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Conference Proceeding

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Introduction: COVID infection has shown to cause thrombocytopenia with multiple different mechanisms including the destruction of platelets with immune system stimulation similar to ITP with little evidence for optimal management. Here, we present a COVID infected patient presented with idiopathic thrombocytopenia with a partial delayed response to the treatment. Case Presentation: A 92-year-old man with a past medical history of coronary artery disease status post remote coronary artery bypass graft, hypertension, diabetes mellitus presented with petechiae, epistaxis, and was found to be profoundly thrombocytopenic with a platelet count of 1x109/L. He also had an asymptomatic COVID 19 infection, a normal coagulation profile, and hemolysis markers. There were adequate megakaryocytes in the marrow with no evidence of dysplasia or thrombotic microangiopathy. There was no splenomegaly. He was treated with IVIG, steroids, and platelet transfusion. The platelet sluggishly responded to 106 X 109/L on day 23rd. Platelet again started to decrease with the nadir of the 60 X 109/L. Prednisone was tapered and Rituximab was added, platelet plateaued at 50-60 X 109/L. Meanwhile, the patient was bed-bound, developed a sacral ulcer, later passed away with sepsis. Discussion: This is the oldest patient known so far to have ITP from COVID infection. Despite IVIG, steroids, and Rituximab the response to treatment was delayed. This has also been observed in other reported cases with suggested several mechanisms of ITP in COVID infection. Also in all COVID cases, a low platelet count has been associated with a fatal outcome suggesting that COVID infection may alter the response of immunomodulation in ITP. This case will educate the clinician for the optimization of treatment on older patients with thrombocytopenia secondary to COVID infection.


American College of Physicians-Michigan, 2021 Michigan Chapter Virtual Residents/Medical Student Day. May 7, 2021. Virtual. Poster.