Primary hepatic lymphoma mimicking acute hepatitis
A 59-year-old man visited the gastroenterology department at our hospital with abdominal bloating. His clinical history did not reveal any specific disease, and his family history was also unremarkable. On physical examination, no abnormality was found, and the results of laboratory investigations were also normal. Initial abdominal US demonstrated mild coarseness of the liver without any focal lesion ().\nFive days after the initial abdominal US, he revisited the emergency department with newly developed symptoms including high fever over 39.5℃, general weakness, cough and sputum. On physical examination performed on his second visit, mild hepatomegaly and tenderness on the right upper quadrant were identified. There were no palpable lymph nodes. The laboratory evaluation showed deteriorated hepatic function: AST of 200 U/L, ALT of 20 U/L, γGT of 223 U/L, ALP of 477 U/L, LDH of 1,060 U/L. The levels of total and direct bilirubin were highly elevated to 27 and 16 mg/dL, respectively. On peripheral blood cell count, all of the blood cell counts declined: red blood cell count of 3.31×106/mL, white blood cell count of 5.5×103/mL, and platelet count of 110×103/mL. Serological tests for hepatitis A, B and C viruses, Ebstein-Barr virus and cytomegalovirus were all negative. Abdominopelvic CT scans taken at the emergency department showed hepatosplenomegaly with collapsed gallbladder, suggestive of acute hepatitis.\nFollow-up abdominal US performed 9 days after the initial study revealed a further decrease in the background echogenicity of the hepatic parenchyma as well as hepatomegaly. The gallbladder was collapsed and accompanied by diffuse wall thickening (). Eight days later, the hepatic echogenicity had become coarser and hepatosplenomegaly was markedly aggravated. Moreover, the gallbladder wall was more thickened and the amount of ascites was increased (). The changes observed on serial US and CT imaging resembled those observed in progressively worsening acute hepatitis, leading to the diagnosis of idiopathic fulminant hepatopathy.\nAs the next step, US-guided liver biopsy was performed using an automatic biopsy gun. Two pieces of specimen were obtained, and the histopathology demonstated numerous lymphocytes mainly infiltrating into the periportal space. On the high-power filed of microscopy, lymphocytes with nuclei of variable size and mitotic activity were seen. The result of immunohistochemical profiles of this specimen revealed peripheral T-cell lymphoma. However, the special stain for γδ T-cell receptor was negative, and the final pathologic diagnosis of peripheral T-cell lymphoma, was reached.\nThe disease was not responsive to chemotherapy using cyclophosphamide hydroxydoxorubicin, vincristine and prednisolone (CHOP), and rapidly progressed to multiple organ failure with severe sepsis and pancytopenia. The patient eventually expired three weeks after admission.