SESSION TITLE: ILD Student/Resident Case Report Posters
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: Hypereosinophilic syndromes (HES) are disorders characterized by chronic peripheral blood hypereosinophilia with eosinophil-mediated damage to organs due to infiltration and release of mediators. It’s a diagnosis of exclusion. HES is rare and only few cases have been reported presenting with eosinophilic pleural effusions (EPE). We report such a case of HES.
CASE PRESENTATION: A 61 year old polish woman presented with shortness of breath and palpitations of 1 month duration. She was seen with similar complaints in another hospital 3 weeks before, was found to have persistent eosinophilia and elevated cardiac enzymes but clean coronaries on angiogram. Physical examination revealed tachycardia, tachypnea with bibasilar crackles. Eosinophil count was 1700cells/mm3. Chest tomography showed cardiomegaly with bilateral pleural effusions, left greater than right. The pleural effusion was eosinophilic and exudative with 62% eosinophils. Echocardiography showed ejection fraction of 30% with areas of hypokinesis. Myocarditis was suspected and suggestive on cardiac MRI. Bone marrow aspiration showed eosinophilia (10%) but no monoclonality and was negative for PDGFRA, PDGFRB and FGFR1. Workup for secondary eosinophilia was negative. Patient responded rapidly to prednisone with a normal eosinophil count within 2 days, resolution of the lung effusions within 4 days and restoration of exercise tolerance to baseline over 2 weeks.
DISCUSSION: Pulmonary disease is common, reported to be up to 63% in Mayo clinic series report in 2011. It results from eosinophilic infiltration of the lung with subsequent fibrosis, heart failure or emboli. Isolated EPE presenting as the only pulmonary involvement of HES is very unusual only 4 cases have been reported. Pleural effusions in HES are been thought to be secondary to cardiac eosinophilic disease not lung involvement directly. The treatment of pleural effusions in HES should be based on treatment of underlying disease usually with timely response. If these effusions fail to resolve alternate etiologies should be evaluated.
CONCLUSIONS: The treatment of pleural effusions in HES should be based on treatment of underlying disease usually with timely response.
Reference #1: H. Kawai et al, “Pulmonary involvement, pleural effusion and electrocardiographical abnormality in hypereosinophilic syndrome,” Nihon Kokyuki Gakkai Zasshi, vol. 39, no. 11, pp. 862-867, 2001
Reference #2: W. Choi et al,“Peripheral T-cell lymphoma-unspecified (PTCL-U) presenting with hypereosinophilic syndrome and pleural effusions,” Korean Journal of Internal Medicine, vol. 21, no. 1, pp. 57-61, 2006.
Reference #3: G. J. Gleich et al, “The hypereosinophilic syndromes: current concepts and treatments,” British Journal of Haematology, vol. 145, no. 3,
DISCLOSURE: The following authors have nothing to disclose: Ijeoma Ezeife, Sahni Ashima, Hemant Mutneja, Judy Emil Dela cruz, David Sumoza
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