• Anna Maria Pisacreta, Ruggiero Mascolo, Mariangela Nivuori, Costanza Caccia Dominioni, Claudia Gabiati, Lucia Trotta, Massimo Pancrazi, Giacomo Di Marco, Chiara Carollo, Alice Pedroli, Francesca Casarin, Enrico Tombetti, Emanuele Bizzi, Massimo Imazio, and Antonio Brucato.
• Department of Internal Medicine, ASST Fatebenefratelli-Sacco, Milan, Italy. Electronic address: anna.pisacreta@unimi.it.
• Eur. J. Intern. Med. 2023 Jul 1; 113: 454845-48.

ObjectivesThis cohort study describes a systemic phenotype of pericarditis, comparing this phenotype with other forms of pericarditis.Patients And MethodsPatients in our center were enrolled in a prospectively maintained registry from 2019 to 2022. 412 patients with idiopathic recurrent pericarditis were analyzed. "Systemic inflammatory" subset was defined as the presence of all the following criteria: fever ≥38C°, CRP ≥2 times normal values, pleural effusion detected with any imaging techniques. The absence of any of the 3 criteria was defined as "isolated" subset.ResultsWe found that 211 (51.2%) of 412 patients (188 female) presented the systemic subset and the variables significantly associated with this subset in univariate analysis (p<0.001) were: higher mean age: 45.5 (±SD 17.2) vs 39.9 (±SD 16.4) years, higher mean CRP values: 128.8 vs 49.9 mg/L, higher proportion of pericardiocentesis: 19% vs 1.5%, higher mean leukocyte count: 13,143.3 vs 9910.3/mm3, higher mean neutrophils number: 10,402.5 vs 6779.8 /mm3 and lower mean lymphocyte count: 1693.9 vs 2079.3 /mm3. As results the neutrophil-to-lymphocyte ratio was higher in systemic inflammatory phenotype: 6.6 vs 3.4 (p< 0.001). Anti-IL1 therapy was started more frequently in the systemic subgroup (26%) than in the isolated subset (7.5%) (p < 0.001). On multivariate analysis neutrophil count and lymphopenia were statistically associated with the systemic subset (p < 0.001).ConclusionThis results demonstrate the relevance of the systemic inflammatory phenotype, characterized by pleural effusions, confirming its analogy with autoinflammatory diseases, thus possibly requiring an eventual escalation of therapy to IL-1 inhibitors.Copyright © 2023. Published by Elsevier B.V.

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