Case Presentation: A 63-year-old male was admitted to the hospital for dizziness secondary to heart failure exacerbation and incidentally found to have thrombocytopenia of 141,000 on admission. Over the next 72 hours, the patient’s platelet count decreased by over 50% to 51,000 while all other cell lines remained stable. The patient had not received any heparin products during or before his hospital course and had normal coagulation studies and negative hemolysis labs. An infectious workup was performed which was significant for positive EBV VCA IgG, EBV EA IgG, and EB-NA IgG as well as negative EBV VCA IgM—consistent with a reactivation of a past infection. CMV and hepatitis serologies were within normal limits. A peripheral smear was significant for atypical lymphocytes and giant platelets. A PCR of peripheral blood was sent which detected EBV DNA. Clinically, the patient was asymptomatic. Given the patient’s benign clinical presentation, the decision was made to defer initiating corticosteroids. On a repeat blood count the following morning, the patient’s platelet count had stabilized. After 72 hours, the patient’s platelet count had risen to 152. On a repeat blood smear, normal platelet morphology was observed. A week later, the patient’s platelet count rose to 264 and was trending laterally.
Discussion: Asymptomatic, mild thrombocytopenia is reported in up to 25-50% of EBV infections, though severe and rapid declines in platelet counts are not commonly observed. Of the reported cases of severe thrombocytopenia in EBV infections, most cases have described primary EBV infections. The current case, however, demonstrates that EBV reactivation may also cause dramatic declines in platelet counts even without other presenting symptoms of EBV. Additionally, the current case corroborates prior observations that patients with EBV who present with thrombocytopenia may not present with the typical symptoms of EBV such as sore throat and lymphadenopathy.Multiple theories also exist for the cause of thrombocytopenia in EBV-infections including hypersplenism, impaired thrombopoiesis, and autoimmune antibody formation. The current patient did not present with splenomegaly, but EBV-induced thrombocytopenia is still most likely multifactorial. Finally, the use of steroids to treat thrombocytopenia in EBV is controversial. Multiple case studies have demonstrated successful recovery of platelet counts after initiating a steroid course for EBV patients with severe thrombocytopenia (< 50,000). In the current case, the patient's platelet counts were borderline (51,000), and steroid treatment was deferred. Platelet counts normalized within a week without treatment, however, indicating that thrombocytopenia in EBV can be self-resolving, even in patients with rapidly declining platelet counts or platelet counts bordering severe thrombocytopenia.
Conclusions: The progression of thrombocytopenia in EBV reactivation may be rapid. In the current patient, platelet counts stabilized and recovered to normal limits within one week without any additional intervention. Our experience supports steroid treatment to be reserved only for patients presenting with severe thrombocytopenia. Finally, isolated rapid onset thrombocytopenia without a clear etiology such as HIT warrants a consideration of atypical Epstein-Barr virus infection.