Hp DNA positive rates in simple hyperplasia, intestinal metaplasia and dysplasia group were 30.3%, 40.0% and 50.0%, respectively, without significant differences among them (P>0.05); the relative CagA mRNA level and the activity of PLA2 in patients with gallbladder mucosa dysplasia were(5.1±0.9) and (188.9±22.3)U/L, both significantly higher than [(1.9±0.4)和(160.5±21.5)U/L, respectively, P<0.05] in patients with simple hyperplasia of gallbladder mucosa or [(3.3±0.6) and (170.9±20.4)U/L, respectively, P<0.05] in patients with intestinal metaplasia of gallbladder mucosa, while the relative CCK-AR mRNA level was (2.9±0.6), significantly lower than [(7.0±1.4), P<0.05] in patients with simple hyperplasia of gallbladder mucosa or [(5.4±1.1), P<0.05] in patients with intestinal metaplasia of gallbladder mucosa. Conclusion Hp infection might accelerate the gallbladder mucosal lesion progression by up-regulating CagA mRNA levels and the activity of PLA2, while by down-regulating CCK-AR mRNA levels, which needs further investigation.

Key words: Calculous cholecystitis, Helicobacter pylori, Cytotoxin-associated gene A, Cholecystokinin-A receptor, Ultrastructure