Fatal Fulminant Hepatitis from Rituximab-induced Hepatitis B Reactivation in a Patient with Follicular Lymphoma: A Case Report and a Brief Review of Literature.

The objective of our study was to recognize hepatitis B reactivation as a complication of rituximab chemotherapy and to realize the importance of screening for prior Hepatitis B virus (HBV) exposure in all patients with hematologic malignancies who will receive rituximab as part of their therapy. Rituximab is a monoclonal antibody targeting CD 20 receptors on the membrane of B cells. In this case report, we described a 79-year-old man who presented to our department with nausea, fatigue, and jaundice. Two months ago, he had received the last dose of the chemotherapy regimen containing rituximab for follicular B cell lymphoma. Ultrasound and computed tomography (CT) scan of abdomen did not show any focal lesions. Liver function tests showed worsening hepatic failure and viral serology demonstrated active HBV infection. Antiviral therapy with entecavir and tenofovir disoproxil fumarate failed to improve his symptoms, and he died of fulminant hepatic failure. Rituximab targets CD 20 receptors positive B cells. It can destroy both cancerous and normal B cells. A decline in immune function can activate occult HBV infection. Prior to initiation of rituximab therapy, screening should be conducted in all cases for HBV associated serological markers. Patients with active or occult HBV infection must be started on appropriate antiviral therapy to prevent any severe outcomes with rituximab-containing regimens.

Mixed Connective Tissue Disorder Complicated by Polymyositis, Sjogren's Syndrome, Pleural Effusion and Pericarditis.

We report a case of a 24-year-old female with a history of asthma and gastroesophageal reflux disease (GERD). She presented to the emergency room with severe chest pain, chest tightness, and shortness of breath following an upper respiratory tract infection. The patient reported that she had a cough and runny nose one week prior to this presentation, followed by a sudden sharp pain in the center of the chest 8/10 in intensity on the visual analog scale and pleuritic in nature, which aggravated by deep breathing and lying down flat. It was relieved by sitting up straight and did not radiate to her left arm or jaw. Computed tomography (CT) scan of the chest, posteroanterior and lateral views, showed a mild left pleural effusion with adjacent left basilar atelectasis/infiltrate. CT angiography of the chest with axial contrast showed mild left pleural effusion as well as a small pericardial effusion with bilateral lower lobe interstitial infiltrates. There was no evidence of pulmonary embolism. Electrocardiogram (EKG) showed no apparent ST segment elevation or depression that would be consistent with pericarditis, or acute ischemia or infarct. There was non-specific T wave abnormality. The patient was prescribed prednisone on a tapering dose. On follow-up visit, her condition significantly improved.