S2835 Extranodal Liver, Pancreas and Spleen Diffuse Large B Cell Lymphoma After Successful Treatment for Chronic Hepatitis C Infection Using Direct Acting Antiviral Therapy

Introduction: Hepatitis C viral infection (HCV) has an estimated prevalence of > 185 millions of people affected worldwide. It is associated with cirrhosis, hepatocellular carcinoma and death. Extrahepatic complications are also common, and include the risk for lymphoma which is higher when compare to general population. Direct acting antiviral therapy (DAA) has shown to have cure rates of more than 95% of cases, however there is an increased risk for malignancy even with evidence of viral cure. We present a case of extranodal non-Hodgkin lymphoma in a patient cured from HCV treated with DAA. Case Description/Methods: 63-year woman with history of increased liver function tests (LFTs) for the last 5 years. Laboratory tests were remarkable for AST: 96, ALT: 144. ALP: 65 and total bilirubin: 0.5. After ruling out other etiologies, work up showed hepatitis C infection genotype 1b with viral load: 346,787 IU/mL.Liver biopsy showed fibrous expansion of most portal areas, occasional portal to portal bridging using Ishak staging (score: 3).She received sofosbuvir and simeprevir for 12 weeks achieving sustained viral response (SVR) at 24-weeks post treatment. After two years, she comes to clinic for follow up.She was asymptomatic, LFTs and alpha-feto protein (AFP) level were normal. Abdominal MRI revealed three well circumscribed poorly enhancing lesions in right hepatic lobe. Liver biopsy revealed morphological and immunohistochemical features with positivity for CD45, BCL-2, BCL-6, CD10, CD20 and MUM-1 neoplastic B cells, diagnostic for diffuse large B cell lymphoma. PET-CTscan showed three large soft tissue hypodensities in liver with increased FDG uptake SUV max of 28.4, 31.8 and 36.0, one pancreatic head mass showing SUV max of 30.8 and small lesion in subcapsular spleen SUV max of 6.3. No abnormal metabolic activity in lymph nodes were noted. Bone marrow biopsy was negative. She was treated with six cycles of cyclophosphamide, doxorubicin, vincristine and prednisone. After 5 years of treatment she is on remission and doing well. Discussion: The relationship for HCV infection and development of lymphomas is well established, but pathophysiology is not well understood. One of the most accepted hypotheses is chronic viral antigen stimulation and genetic mutations to lymphocytes arising from HCV-induced replication proteins. Physicians need to be aware that DAA therapy is clearly effective for intra- and extrahepatic manifestations of the virus, but these patients are still at risk for malignancy regardless HCV serologic status.Figure 1.: PET-CT SCAN showing in the lower half of the right liver lobe three large foci of increased tracer uptake, the larger lesion located on the anterolateral aspect of segment VIII measuring 4.3cm AP, also shows a soft tissue mass in pancreatic head with caudal extension that measures 3.7cm AP. There is no main pancreatic duct dilation (b), and a small lesion on superior-posterior aspect subcapsular area of the spleen (c).Table 1.: Laboratory results at the time of diffuse large B-cell lymphoma diagnosis: H: high abnormal level; WBC: white blood cell count; RBC: red blood cell count; AST: aspartate transaminase; ALT: alanine transaminase; ALP: alkaline phosphatase; INR: international normalized ratio; CEA: carcinoembryonic antigen; CA 19-9: cancer antigen 19-9; IgG: immunoglobulin G; IgA: immunoglobulin A; IgM: immunoglobulin M;HCV-Ab: hepatitis C antibody; HBs-Ag: hepatitis B antigen; HBs-Ab: hepatitis B antibody; HBc-Ab: hepatitis B core antibody; HIV: human immunodeficiency virus.