Dear Editor: Upper gastrointestinal tract inflammation of Crohn’s disease became increasing recognized as a result of more frequent upper endoscopic examination. However, the diagnosis of upper gastrointestinal Crohn’s disease is still neglected easily, especially in the patients with Helicobacter pylori infection; they are even considered as gastritis or gastric ulcer incorrectly. A 26-year-old man visited our hospital, complaining of vomiting, abdominal pain, and weight loss for 3 years. Three years ago, he underwent an upper endoscopy with biopsies in a local hospital, he was diagnosed with multiple gastric ulcers, accompanying with H. pylori infection. Then, he accepted quadruple therapy. After 5 months, he still felt these symptoms. Therefore, upper endoscopy was performed again in the local hospital; the result still showed multiple gastric ulcers but with H. pylori eradication. He continued to be treated with proton pump inhibitors for more than 2 years. However, these symptoms were not controlled obviously, and he suffered from anal fistula under no inducing factors 1 month ago. Because these symptoms did not improve with medication, he accepted endoscopy and other examinations in our institute. Upper endoscopy showed Crohn’s disease was suspected. Small bowel barium X-ray confirmed ileum multiple zonal stenosis with enteric cavity distension and multiple cobblestone filling defect of partial mucosae. Colonoscopy did not demonstrate other abnormalities. Abdominal computerized tomography showed thickened and edematus terminal ileum and lymph nodes image-developing for root of mesentery; these appearances are consistent with Crohn’s disease. He is currently treated with mesalazine therapy; his symptoms have been controlled. The incidence of upper gastrointestinal Crohn’s disease are difficult to ascertain, since most reported cases were poorly documented and were reported when diagnostic criteria were poorly standardized and endoscopy was not widely available. Japanese experts considered that the incidence exceeded the values of some reports greatly. Therefore, we should think highly of upper gastrointestinal Crohn’s disease, especially in patients with upper gastrointestinal symptoms in the first visit. The identification of H. pylori as a major gastric pathogen leads to an increased awareness of the different types of gastritis or gastric ulcer. H. pylori is recognized as the most common cause of upper gastrointestinal lesions; we could pay more attention to H. pylori infection for the patients with epigastric discomfort. However, the prevalence rate of H. pylori infection is low in Crohn’s disease. Although upper gastrointestinal tract inflammation is common in Crohn’s disease patients, the majority of cases are not associated with H. pylori infection, and high-dose proton pump inhibition and H. pylori eradication failed to induce healing. In our patient, the symptoms of upper gastrointestinal tract did not disappear along with proton pump inhibition treatment and H. pylori eradication. Therefore, the H. pylori infection status of suspected Crohn’s disease patients with upper gastrointestinal lesions should be checked to distinguish Crohn’s disease or H. pylori infection-related pathogenesis. Diagnosis of Crohn’s disease is based on clinical, radiological, endoscopic, and histologic features. However, histologically, granulomas were found in only 9% of the gastroduodenal Crohn’s disease patients whose biopsy Int J Colorectal Dis (2009) 24:121–122 DOI 10.1007/s00384-008-0600-3