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Interleukin (IL)‐1β is a potent inhibitor of gastric acid secretion and its genetic polymorphism is linked to the severity of reflux esophagitis. Proton‐pump inhibitor (PPI) metabolized by P450 2C19 (CYP2C19) is the chief medication in reflux esophagitis treatment. The CYP2C19genotype may influence the therapeutic effect of PPI for reflux esophagitis. From November 2009 to June 2012, 184 patients were enrolled in this study with endoscopy examination, 8 weeks of esomeprazole treatment, and 20 weeks of follow‐up with questionnaire. These patients also received endoscopy examination after 20 weeks. Blood was collected for genetic polymorphism analysis with polymerase chain reaction. After 8 weeks of treatment with esomeprazole, all of these 184 patients had achieved complete symptom relief. However, in the following 12 weeks, 58.70% (108/184) complained of symptom relapse, 45.65% (84/184) patients had persistent esophageal erosion verified by endoscopy, and in total, 76.09% (140/184) patients had treatment failure at the end of 20 weeks. There were no influences between the genetic polymorphisms of CYP2C19and IL1Bto treatment failure (p= 0.896). Therefore, prolonging PPI treatment and further lifestyle modification might be warranted for symptomatic mild esophagitis. There were no relationships between IL‐1β and CYP2C19 in the treatment effect in mild reflux esophagitis.

Eradication of Helicobacter pyloriinfection has become an important issue recently, because this bacterial species cluster can cause many gastrointestinal diseases. Elevated antibiotic resistance is related to an increasing failure rate of H. pylorieradication. Standard triple therapy is still the first‐line therapy; however, according to the Maastricht IV Consensus Report, it should be abandoned in areas of high clarithromycin resistance. Alternative first‐line therapies include bismuth‐containing quadruple therapy, sequential, concomitant, and hybrid therapies. Quinolone‐based triple therapy may be considered as first‐line therapy in areas of clarithromycin resistance >15–20% and quinolone resistance <10%. Unique second‐line therapy is still unclear, and bismuth‐containing quadruple therapy or levofloxacin‐based triple therapy can be used as rescue treatment. Third‐line therapy should be under culture guidance to select the most effective regimens (such as levofloxacin‐based, rifabutin‐based, or furazolidone‐based therapies). Antibiotics resistance, patient compliance, and CYP 2C19 genotypes could influence the outcome. Clinicians should use antibiotics according to local reports.

Alpha‐fetoprotein is a well‐known tumor marker in the screening and follow‐up of hepatocellular carcinoma. In Taiwanese society, a high prevalence of hepatitis and hepatoma and elevation of alpha‐fetoprotein associated with liver function impairment usually suggested clinics undertake further examination for liver or genital tumor. We report the case of 45‐year‐old man who was found to have an alpha‐fetoprotein‐producing esophageal adenocarcinoma with an initial presentation of liver function impairment and rapid elevation of alpha‐fetoprotein. Esophageal cancer was diagnosed via endoscope and a biopsy proved the presence of adenocarcinoma. A small endoscopic biopsy specimen failed to identify the alpha‐fetoprotein positive tumor cell. Esophagectomy was performed and histopathological study of surgical specimen revealed grade II adenocarcinoma with regional metastatic lymphadenopathy. Immunohistochemical study was focal positive for alpha‐fetoprotein. Serum alpha‐fetoprotein declined transiently after esophagectomy and fluctuation of alpha‐fetoprotein level was noted during the treatment with adjuvant chemotherapy. Finally, 19 months after the operation, the patient died due to multiple organ metastases with multiple organ failure. Thus, a small specimen for upper endoscopy may not be sufficient in the presence of alpha‐fetoprotein‐producing adenocarcinoma. Monitoring of serum alpha‐fetoprotein may be useful in the evaluation and follow‐up of esophageal alpha‐fetoprotein‐producing adenocarcinoma.