Case Presentation: 72-year-old lady with past medical history of CAD, COPD and a recent hospitalization for COVID19 Pneumonia and was discharged with Levofloxacin for 1 week. Her labs upon discharge were noted to be: Hb 11.7 gm/dl, WBC 6.9x 109/L, and platelet count 194 x109/L.. One week after getting discharged from the hospital, the patient presented again with epistaxis for one day. She denied any trauma, sinusitis or any past medical history of epistaxis. Physical exam at the time of this presentation revealed scattered petechiae on lower extremities. Her skin findings at the time of initial presentation are shown in figure 1. Labs upon arrival included Hb 9.7 g/dl, WBCs 11.0×109/L, and platelets 2 x109/L. Two units of platelets were transfused immediately. Upon further evaluation, her D-dimer was 674 ng/mL and LDH 765 U/L. She tested negative for HIT antibody, Serotonin release assay, Hep C antibody, and HIV screen. Also, VIT B12 , folate levels, and ADAMTS13 activity were within normal range. Peripheral blood smear revealed morphologically normal appearing platelet however markedly reduced in number, absence of clumping, schistocytes or any findings suggestive of bone marrow failure. A presumed diagnosis of COVID19 induced ITP was made however there was also a suspicion of Drug induced ITP secondary to Levofloxacin use. Patient was given high dose steroids and IVIG. Her platelet count trended upwards and was found to be 53×109/L on day 10 of second admission. Treatment response observed in our patient has been shown in figure. 2
Discussion: Several risks factors have been described for ITP including environmental factors (of which infection is included) and genetic predisposition [5]. Thrombocytopenia has been shown to be associated with COVID-19 but it is commonly seen in the initial disease process. Several cases of ITP related to COVID-19 have been reported, but few with severe thrombocytopenia occurring as a late manifestation of disease process. The theorized mechanism behind COVID-19 associated thrombocytopenia include endothelial damage, platelet aggregation and formation within the lung, bone marrow suppression, and problems surrounding immune clearance [6]. Levofloxacin is known to cause a wide array of adverse effects. Additionally, multiple case reports have found levofloxacin to be a causative agent of drug induced ITP. D-ITP typically occurs within 1 week after initiation of the offending agent. It is thought that a specific antibody to platelet surface proteins develops and thus, immune destruction occurs [7].Given that autoimmune diseases are becoming increasingly associated with COVID-19 and the fact that our patient was discharged on levofloxacin. We believe there is a good probability that she developed ITP from the combination of both risk factors. Her promising response tosteroids and intravenous immunoglobulins, along with a negative workup for other possible causes of thrombocytopenia make her ITP development secondary to above mentioned mechanisms more plausible.
Conclusions: It is of the utmost importance to consider the development of ITP as a potentially fatal manifestation of levofloxacin use in COVID-19 patients. This case also highlights the importance of close follow up in patients diagnosed with COVID-19 and treated/discharged with levofloxacin. At this moment, we need more data to further assess the incidence of ITP in COVID-19 patients and moreover, in those treated with levofloxacin.
