Case Report Epstein–Barr Virus Primary Infection Complicated by Hemophagocytic Lymphohistiocytosis and Plasmablastic Lymphoma in a HIV-Negative Patient Nan Chen , Mike Perez, and Martha Mims Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA Correspondence should be addressed to Nan Chen; nanc@bcm.edu Received 9 August 2019; Accepted 19 September 2019; Published 7 October 2019 Academic Editor: Kostas Konstantopoulos Copyright © 2019 Nan Chen et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. EBV (Epstein–Barr virus) viremia causes immune dysregulation through various mechanisms, and we are understanding more that mutations in B, T, and NK (natural killer) cell signaling pathways allow EBV complications such as HLH (hemophagocytic lymphohistiocytosis) and lymphomas to arise. Here, we report a 20-year-old previously healthy, HIV- (human immunodeficiency virus-) negative male who presented with fevers, sore throat, and lymphadenopathy (LAD). He was found to have EBV viremia, pancytopenia, and elevated LFTs (liver function tests) suspicious for HLH. Bone marrow biopsy and elevated IL-2 (interleukin) receptor confirmed this diagnosis. Additionally, gastric biopsy confirmed diagnosis of plasmablastic lymphoma (PBL), a rare, aggressive HIV- and EBV-associated lymphoma. Both bone marrow and gastric biopsy showed evidence of EBV. Patients with EBV complications should have a rigorous workup to characterize the full extent of immune dysregulation including genetic testing at a high-volume center. 1. Case Presentation e patient was a healthy 20-year-old M who presented with 3 weeks of intermittent fever, sore throat, and painful bi- lateral cervical lymph nodes. He went to an outside emer- gency room 5 days prior to presentation and was diagnosed with infectious mononucleosis via positive monospot and discharged with symptomatic treatment. He presented to our institution for 2 days of hematemesis, melena, jaundice, and continued fevers. On interview with his family, he had a healthy childhood without prior hospitalizations and one healthy younger male sibling. On physical exam, he was febrile and tachycardic. He had bilateral cervical lymphadenopathy, decreased breath sounds in his bilateral lung bases, and hepatosplenomegaly. Initial laboratory testing showed the following: Hgb (hemoglobin) 12.3 g/dL, WBC (white blood cell) 5.2 k/uL, platelets 68 k/uL, aspartate aminotransferase 361 U/L, alanine aminotransferase 242 U/L, alkaline phosphatase 332 U/L, total bilirubin 10.7 mg/dL, prothrombin time 34.3 seconds, fibrinogen 95 mg/dL, and d-dimer 6.5 ug/mL. HIV (human immuno- deficiency virus) and hepatitis panel were negative. CT (computed tomography) of chest, abdomen, and pelvis showed diffuse lymphadenopathy in axillary, mediastinal, hilar, retroperitoneal, and inguinal regions, numerous pul- monary nodules bilaterally, and hepatosplenomegaly. Over the following 24 hours, the patient’s clinical condition de- teriorated, and the following day, he was intubated for hypoxemic respiratory failure, started on broad-spectrum antibiotics, and given supportive transfusions. EBV viremia was confirmed with a viral load of 2 million copies/mL (Figure 1). An EGD (esophagogastroduodenoscopy) was performed for bleeding, revealing multiple friable, superficial ulcers throughout the distal esophagus and stomach inconsistent with peptic ulcer disease, and biopsies were collected. With dropping blood counts, triglycerides of 289 mg/dL and ferritin of 13,000 ng/mL (Figure 2), there was concern for hemophagocytic lymphohistiocytosis (HLH), and a marrow exam was performed along with a left inguinal lymph node Hindawi Case Reports in Hematology Volume 2019, Article ID 7962485, 4 pages https://doi.org/10.1155/2019/7962485