Endoscopic Esophageal Variceal Ligation May Increase The Risk Of Duodenal Ulcer

Aim: To explore the incidence of duodenal ulcer(DU), as well as other clinical characteristics occurring after endoscopic variceal ligation(EVL) of the esophagus, and the possible mechanism of action.Methods: A total of 47 patients with esophageal varices(EV)who had also undergone EVL and gastroscopic follow-up within three months of the procedure was retrospectively analyzed.The status of age,sex,pathogenesis,the status of Helicobacter pylori(H.pylori) infection,Child-Pugh classification,the grades of portal hypertensive gastropathy(PHG),the number of ligation treatment and the number of ligating bands were collected.Sixty EV patients without EVL treatment, but with clinical data available,served as the control group.Results: There was no difference between the EVL group and the control group in the general characteristics of patients(p>0.05).The incidence of DU in the EVL group(29.8%, 14/47)was higher than that in the control group(6.7%,4/60),(p<0.05).The H.pylori infection rate in EVL group was 19.15%(9/47),while in control group was 21.67%(13/60),(p>0.05).The H.pylori positiverate(12.5%, 1/8)in patients exhibited new DU after EVL was comparable to that in patients without DU in the EVL group(12.1%, 4/33),(p>0.05).Patients presenting with DU after EVL received(18.79±8.48) bands of ligating bands, while in those who did not exhibit DU received(13.85±6.47) bands,(z=-2.042, p=0.041).A Logistic regression analysis showed that the incidence of DU after EVL was related to the number of ligating bands employed during EVL,but was not related to H.pylori infection Helicobacter pylori(H.pylori) infection, Child-Pugh classification,the grades of portal hypertensive gastropathy(PHG) and the number of ligation treatment.Conclusions: EVL may increase the risk of DU in EV patients,and the incidence of DU is related to the number of ligating bands employed during EVL,but is not related to H.pylori infection and the number of ligation treatment.These results also suggest thatchanges to portal hypertension-induced collateral circulation after EVL may constitute a key mechanism.