Immune thrombocytopenia during the COVID‐19 pandemic

Abstract

Given past experience with widespread viral infections, for example influenza, we expected that SARS-CoV-2 would create a large number of de novo cases of immune thrombocytopenia (ITP). Perhaps a silver lining on the cloud of SARSCoV-2 is that for patients with ITP, the virus is not having a major effect, as evidenced by few reports of ITP in conjunction with SARS-CoV-2 infection. We performed a retrospective review of patients ≥18 years diagnosed with COVID-19 and ITP seen at New York Presbyterian–Weill Cornell Medicine (NYP-WCM) or Shandong Provincial Chest Hospital–Shandong University (SPCH-SDU) from February to August 2020. Ten patients from NYPWCM and two from SPCH-SDU were identified (Table I). The study was approved by the Institutional Review Board of NYP-WCM and the Medical Ethical Committee of SPCHSDU. There were 10 patients with pre-existing ITP and two with presumed new SARS-CoV-2-associated ITP (Table I). Patient 8 was diagnosed with ITP during hospitalization for COVID19 and Patient 10 developed isolated ITP six weeks following SARS-CoV-2 infection; neither had a prior history of thrombocytopenia. For those with pre-existing ITP, SARS-CoV-2 infections were managed as outpatients (n = 3), ER visits (n = 2), and hospitalizations (n = 5). During active COVID-19, five patients required ITP treatment for platelet nadirs of 8–33 9 10/l. Patient 7 received platelet transfusion, steroids and intravenous immunoglobulin (IVIg). Patients 1 and 9 received IVIg alone. Patient 1 had been on weekly romiplostim, twice daily mycophenolate mofetil (MMF) and IVIg as needed since 2017. She had fevers, fatigue, body aches and was ITP-Bleeding Assessment Tool: Skin 1 (petechiae), Mucosae 1 (epistaxis). Due to morbid obesity, limited mobility, and advanced age, she received weekly home infusions of IVIg 80 g for counts <10– 20 9 10/l. Patient 9, on prednisone 15 mg daily for platelets 20–30 9 10/l, was hospitalized at SPCH-SDU. He received IVIg 10 g daily for two days with platelet improvement from 18 to 28 9 10/l. Patient 8 received inpatient IVIg 15 g daily for three days, methylprednisolone 80 mg BID, and convalescent plasma for SARS-CoV-2-associated ITP with platelets increasing from 33 to 83 9 10/l. Several weeks following SARS-Cov-2 diagnosis, Patient 10 received IVIg with steroids for de novo ITP with platelet improvement from 6 to 82 9 10/l. Patient 7 had chronic ITP with platelets of 8 9 10/l requiring platelet transfusions. In the setting of multiorgan failure, he declined additional treatment and passed away. Two patients received steroids alone for exacerbations of known ITP during infection with SARS-CoV-2. Patient 11’s platelets dropped from 60–70 to 23 9 10/l two weeks after diagnosis. His platelets improved to 180 9 10/l on prednisone 20 mg daily. Patient 4’s platelets dropped from a baseline of 60–70 to 26 9 10/l. She received dexamethasone 40 mg for four days with platelets rising to 105 9 10/l. Five patients (Patients 2, 3, 5, 6, 12) did not modify their ITP treatment despite COVID-19. Three (Patients 2, 3, 6) were on treatment (eltrombopag, steroids, rituximab, respectively). Patient 5 was discharged from the ER with haematology follow-up for platelets 26 9 10/l and Patient 12 was diagnosed with SARS-Cov-2 on routine screening for caesarean section with platelets 94 9 10/l. Patients 3, 4, 6, 8 were hospitalized and received prophylactic anticoagulation with enoxaparin 40 mg SC daily (NYPWCM) or nadroparin 3 800 U SC daily (SPCH-SDU) without bleeding events. Patient 6 developed deep vein thrombosis (DVT) and pulmonary embolus (PE) despite prophylactic enoxaparin. He received therapeutic heparin and was discharged on apixaban. Patient 2 presented with a new headache due to cerebral venous sinus thrombosis and was discharged on apixaban. Treatments of ITP, ongoing or newly initiated, can impact the course and outcome of SARS-CoV-2. Thrombosis is a major concern in patients with SARS-CoV-2 infection and immunosuppression could worsen infection. The American Society of Hematology offers recommendations limited by data to expert opinion for ITP management in SARS-CoV-2 infection. IVIg is not immunosuppressive, rapidly increases platelets, and has anti-inflammatory effects. To avoid prolonged visits and SARS-CoV-2 exposures, home administration (like Patient 1) is useful. Steroids may risk increasing viral susceptibility early in infection; however, published reports and our own experience suggest steroid use does not often lead to worse outcomes in COVID-19. No consensus exists regarding increased severity of COVID-19 infection in patients who have received rituximab or are on other chronic immunosuppressants. Anti-CD20 agents impair humoral responses to de novo infections and vaccines for at least 4–6 months. We agree with avoiding immunosuppressives or rituximab during the COVID-19 pandemic pending reasonable alternatives. We also caution use of splenectomy due to increased thrombotic risk and risk of overwhelming sepsis. correspondence