An 80-year-old man presented to our hospital complaining of epigastric pain. His levels of hepatobiliary system enzymes were elevated. Computed tomography (CT) showed no obvious common bile duct stones but mild bile duct dilatation was present. He was admitted to the hospital for treatment of suspected cholangitis. Repeated endoscopic bile duct drainage did not improve the liver damage. Although serum immunoglobulin (Ig) G was mildly elevated, viral markers and autoantibodies were negative. Liver biopsy showed nonspecific, chronic active hepatitis but did not lead to a definitive diagnosis. Additional blood tests showed high IgG4 levels and IgG4 immunostaining of liver biopsy pathology showed IgG4-positive plasma cell infiltration in the portal. Based on the above, the patient was diagnosed with IgG4-related autoimmune hepatitis, and prednisolone (PSL) was started; the liver damage promptly improved. This case demonstrates that measurement of serum IgG4 and IgG4 immunostaining of liver tissue may be useful for the diagnosis of liver disorders of unknown origin.

Spontaneous regression of hepatocellular carcinoma (HCC) is rare. Here, we present a rare case of spontaneous regression of a rapidly-grown hepatocellular carcinoma. An 83-year-old man had repeatedly received therapy for recurring HCC for 11 years. The HCC, 1 year ago, had rapidly grown to 68 mm in diameter from 30 mm 3 months prior. The patient refused treatment stating dementia as a reason. After 1 year, the patient returned to our hospital. During this 1 year, the concentration of alpha-fetoprotein (AFP) had remarkably decreased to 2.05 ng/ml from its previous value of 2772 ng/ml. The value of protein induced by the absence of vitamin K or antagonist II (PIVKA-II) had also decreased to 55.11 mAU/ml from 23023 mAU/ml. The contrast-enhanced computed tomography showed that the HCC had shrunk to a diameter of 10 mm. Tumor regression may have been caused by a disturbance in hepatic circulation associated with rapid growth, the location, the formation of a capsule, and the portal vein thrombus.

A 40-year-old man was referred to our hospital for investigation and treatment of abdominal pain. A dynamic computed tomography scan showed extensive intrahepatic thrombosis in the main trunk of the portal vein and the mesenteric vein. The patient was treated with freeze-dried human antithrombin III concentrate for 15 days, and the thrombus shrunk in size. As maintenance treatment, we administered warfarin and the thrombus did not increase. Liver biopsy showed mild fibrosis and no evidence of idiopathic portal hypertension. We found decreased protein C activity in the blood, which suggested the portal vein thrombosis was due to a protein C deficiency. Analysis of the protein C gene (PROC) mutation revealed a heterozygous stop-gain variant (p.Trp2*), confirming the diagnosis of congenital protein C deficiency. In cases of noncirrhotic or non-neoplastic portal vein thrombosis, it is important to check not only for liver disease but also for blood coagulation disorders.

A 68-year-old female patient with autoimmune hepatitis receiving prednisolone was referred to our institution for a mass lesion on segment VII of the liver. After undergoing contrast-enhanced ultrasonography, contrast-enhanced CT, Gd-EOB-DTPA-enhanced MRI, and ¹³¹I-adosterol scintigraphy, the mass was suspected to be a hepatic adrenal rest tumor (HART). We then performed a liver biopsy, which revealed adrenal cortex-like cells. Pathological diagnosis identified the mass as a HART. After various hormonal tests, the tumor was confirmed to be hormonally nonfunctional. HARTs are sometimes difficult to distinguish from malignant tumors because of the difficulty in obtaining characteristic image findings, and surgical resection is often selected as the treatment approach. In this rare case, percutaneous liver biopsy and ¹³¹I-adosterol scintigraphy were useful for diagnosis, due to which an unnecessary liver resection was avoided.

Here, we present a case of a female patient who was in her 70s. She was treated with IFN for hepatitis C-related compensated cirrhosis 8 years ago but had discontinued the treatment. She was given Daclatasvir hydrochloride+Asunaprevir 4 years ago; however, it was ineffective. She was given Sofosbuvir+Velpatasvir+Ribavirin 2 years and 4 months ago, and achieved SVR. She underwent partial hepatectomy, 7 months ago, for a single-moderately differentiated-3 cm hepatocellular carcinoma. In January X, she was admitted to the hospital because of multiple intrahepatic tumors shown on MRI. Further evaluation revealed tumors in the breasts and upper left arm and the patient died 1 month after admission. The pathological autopsy revealed that multiple systemic tumors were adenocarcinoma of unknown primary origin, except one hepatic tumor that was hepatocellular carcinoma. There are few reports of developing solid cancers other than hepatocellular carcinoma after treatment with direct-acting antivirals. Here, we report a similar case with a review of previously published literature on the same.

We performed a questionnaire survey among ophthalmologists on how they handle the results of viral hepatitis tests. Of 307 responses (28.6% of sent questionnaires), 80.1% were analyzed, which were from the ophthalmologists who order viral hepatitis tests. To hepatitis test-positive patients, 69.4% of the ophthalmologists responded "inform always," but to test-negative patients, 68.3% answered "don't inform." The younger ophthalmologists significantly more often replied "don't inform." Ophthalmologists who answered "consult hepatologists" were only 7.6% and 37.1% for test-positive patients with primary-care physicians and those without, respectively. Ophthalmologists who responded "consult hepatologists" are significantly fewer among those working at clinics. As reasons for the difficulty of the consultation, 64.6% and 43.1% answered "patients are visiting primary-care physicians" and "which hepatologist to consult is uncertain," respectively.