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.
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.
INTRODUCTION: Esophageal variceal bleeding is one of the leading causes of death in patients with cirrhosis, requiring rapid endoscopic intervention and vasoactive medication administration. When this fails, balloon tamponade using Sengstaken–Blakemore (SB) tube is an effective temporizing measure in up to 90% of patients. However, it can result in esophageal perforation, with potentially fatal septic mediastinitis. Mediastinitis from esophageal perforation carries mortality rates as high as 40-67%, with mortality rate increasing as time to perforation detection increases. Hence a high level of suspicion and rapid identification are key. CASE DESCRIPTION/METHODS: A 56 year old male with history of decompensated Hepatitis C related cirrhosis, recurrent variceal bleeds and portal vein thrombosis (on warfarin), presented with massive hematemesis due to variceal bleed. Despite endoscopy (EGD) with banding, re-bleeding occurred, with rapid drop in hemoglobin from 9 to 5 g/dl. Despite multiple attempts, SB tube was unsuccessful due to resistance. Therefore, the patient was emergently transferred to a tertiary care center for specialist management. Upon presentation, he was found to be in fluid/blood unresponsive shock, requiring high dose vasopressor support. An emergent EGD revealed a 1 cm esophageal perforation above the gastroesophageal junction. CT chest revealed pneumomediastinum. He underwent esophageal stent placement 24 hours later, and was concomitantly treated with antibiotics, antifungals, vasopressors and chest tube insertion for mediastinitis. He slowly stabilized following these interventions, and within 1 week was transferred out of the ICU. DISCUSSION: In patients with fluid/blood unresponsive shock following esophageal manipulation with an SB tube, a high level of suspicion for esophageal perforation and mediastinitis should be maintained. In the past, Xray and esophagogram were thought to be helpful in establishing the diagnosis, however, it is now recognized that going straight to contrast-enhanced CT thorax has the highest yield and will establish diagnosis expediently. This is a necessity, as studies have shown a dramatic reduction in mortality if the diagnosis is made within the first 24 hours, with subsequent initiation of antibiotics and antifungals. Lastly, early consideration for esophageal stenting has also shown to reduce mortality, by tamponading the bleeding varices as well as the perforation.
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