Associazione Nazionale Medici Cardiologi Ospedalieri

CONGRESS ABSTRACT

CONGRESS ABSTRACT

Haemophilus Influenzae-related pleuro-pericarditis conditioning cardiac tamponade in a patient with B lymphocyte depletion and hypogammaglobulinemia after CAR-T therapy

Griffith Brookles Carola Torino (Torino) – Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino | Bongioanni Lorenzo Torino (Torino) – Azienda Ospedaliero-Universitaria Città della Salute e della Scienza di Torino | Nangeroni Giulia Orbassano (Torino) – Azienda Ospedaliero-Universitaria San Luigi Gonzaga | Biolè Carloalberto Orbassano (Torino) – Azienda Ospedaliero-Universitaria San Luigi Gonzaga | Cerrato Enrico Orbassano (Torino) – Azienda Ospedaliero-Universitaria San Luigi Gonzaga | Chinaglia Alessandra Orbassano (Torino) – Azienda Ospedaliero-Universitaria San Luigi Gonzaga | Bianco Matteo Orbassano (Torino) – Azienda Ospedaliero-Universitaria San Luigi Gonzaga

Introduction: Bacterial pericarditis is a rare but rapidly progressing form of pericarditis, mostly affecting immunosuppressed patients. We report a case of Haemophilus influenzae-related pleuro-pericarditis resulting in cardiac tamponade in a patient with severe hypogammaglobulinemia after Chimeric Antigen Receptor T-cell (CAR-T) therapy for a diffuse large B-cell lymphoma (DLBCL).  Case report: A 69-year-old man presented for dyspnea in the last few days. He had a history of DLBCL, in remission after radiotherapy and CAR-T therapy. He had undergone catheter ablation for paroxysmal atrial fibrillation, recently starting amiodarone for a relapse. On arrival he was hypotensive; ECG showed sinus rhythm (SR) with mild diffuse anterior ST elevation. Echocardiography showed large circumferential pericardial effusion with cardiac tamponade, leading to urgent pericardiocentesis and drainage of 350 mL of orange fluid. Cultures grew H. influenzae, indicating bacterial pericarditis. He had started amoxicillin and azithromycin for pneumonia; after cultures’ results, amoxicillin was switched with ceftriaxone. Acetylsalicylic acid and colchicine were initiated, with a switch to prednisone (0.1 mg/kg/day) for signs of constriction. A second pericardiocentesis was performed for relapsing pericardial effusion, draining 300 mL of fluid. Hematologic tests showed B lymphocyte depletion and severe hypogammaglobulinemia, leading to immunoglobulin (Ig) supplementation. He was discharged and advised to continue prednisone, gradually tapering it. At 1 and 6-month follow-up, he was asymptomatic, in SR, with a progressively reducing mild pericardial effusion despite suspension of prednisone. Amiodarone was suspended, while he continued regular Ig supplementation for persistent hypogammaglobulinemia. Discussion: Bacterial pericarditis has become an uncommon cause of pericardial inflammation due to widespread use of antibiotics. In our case, infection was secondary to H.influenzae-pneumonia, as the patient’s severe hypogammaglobulinemia increased his susceptibility to encapsulated bacteria. Specialistic tests were essential to identify this condition and enable targeted therapies. Conclusion: Bacterial infection should always be considered in patients with pericardial effusion, especially when immunosuppressed. Microbiological analysis of pericardial fluid is essential to detect the causative pathogen and guide antimicrobial therapy, possibly leading to a favorable prognosis.