IJCS | Volume 33, Nº3, May / June 2020

DOI: 10.5935/2359-4802.20190033 295 CASE REPORT International Journal of Cardiovascular Sciences. 2020; 33(3):295-298 Mailing Address: Maria Trêpa Largo Prof. Abel Salazar, nº 1. Postal Code: 4099-001, Porto – Portugal. E-mail: maria_trp@hotmail.com Acute Pericarditis in Crohn's Disease under Pharmacological Immunosuppression: A Diagnostic and Therapeutic Dilemma Maria Trêp a, Isabel Neve s, M arta Salgad o, Graziela Carvalheira s, Vasco Dia s Centro Hospitalar do Porto, Porto - Portugal Manuscript received Ocotober 28, 2018; revised manuscript October 28, 2018; accepted November 22, 2018. Crohn Disease; Pericarditis, Tuberculous; Fever; Tuberculosis; Anti-Bacterial Agents; Antibiotic- Prophylaxis. Keywords Introduction Acutepericarditis inyoungpatientsusuallyhas abenign course. However, in those with autoimmune diseases it is mandatory to consider the risk of opportunistic infections, and of association with the underlying disease or immunomodulatory drugs. This case report aims to show possible strategies for diagnosis and treatment of this particularly complex group of patients. Case Report A 40-year-oldwoman, with Crohn’s disease diagnosed in 2009 was admitted to the emergency department with a 1-week history of fever, dyspnea and pleuritic chest pain. She was taking adalimumab (anti-TNF α ), and azathioprine was started after a negative screening for tuberculosis (TB) done by interferon gamma release assay (IGRA). Upon admission, examinations revealed pulmonary and peripheral congestion, and hypoxemia (PaO 2 : 60 mmHg). C-reactive protein was elevated (92 mg/L) and there was normocytic anemia (Hb: 7.9mg/dL) and lymphopenia (670/µL). Electrocardiogram showed T wave flattening and transthoracic echocardiogram (echo) showed moderate pericardial effusion and thickening of layers. Bi-ventricular function was normal. A diagnosis of acute pericarditis complicated by effusion was assumed. Given the clinical context, she was admitted for further management. She underwent exhaustive examination from which we inferred: (1) no criteria for myopericarditis; (2) no conditions for pericardial drainage (especially effusion on the posterior wall); (3) no microbiological isolates (i.e., bronchial lavage without Koch bacillus isolation); (4) undetermined interferon- γ release assay (IGRA) in two different occasions; (5) negative serology for acute infections (HIV, CMV, EBV, HSV 1 and 2, toxoplasmosis, parvovirus); (6) positive immunological tests foranti-nuclear antibodies (ANA), anti-histones and immunoglobulins G and M; (7) thoracic/abdominal/pelvic computed tomography angiography (Figure 1) with mediastinal and hilar adenopathies (not accessible) with no other findings. The anti-TNF α was discontinued and she was started on ibuprofen and colchicine, showing an initially good clinical response and decrease of pericardial effusion. However, reassessment 15 days after discharge showed an increase in pericardial effusion and echo criteria for constrictive pericarditis: septal bounce, increased respiratory variability (~40%) of the transtricuspid flow, and dilatation and reduced variability of the inferior vena cava (Figure 2). Given the unfavorable course, four possible etiologies of pericarditis were considered: (1) idiopathic/viral, (2) bacterial (especially TB), (3) extra-intestinal manifestation of inflammatory bowel disease (IBD) and (4) association with immunomodulation therapy. The case was presented in a multidisciplinary meeting (including Cardiology, Internal Medicine and Immunology specialists) that concluded that there were no definitive criteria for the cause of pericarditis. However, because of the evidence suggestive of TB (immunosuppression, mediastinal adenopathy and incipient constrictive pericarditis), the real possibility of an adverse outcome if TB was not treated, as well as an increased risk of worsening with the use of corticosteroid