Primary Liver Diffuse Large B-Cell Lymphoma following Complete Response for Hepatitis C Infection after Direct Antiviral Therapy.

INTRODUCTION: Hepatitis C infection is highly prevalent worldwide and has a well-known association with B-cell lymphoid malignancies. Antiviral therapy has successfully decreased the rate of liver cirrhosis and improved the outcome in patients with hepatitis C-associated lymphomas. However, although there are a few case reports of aggressive lymphomas after successful hepatitis C therapy, the mechanism behind this association remains unclear. CASE PRESENTATION: We present the case of a 55-year-old man with chronic hepatitis C infection and liver cirrhosis who received antiviral therapy with sofosbuvir and ribavirin and achieved a sustained complete virological response. One year after successful therapy, there was an unexplained decline of his liver function and atypical liver nodularity, which led to the diagnosis of a primary liver diffuse large B-cell lymphoma. DISCUSSION: We review the evidence supporting possible mechanisms of lymphomagenesis after successful hepatitis C therapy, particularly involving late "second-hit" mutations after viral-induced DNA damage and antiviral therapy facilitating the emergence of latent malignant B-cell clones by decreasing local inflammation and immune surveillance. More reports may help elucidate any association between hepatitis C antiviral therapy and late lymphoid malignancies.

Pancreatic Collision Tumor of Ductal Adenocarcinoma and Neuroendocrine Tumor.

A pancreatic collision tumor is a rare entity that can be challenging to diagnose. We present a very rare case of a pancreatic collision tumor composed of both a neuroendocrine tumor and a ductal adenocarcinoma. Preoperative diagnosis was clinically challenging because both the radiology and fine-needle biopsy were consistent with a typical neuroendocrine mass. However, gross examination of the mass postoperatively revealed neuroendocrine cells with rare foci of ductal adenocarcinoma without a transition zone. Awareness of this entity is important so that medical practitioners consider pursuing surgical management of pancreatic lesions that otherwise would be managed exclusively with surveillance.

Hypotension associated with advanced hodgkin lymphoma.

Hypotension is an extremely rare manifestation of Hodgkin lymphoma. We report the case of a patient who presented with new onset hypotension and was diagnosed with urosepsis and septic shock requiring pressor support for maintaining his blood pressure. computed tomography (CT) scan of abdomen showed liver lesions, which were new on comparison with a CT abdomen done 3 weeks back. Biopsy of the liver lesions and subsequently a bone marrow biopsy showed large atypical Reed-Sternberg cells, positive for CD15 and CD 30 and negative for CD45, CD3 and CD20 on immuno-histochemical staining, hence establishing the diagnosis of Hodgkin lymphoma. The mechanism involved in Hodgkin lymphoma causing hypotension remains anecdotal, but since it is mostly seen in patients with advanced Hodgkin lymphoma, it is hypothetically related to a complex interaction between cytokines and mediators of vasodilatation. Here we review relevant literature pertaining to presentation and pathogenesis of this elusive and rare association.

Acute splenic sequestration crisis in an adult with sickle beta-thalassemia.

Acute splenic sequestration crisis (ASSC) is a major cause of morbidity and mortality in children with sickle cell disease. Reports of ASSC in adults with sickle beta-thalassemia (S-beta(thal)) are rare and consist of isolated case reports comprising a total of seven patients, three of whom died during the crisis. We report a 22-year-old man with S-beta(thal) who developed ASSC 1 day after suffering multiple blunt trauma. Systemic inflammatory response to severe blunt trauma may have precipitated ASSC in our patient. ASSC in adults with S-beta(thal) is a potentially life-threatening complication with a high risk of recurrence. Splenectomy is recommended after the first attack of ASSC in adults with S-beta(thal).