CAN YOU SPELL COVID-19 WITH ITP?

Case Presentation: 59 year old man with hypertension initially presented to the hospital with bleeding, oral lesions. They developed four days prior to presentation. They manifested as bullae which eventually “popped” and bled. Patient had no other associated symptoms, including fever, chills, dizziness, chest pain, dyspnea, or irregular bleeding. He works as a city bus driver with high risk for SARS-CoV2 exposure. His vitals were stable. His exam was notable for four lesions that were located on right inner commissure, right buccal mucosa, anterior tongue, and left hard palate. Their sizes ranged from 1 cm to 3 cm. They were reddish purple in color with friable and exophytic quality. Patient also had petechiae on lower labial mucosa. His labs revealed isolated and profound thrombocytopenia with platelet count of less than 1000 (two months ago, his platelet count was >200,000). Blood smear showed mild platelet clumping without any schistocytes. His INR, PTT, PT and D-dimer were mildly elevated. Fibrinogen was 500 mg/dl. His inflammatory markers including C-reactive protein, ferritin, and lactate dehydrogenase were markedly elevated. Otherwise, all other labs were normal, including white blood cell count, hemoglobin level, and serum creatinine. CT head without contrast was negative for any form of acute bleeding. Acute hepatitis panel and HIV were negative as well. Finally, his nasal swab was positive for SARS-CoV2.

Discussion: The patient was diagnosed with immune thrombocytopenic purpura (ITP) secondary to COVID-19. Hematology was consulted and patient was treated with high dose steroids and IVIG therapy. His platelet count increased by 50% within 48 hours of treatment. Through September, 2020 there have been at least 45 cases of ITP caused by COVID-19, most of which were diagnosed retrospectively. It is a difficult condition to diagnose for clinicians as COVID-19 is associated with multiple complications, especially sepsis induced coagulopathy (SIC), thrombotic thrombocytopenic purpura (TTP), and disseminated intravascular coagulopathy (DIC). Moreover, other viral infections such as Hepatitis B and C, HIV, cytomegalovirus, and zoster varicella can commonly cause ITP. Drugs and autoimmune diseases should also be considered when suspecting ITP. Our patient had no systemic symptoms. He had normal white blood cell count, hemoglobin level, serum creatinine, and fibrinogen level with negative blood cultures, urinalysis, HIV test, and hepatitis panel. Only his SARS-CoV2 PCR was positive. These findings enabled us to make the diagnosis of ITP prospectively and start treatment early. Although the actual mechanism behind ITP caused by COVID-19 is still unknown, several mechanisms such as bone marrow suppression, reduced production of thrombopoetin, molecular mimicry, abnormal cytotoxicity of T-cells, and epitope spreading have been suspected. However, treatment has remained the same. Most patients including ours responded well to high dose dexamethasone and IVIG therapy. Very few cases of relapses have been identified so far.

Conclusions: SARS-CoV2 is truly a novel virus with unknown complications. Patients with isolated and unclear thrombocytopenia should undergo COVID-19 testing.