Endoscopic severe mucosal atrophy indicates the presence of gastric cancer after Helicobacter pylori eradication -analysis based on the Kyoto classification.

BACKGROUND: Gastric cancer after Helicobacter pylori (HP) eradication is a crucial clinical challenge today as HP eradication therapy is widely performed. Detecting gastric cancer after HP eradication tends to be difficult with normal white-light endoscopy. In the present study, we aimed to identify easily-evaluated endoscopic findings that indicate the presence of gastric cancer after HP eradication so that endoscopists can consider additional detailed examinations at the site. METHODS: We analyzed the endoscopic images of 43 patients who underwent endoscopic submucosal dissection for early gastric cancer after HP eradication and 119 patients with an HP eradication history who underwent esophagogastroduodenoscopy for a medical checkup. Endoscopic findings were evaluated according to the Kyoto classification of gastritis (atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness) and map-like redness. RESULTS: Patients with gastric cancer had significantly higher total Kyoto risk scores; more atrophy, intestinal metaplasia, and diffuse redness; and a significantly higher prevalence of map-like redness compared with those without gastric cancer, in the univariate analyses. We used logistic regression analysis with forward selection based on the likelihood ratio to develop a model using atrophy and diffuse redness. Receiver operating characteristic analysis showed that a score of A2 in the Kyoto classification of gastritis (open-type atrophic pattern in the Kimura-Takemoto classification) was an endoscopic marker for the presence of post-HP-eradication gastric cancer. CONCLUSIONS: Endoscopic severe gastric mucosal atrophy is useful to screen patients for gastric cancer after HP eradication.

[Multiple hepatic sclerosed hemangiomas that are difficult to diagnose preoperatively:a case report].

An 83-year-old woman was admitted to our hospital because of a space-occupying lesion (SOL) in the liver. Enhanced computed tomography (CT) showed a nodule measuring 20mm in size in the posterosuperior segment of the right hepatic lobe (S7) and another nodule measuring 14mm in size in the anterosuperior segment of the right hepatic lobe (S8). The margins of these nodules showed faint enhancement in the arterial phase and presented as low-density areas in the equilibrium phase. The S8 SOL could not be easily identified using ultrasonography (US). However, the S7 SOL could be clearly identified as a nodule accompanying the marginal enhancement in the early vascular phase and a defect in the late vascular phase using contrast-enhanced US. On gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging, both nodules were described as low-intensity lesions in the T1 phase, high-intensity lesions in the T2 phase, faint high-intensity diffusion-weighted images, and clear low-intensity lesions in the hepatobiliary phase. On positron-emission CT, there was no uptake of 18F-fluorodeoxyglucose in these nodules. Hepatectomy was performed because we were unable to rule out a malignant tumor. Histopathologically, these lesions demonstrated collapsed vascular spaces against a background of rich paucicellular fibrous stroma and were diagnosed as sclerosed hemangiomas. The occurrence of multiple sclerosed hemangiomas is rare and often difficult to diagnose because of variable findings on imaging studies. We report a case of multiple hepatic sclerosed hemangiomas, which was difficult to diagnose preoperatively. Moreover, we have reviewed the literature, particularly with respect to the relevant imaging findings.

Nivolumab Therapy for Synchronous ALK-Positive Lung Cancer and Gastric Cancer.

Nivolumab is an immune checkpoint inhibitor with demonstrated efficacy against several malignant tumors. Alterations in driver oncogenes such as EGFR and ALK are a poor prognostic factor in nivolumab therapy for non-small cell lung cancer (NSCLC), whereas a smoking history is a well-known, favorable prognostic factor. However, an efficacy of nivolumab therapy for multiple primary malignant tumors (MPMTs) has not been reported, and its efficacy for driver oncogene-positive NSCLC in smokers is unclear. Herein, we report the case of a patient with a history of heavy smoking who developed synchronous ALK-positive NSCLC and gastric cancer that responded to nivolumab therapy. A 76-year-old man who was a heavy smoker presented to our hospital with symptoms of hoarseness and dysphagia. He was ultimately diagnosed with ALK-positive advanced NSCLC. An ALK inhibitor (alectinib) was administered, and the lung cancer lesions showed improvement. The alectinib therapy was continued for 5 months. Thereafter, the lesions in the left lower lobe of the lung showed regrowth. During the same period, the patient experienced epigastric pain. Gastrointestinal endoscopy examination revealed gastric cancer. He was administered nivolumab to treat both the lung cancer and the gastric cancer. Two months later, both the lung lesions and the gastric lesions had diminished in size. Nivolumab therapy might be an effective therapy for synchronous MPMTs and NSCLC in heavy smokers, even if the lung cancer possesses driver oncogene mutations.