A 66‐year‐old man was admitted to our department due to cholestatic liver injury. He had received five cycles of pembrolizumab for small‐cell lung cancer. Imaging showed the possibility of sclerosing cholangitis (SC) with hemobilia. Histologically, CD8+ T cells had infiltrated the biliary epithelium of the extrahepatic bile duct. We reached the diagnosis of secondary SC induced by pembrolizumab. Although we treated him with high‐dose corticosteroids, laboratory data showed only a moderate response. Clinicians should recognize that immune checkpoint inhibitors can sometimes cause severe and irreversible SC.

A 72-year-old woman with advanced lung cancer had received systemic chemotherapy including atezolizumab. About three months after the initial administration of atezolizumab, her liver enzyme levels increased. The histopathological findings of the initial liver biopsy revealed acute inflammatory infiltrate, predominantly CD3 + , CD4 + and CD8 + T lymphocytes, in the hepatic lobules. We diagnosed her with atezolizumab-induced immune-related acute hepatitis. Oral corticosteroid therapy successfully improved the elevation of serum aminotransferases. A sequential liver biopsy demonstrated the rapid progression of liver fibrosis. Because hepatocellular carcinoma occurs most often in advanced cases of chronic liver disease, we should pay close attention to immune-related acute hepatic injury when treating patients with advanced liver diseases using atezolizumab.

A 52-year-old woman developed vomiting and disturbance of consciousness after consuming raw fish and sushi on a trip. A blood test showed hyperammonemia (310 μg/dL) with a normal liver function. She fell into a deep coma, and her serum ammonia level increased to 684 μg/dL. L-arginine was administered as a diagnostic treatment for urea cycle disorder (UCD) and serum ammonia, and her consciousness levels improved. She was diagnosed with ornithine transcarbamylase deficiency (OTCD) by analyses of plasma amino acids, urinary orotic acid, and the OTC gene mutation. UCD should be considered for patients with hyperammonemia without severe liver function abnormalities.

A 75-year-old man visited our hospital for the examination of a tumor in the pancreas. Computed tomography showed an 85×85-mm low-density tumor in the pancreas. The tumor was pathologically diagnosed as poorly differentiated carcinoma by endoscopic ultrasound-guided fine-needle aspiration. Although we started chemotherapy, the patient died 84 days after the diagnosis. An autopsy demonstrated a ruptured anaplastic carcinoma with mucoepidermoid carcinoma of the pancreas. Anaplastic carcinoma with mucoepidermoid carcinoma is a very rare histologic subtype of pancreatic carcinoma, so pathological findings are important for predicting the patient's prognosis. Physicians should be aware of this rare but fatal disease.

Objectives: Esophageal variceal bleeding can be fatal in patients with liver cirrhosis. The aim of this study was to investigate the relationship between gastroesophageal flap valve (GEFV) and esophageal variceal bleeding. Methods: Subjects were cirrhotic patients with endoscopically diagnosed esophageal varices treated at our hospital between 2005 and 2019, excluding those with F3 form and red color (RC) signs at first endoscopy. Sixty-five patients with normal GEFV (Hill grade I or II) and 42 with abnormal GEFV (Hill grade III or IV) were enrolled. Propensity score matching eliminated the baseline differences, resulting in a sample size of 30 patients per cohort. The primary endpoint was esophageal variceal bleeding, and the secondary endpoint was variceal bleeding or appearance of RC sign. We analyzed the cumulative incidences and predictors of each endpoint. Results: The 3-, 5-, and 10-year cumulative incidences of the primary endpoints were all 3.4% in the normal GEFV group, and 19.0%, 24.6% and 34.0% in the abnormal GEFV group, respectively (log-rank P = 0.011). Cumulative incidence of the secondary endpoint was 13.8%, 33.1% and 39.2% in the normal GEFV group, and 42.2%, 54.6% and 84.9% in the abnormal GEFV group, respectively (log-rank P = 0.001). In multivariate Cox regression analyses, hazard ratios of abnormal GEFV of the primary and secondary endpoints were 12.79 (95% confidence interval 1.331-122.8) and 3.600 (1.653-7.840), respectively. Conclusions: Abnormal GEFV was an independent risk factor for esophageal variceal bleeding and appearance of RC sign.

Two men (24 and 34 years of age) with a single hypervascular liver tumor were admitted to our hospital. The tumors were diagnosed as hepatocellular adenoma (HCA) by an ultrasound-guided biopsy and classified as inflammatory type by immunohistochemical staining. Considering the risk of malignant transformation, they underwent surgical resection. Although the serum levels of protein induced by vitamin K absence/antagonist-II (PIVKA-II) were slightly elevated, they normalized after the resection. The diagnosis of HCA including malignant transformation is often difficult by image findings alone. Careful immunohistochemical examinations are very useful for the diagnosis and classification of subgroups, including malignant transformation. In addition, we proved that HCA without malignant transformation expresses PIVKA-II.

A 69-year-old man was diagnosed with a liver abscess and received antibiotics at a local hospital. He was referred to our hospital due to a persistent fever. He had hepatic masses protruding from the liver surface toward the transverse colon. We reached a diagnosis of inflammatory pseudotumor (IPT) by a percutaneous liver biopsy. Colonoscopy showed direct invasion of IPT to the colon. His condition improved by the intravenous administration of antibiotics. Hepatic IPT is often misdiagnosed as a malignant tumor. We should consider IPT when we encounter hepatic tumors, and a percutaneous liver biopsy is useful for avoiding unnecessary excessive treatments.

An 83-year-old man underwent transcatheter arterial chemoembolization (TACE) for a 20-mm hepatocellular carcinoma (HCC) in Couinaud’s segment 4. Computed tomography (CT) 4 months after TACE showed tumor thrombus in the portal vein in addition to diffuse metastases and arterioportal shunts in the left lobe. Although we performed the best supportive care, the tumor thrombus in the portal vein and tumors in the left lobe had completely disappeared on CT 16 months after the TACE. Rapidly grown portal vein tumor thrombus and arterioportal shunt might be the causes of spontaneous regression of HCC, probably associated with tumor hypoxia.