Pb2306: relapse of immune thrombocytopenia and myocarditis

Background: Immune thrombocytopenia (ITP) is an acquired thrombocytopenia caused by autoantibodies against platelet antigens. ITP most often occurs within a few weeks following a viral infection, but it is also associated with other infections, drugs, hematopoietic malignancies and autoimmune diseases. Myocarditis is an inflammatory disease of cardiac muscle caused by a variety of infectious and noninfectious conditions. Autoimmune mechanisms have been implicated in the pathogenesis of myocarditis with or without a virus trigger. Aims: Our aim is to present an unusual case of myocarditis in a 17-year-old male, with a history of ITP presenting simultaneous relapse of ITP. Methods: A 17-year-old male with a history of ITP presented at the Emergency Department complaining of gingival bleeding, left shoulder pain and fever. Clinical examination showed extremity petechiaes and tachycardia, there was an ST elevation in V2-V6 leads on ECG and laboratory data included PLTs 2000/μL and elevated high sensitivity troponin (1.240pg/mL). He was treated immediately as a relapse of ITP with corticosteroids and he received b-blockers due to persistent tachycardia. Viral and immunological tests were negative. Results: Gradually, during hospitalization, there was an elevation of PLT count and a decrease in serum troponin levels with improving and finally normal ECG findings. The patient was discharged and continued treatment with prednisolone and b-blocker. He was reassessed after one month and troponin levels, PLT counts and ECG were normal. However, the cardiac Magnetic Resonance Imaging (MRI) revealed fibrosis with signal intensity and gadolium enhancement in the anterolateral and inferior segments. After three months a follow up cardiac MRI showed reduction of fibronitic tissue size. Summary/Conclusion: Autoimmunity plays a major role in the pathogenesis of both ITP and myocarditis. It seems that they share common autoimmune pathways and further research of which is important for understanding pathophysiology behind these clinical entities and improving their treatment.