HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTION PRESENTING WITH PROGRESSIVE RASH

ABSTRACT

CASE A 25-year-old female with no medical history presented with progressive petechial rash at the chest, trunk, bilateral forearms, and thighs. Patient had the COVID-19 vaccine three weeks prior. However, denied recent travel or tick bites. No home medications nor recent hospitalizations, other than a tooth extraction a month earlier. On physical exam, the patient's vitals were unremarkable and had non-blanching petechial rash noted on her torso and bilateral extremities. Labs were significant of platelet count 1,000/mcL, hemoglobin 12.9 mg/dL, WBC 7.52 x103 /mcL, absolute lymphocytes 3.33x103 /mcL. Patient was administered two units of platelets followed by intravenous immunoglobulin (IVIG) and dexamethasone. No bleeding or hemodynamic instability was identified. Platelet count improved to 100,000/mcL over the next 24 hours. Further work-up revealed a positive HIV-1 antibody, absolute CD4 256 cells/mcL, viral load 27,300 copies/mcL. Once starting antiretroviral therapy (ART);bictegravir, emtricitabine, and tenofovir alafenamide, platelet count increased within a month to more than 200,000/mcL. IMPACT/DISCUSSION: Thrombocytopenia is defined as platelet count below 150,000/mcL. HIV-induced cytopenias are common, mainly neutropenia. However, sentinel events of thrombocytopenia are very rare in otherwise healthy individuals. A review of 5,290 HIV patients at the University of British Columbia from 1996 to 2012 revealed only 0.6% incidence of severe thrombocytopenia which they defined as platelet count <20,000/mcL. The exact pathophysiology is not clearly understood, but it is possible that antibodies against HIV cross-react with platelets or possible immune alteration. This is suggested by the prompt resolution of thrombocytopenia once ART is initiated. Immune thrombocytopenia (ITP) is a diagnosis of exclusion typically presenting with thrombocytopenia while other cell lines are normal. The greatest concern is when platelet counts drop less than 20,000/mcL due to fears of intracranial bleeding. Literature is not decisive in a correlation between platelet counts and risk of bleeding, yet it is suggested that circulating platelets are younger and more effective to maintain hematopoiesis in ITP when compared to other causes of thrombocytopenia. Treatment approach for ITP depends on the bleeding risk. In the presence of bleeding, urgent platelet transfusion, glucocorticoids, and IVIG are the mainstay of treatment. In absence of bleeding, individualized assessment of the condition is recommended to either monitor or treat. Platelet counts below 20,000-30,000/mcL require steroids or IVIG. In our case, she surprisingly presented only with minor petechial bleeding. Prompt initiation of ART, close monitoring of platelet response and CD4 count, as well as identifying resistant thrombocytopenia is indicated once patient is medically stable. CONCLUSION: Sole presentation of ITP due to HIV infection is rare. Risks of critical bleeding and further management are crucial to prevent fatal outcomes.