Published online Oct 21, 2017. doi: 10.3748/wjg.v23.i39.7150
Peer-review started: August 19, 2017
First decision: August 30, 2017
Revised: September 21, 2017
Accepted: September 28, 2017
Article in press: September 28, 2017
Published online: October 21, 2017
Processing time: 64 Days and 7.5 Hours
Esophageal varices (EVs) develop as a result of portal hypertension, which is mainly due to liver cirrhosis (LC) in alcoholics. Excessive alcohol consumption has been reported to be associated with the presence of a short-segmental columnar-lined esophagus (CLE) in East-Asian studies. It has not been evaluated whether associations exist between the presence of EVs and the presence of CLE in alcoholics.
Our empirical impression based on the results of endoscopic screening examinations of Japanese alcoholic men is that EVs are less common among men with short-segmental CLE. The development of CLE is accompanied by several histological changes around the palisade vessels at the lower end of the esophagus. Some of the histological changes accompanying the development of CLE may protect against the development of EVs.
To determine whether and to what extent associations exist between the presence of EVs and the presence of CLE in Japanese alcoholic men based on the results of endoscopic screening examinations.
The subjects were 1614 Japanese alcohol-dependent men (≥ 40 years of age) who had undergone upper gastrointestinal endoscopic screening. Digitalized records of high-quality endoscopic images that included the squamocolumnar junction and esophagogastric junction were retrospectively jointly reviewed by four expert endoscopists for the purpose of diagnosing CLE. The authors investigated whether and to what extent there were associations between the presence of CLE and the presence of EVs, especially in the group with LC.
CLE ≥ 5 mm in length was found in 355 subjects, LC without EVs in 152 subjects, LC with EVs in 174 subjects, and EVs without LC in 6 subjects. Advanced EVs, i.e., nodular, large or coiled forms, red color sign, or post-treatment, were found in 88 subjects. The incidence of CLE ≥ 5 mm decreased in the following order (P < 0.0001): 23.3% in the group without EVs, 17.4% in the group with small and straight EVs, and 5.7% in the group with advanced EVs. The multivariate ORs (95%CI) for EVs and advanced EVs in the group with LC were lower when CLE ≥ 5 mm was present [0.46 (0.23-0.93) and 0.24 (0.08-0.74), respectively, vs 0-4 mm CLE]. To clarify the pathological backgrounds of the negative association between the presence of CEL and the presence of EVs, the further pathological studies of autopsied cirrhotic subjects may be warranted.
The presence of CLE was negatively associated with the presence of EVs, and even more negatively associated with the presence of advanced forms of EVs. Since the first resistance vessels to EVs are the mucosal palisade vessels and submucosal veins at the lower end of the esophagus, the development of CLE may impede the development of EVs. Helicobacter pylori infection and chronic atrophic gastritis protect against the development of GERD and CLE. If the observed associations between CLE and EVs and advanced EVs reflected causal relationships, the current trend toward to lower Helicobacter pylori infection rates in Japan may influence EV rates and advanced EV rates in the future, and examination for CLE may benefit alcoholics with advanced liver disease by identifying their risk for the development or progression of EVs. The further studies should be conducted prospectively in the longitudinal fashion to test this finding.