We examined 171 patients with novel coronavirus disease 2019 (COVID-19) with liver injury in the respiratory failure groups and the nonrespiratory failure groups and investigated 41 patients with moderate II COVID-19 with respiratory failure who received dexamethasone (Dex) monotherapy in the liver injury group and the nonliver injury group at the time before treatment. The respiratory failure group had 64% more liver damage than the nonrespiratory failure group, was older, had more men, and had significantly more complications from lifestyle-related diseases such as hypertension and diabetes. Obesity was more common in the liver injury group prior to Dex monotherapy, and the liver CT value was significantly lower than in the nonliver injury group. Liver injury worsened in 41% of patients after Dex monotherapy, but there was no significant difference in the frequency before Dex monotherapy between the liver injury group and the nonliver injury group, and the degree of liver injury was mild in all cases, improving in 38% of the liver injury group. Dex monotherapy was a safe treatment for moderate II COVID-19, which frequently resulted in liver injury.

During a medical health check, a 29-year-old man was presented to our hospital with iron deficiency anemia. He had no significant medical history in his family. Despite being diagnosed with ocular sarcoidosis 5 years ago, he had no vision problems. Physical examination revealed normal vital signs and a nontender abdomen;however, his eyelid conjuvitis was pale, and he became aware of fatigue when moving vigorously. He had upper gastrointestinal endoscopy and colonoscopy, but there was no evidence of bleeding detected. A contrasted mass 30mm in size was discovered on abdominal contrast-enhanced computed tomography at the dorsal wall of the proximal jejunum. Positron emission tomography showed an accumulation image in the bilateral hilar lymph and upper jejunum. A 30-mm submucosal tumor with a central depression in the upper jejunum was discovered using a double-balloon enteroscopy. We performed biopsies from the depression margin and tattoo marking on the oral side of the tumor. Even though the biopsies specimen revealed granulation tissue, the patient was referred to surgery and underwent a partial jejunum resection because the tumor was diagnosed as the cause of anemia. The operation went smoothly, and the patient was discharged on the seventh postoperative day. Histological examination showed a proliferation of densely packed spindle cells with prominent nuclear palisading. The immunohistochemical examination revealed that c-kit and CD34 were highly expressed, whereas desmin and S-100 proteins were not. Ki-67 expression demonstrated a very low proliferative index (2%). We discovered gastrointestinal stromal tumors (GIST), as well as an ectopic pancreas. GIST is extremely rare in young people, and the coexistence of ectopic pancreas and sarcoidosis has never been reported.

Sleeve gastrectomy was covered by Japan's national health insurance as bariatric surgery for morbid obesity in 2014. There are a few cases of gastric bypass surgery, which is a different procedure. Given that the current incidence of gastric cancer in Japan is higher than that in the EU and US, the difficulty that gastric bypass surgery presents in examining the bypassed stomach necessitates a cautious approach to the indication of gastric bypass surgery in Japan. We present the case of a woman in her fifties who developed gastric cancer in the bypassed stomach 12 years after undergoing a laparoscopic Roux-en-Y gastric bypass. When a patient develops anemia and abdominal symptoms after bariatric surgery, the surgical procedure should be considered in the inspection.

A 65-year-old man had unresectable intrahepatic cholangiocarcinoma with a malignant biliary stricture. We used an endoscopic plastic stent to drain the bile. Despite receiving standard chemotherapy, the tumor eventually progressed and cancerous peritonitis developed. We had to exchange plastic stents frequently because of stent occlusion. We had a re-biopsy with EUS-FNA and tested for microsatellite instability, which came back as MSI-high. We administered pembrolizumab, which resulted in a significant reduction of tumor size. We were able to administer long-term chemotherapy without serious side effects by repeatedly exchanging plastic stents for stent occlusion. He has maintained partial response for more than 20 months after receiving pembrolizumab.

Concomitant pancreatic ductal adenocarcinoma (PDA) is observed in a subset of patients with intraductal papillary mucinous neoplasm (IPMN) of the pancreas, and early detection of those progressing lesions is difficult. We present a case with a de novo carcinoma in situ (CIS) discovered incidentally around the resection margin of IPMNs. A man in his 70s with a history of acute pancreatitis at the age of 50 years and no family history of PDA had a pancreatoduodenectomy for three isolated branch duct IPMNs that caused recurrent pancreatitis. During the 2-year follow-up period, the index lesion in the pancreatic head grew significantly, whereas the other cysts remained small and without mural nodules. The majority of the cysts are histologically composed of low-grade dysplasia and are classified as gastric-type IPMN. CIS with nuclear overexpression of p53 was located in the main pancreatic duct and adjacent brunch duct, which involved the pancreatic resection margin. The precise pathological analysis combined with multiregion sequencing revealed the CIS harbored KRAS G12V and TP53 R248W. Conversely, IPMNs contained GNAS mutant cells as well as components containing additional KRAS mutations. These findings suggested that the CIS formed independently of the multiple IPMNs and appeared to be an early manifestation of concomitant PDA with coexisting IPMNs. Despite widespread agreement on the resection of the radiographically significant IPMN lesion (s), the latent invasive cancer was not eradicated. A detailed pathological and molecular assessment of the resected materials may aid in a better management strategy for concurrent lesions.

A 70-year-old woman who was diagnosed with liver cirrhosis as a result of primary biliary cholangitis and heart failure by myocardial infarction 1 month ago complained of dyspnea and was admitted to our hospital. Image inspections showed right massive pleural effusion, so we performed thoracentesis and drainage. Despite no history of trauma or malignancy, we obtained milky white-yellow pleural effusion by drainage and it turned out to be transudative chylothorax. Because there were no signs of heart failure exacerbation or other diseases, we suspected that the transudative chylothorax was caused by liver cirrhosis. For cardioprotection and improvement of portal hypertension, we used conservative treatments such as increasing diuretic dosage, inducing branched-chain amino acids, and switching β-blocker medication from bisoprolol to carvedilol. Even though thoracentesis and drainages were performed twice for improvement of hypoxemia, right pleural effusion gradually decreased with the disappearance of dyspnea and she was discharged from our hospital on the 20th hospital day. We have been following her for 10 months and have found no evidence of pleural effusion. Although liver cirrhosis complicated with chylothorax is rare, several case reports have shown all patients with chylothorax caused by liver cirrhosis were transudative. It is assumed that portal hypertension by liver cirrhosis is associated with transudative chylothorax. This patient's case is complicated by insufficient ascites to be punctured. Other studies have reported that chylothorax occurs as a result of chylous ascites passing through the diaphragm in patients with liver cirrhosis;however, our case does not appear to fit the mechanism. Another study has proposed that portal hypertension increased lymph fluid production in the liver, this flow in the thoracic duct, and increased intrathoracic pressure resulting in the occurrence of chylothorax. We believe that switching β-blocker medication from bisoprolol to carvedilol is one of the reasons this patient's right chylothorax gradually decreased. According to one case study, a nonselective β-blocker improves chylothorax by lowering portal hypertension. As a result, a nonselective β-blocker such as carvedilol that improves portal hypertension may contribute to a reduction in cirrhotic chylothorax in this case. Bisoprolol, a selective β-blocker, has no effects on portal pressure and intrathoracic pressure. Our case report suggests that portal hypertension causes transudative chylothorax complicated by liver cirrhosis and that medication for portal hypertension improvement, such as a nonselective β-blocker, is one option for treatment.