IVIG was recommended to be used when immediate platelet count elevation is needed7. a normal white cell count, hemoglobin (Hb) of 12.0 g/d, and platelet count (175 000/mm3). Creactive protein (CRP) and Ddimer were elevated at 10.9 mg/dL and 970 ng/mL. A nasopharyngeal swab was positive for COVID19. Chest Xray showed bilateral lung infiltrates. The patient was admitted to the regular medical floor and started on hydroxychloroquine, intravenous piperacillin/tazobactam, and azithromycin. On day 13, the patients oxygen requirements increased and 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(Physique1). At the same day, his Hb was 10.4 g/dL. Ddimer and fibrinogen were elevated at 13 180 ng/mL and 446 mg/dL. PT, partial thromboplastin time, and INR were 21.9 seconds, 40.5 seconds, and 2.0 respectively. Peripheral blood smear did not show any schistocytes. The international society on Acemetacin (Emflex) thrombosis and hemostasis (ISTH) DIC score was 7. The 4T score for possible heparininduced thrombocytopenia (HIT) was 4 (intermediate probability), and antiplatelet factor 4 antibody and antinuclear antibodies were negative. Drugdependent platelet antibodies were unfavorable for tazobactam IgG or IgM antibodies; however, the test was positive for nondrugrelated IgG antiplatelet antibodies. 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. == 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 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 models of platelets were transfused, and platelet count continued to be less than 2000/mm3; however, 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/mm3and 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 COVID19 is usually a respiratory tract disease, multiple systems can be affected including hematopoietic and lymphatic systems among others. Thrombocytopenia has been reported by multiple studies and was linked to disease mortality2. ITP induced by COVID19 is usually rare and has been reported in few cases3,4,5. Our Rabbit Polyclonal to SHANK2 case presented with viral pneumonia secondary to COVID19 and Acemetacin (Emflex) 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 usually a diagnosis of exclusion; it can be diagnosed after excluding all possible causes of thrombocytopenia1. In a recently published case statement, COVID19 patient developed acute thrombocytopenia, skin purpura, and epistaxis on day 4 after admission, other Acemetacin (Emflex) possible causes of thrombocytopenia were excluded, and ITP was concluded to be the most probable diagnosis3. In another case series, three COVID19 patients developed ITP, two of the three patients presented with skin purpura and mucosal bleeding. The third individual developed acute transfusionresistant thrombocytopenia and died after intracerebral hemorrhage4. The patient in our case designed acute thrombocytopenia, and possible causes such as DIC, HIT, thrombotic thrombocytopenic purpura, and druginduced 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 Acemetacin (Emflex) to have positive IgG antibodies against the platelets and did not respond to platelet transfusion which makes Acemetacin (Emflex) ITP the most likely diagnosis. Our individual did not experience any bleeding events although he had severe thrombocytopenia, this may be explained by the fact that diagnoses and management were established in a timely.