Red arrow indicates the date of treatment initiation with dexamethasone and intravenous immunoglobulins Since INR was subtherapeutic on the day of admission (INR?=?1.1), oral warfarin was started. he was transferred to the intensive care unit (ICU) for monitoring. On the same time, his platelet count decreased acutely to less than 2,000/mm3 (Physique?1). At the same day, his Hb was 10.4?g/dL. D\dimer and fibrinogen were elevated at 13?180?ng/mL and 446?mg/dL. PT, partial thromboplastin time, and INR were 21.9?seconds, Auristatin F 40.5?seconds, and 2.0 respectively. Peripheral blood smear did not show any schistocytes. The international society on thrombosis and hemostasis (ISTH) DIC score was 7. The 4T score for possible heparin\induced thrombocytopenia (HIT) was 4 (intermediate probability), and antiplatelet factor 4 antibody and antinuclear antibodies were negative. Drug\dependent platelet antibodies were unfavorable for tazobactam IgG or IgM antibodies; however, the test was positive for non\drug\related IgG antiplatelet antibodies. Auristatin F Ultrasound of the lower extremities on day 13 showed acute left tibial deep vein thrombosis (DVT). Computed tomography of the chest was unfavorable for pulmonary embolism. Open in a separate window Physique 1 Changes in platelet count level during admission. Day 1 (baseline) represents the day of admission. Red arrow indicates the date of treatment initiation with dexamethasone and intravenous immunoglobulins Since INR was subtherapeutic on the day Auristatin F of admission (INR?=?1.1), oral warfarin was started. On day 9, INR was 3.3 and warfarin was held. The patient received a single dose of prophylactic enoxaparin the next day, 3?days before the acute drop in platelet count. Argatroban was started for possible HIT (although unlikely) and then stopped when HIT excluded. Three units of platelets were transfused, and platelet count continued to be less than 2000/mm3; however, Auristatin F no bleeding developed at any point. On day 15, the patient was started on dexamethasone 40?mg daily (received 4 doses) and 1?g/kg intravenous immunoglobulin (IVIG) daily for 2?days. By the end of the treatment course, his platelet count was 79?000/mm3 and he was restarted on systemic heparin. The patient required endotracheal intubation and family decided to go with comfort care. Patient passed away after 20?days of admission. Although COVID\19 is a respiratory tract disease, multiple systems can be affected including hematopoietic and lymphatic systems among others. Thrombocytopenia SLC7A7 has been reported by multiple studies and was linked to disease mortality 2 . ITP induced by COVID\19 is rare and has been reported in few cases 3 , 4 , 5 . Our case presented with viral pneumonia secondary to COVID\19 and developed secondary ITP. Immune thrombocytopenic purpura is an acquired hemorrhagic disease characterized by thrombocytopenia and autoantibodies against platelet antigens. Clinically patients with ITP may be asymptomatic or can present with bleeding. ITP is a diagnosis of exclusion; it can be diagnosed after excluding all possible causes of thrombocytopenia 1 . In a recently published case report, COVID\19 patient developed acute thrombocytopenia, skin purpura, and epistaxis on day 4 after admission, other possible causes of thrombocytopenia were excluded, and ITP was concluded to be the most probable diagnosis 3 . In another case series, three COVID\19 patients developed ITP, two of the three patients presented with skin purpura and mucosal bleeding. The third patient developed acute transfusion\resistant thrombocytopenia and died after intracerebral hemorrhage 4 . The patient in our case developed acute thrombocytopenia, and possible causes such as DIC, HIT, thrombotic thrombocytopenic purpura, and drug\induced thrombocytopenia have been excluded. Although the patient had acute DVT that may contribute to consumptive thrombocytopenia, the timing, magnitude, and acuity of thrombocytopenia are unlikely to be due to DVT alone. Also, the patient was found to have positive IgG antibodies against the platelets and did not respond to platelet transfusion which makes ITP the most likely diagnosis. Our patient did not experience any bleeding events although he had severe thrombocytopenia, this Auristatin F may be explained by the fact that diagnoses and management were established in a timely manner. Immune thrombocytopenic purpura treatment consists of systemic steroids and IVIG as first line. Second\line treatment options include splenectomy, rituximab, immunosuppressive therapy, and thrombopoietin receptor agonists (TRAs). More than 70% of the patients respond to conventional therapy. TRAs are reserved for patients resistant to first\ and second\line therapies and are considered safe and effective 6 . Recent guidelines published by Pavord S et al recommended steroids as a first\line therapy for ITP secondary to COVID\19. TRA may be.