OVERLAPPING ACUTE AND CHRONIC EOSINOPHILIC PNEUMONIA: A CASE REPORT

Abstract

SESSION TITLE: Medical Student/Resident Diffuse Lung Disease SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Lung limited eosinophilic diseases include acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP) which are regarded as two different diseases that differ in severity and timeline.[1] We present a case labeled as idiopathic AEP with features suggestive of a chronic pathology and overlap with CEP. CASE PRESENTATION: An 81 year-old caucasian non-smoking female presented with three days of shortness of breath and non-productive cough. She denied any sick contacts, recent travel or contact with farm animals. Her initial exam showed tachycardia, hypoxia and decreased breath sounds on auscultation with diffuse crackles. Labs showed leukocytosis of 17.5 K/uL with 21% eosinophils and an absolute eosinophil count of 3.7 K/uL. Her computed tomography (CT) of the chest showed extensive ground glass infiltrates with interlobular septal thickening and a crazy paving pattern.(Images A, B, C) Bronchoscopy and bronchoalveolar lavage showed total nucleated cell count of 2,783 with 78% eosinophils, negative cytology and normal flow cytometry. Serologies were negative for parasitic and fungal infections. AEP was diagnosed and the patient was started on a prednisone taper. During her outpatient follow up after two months, she was symptom free. Given no identified inciting factors with resolution of symptoms in less than two weeks, she was labeled as idiopathic AEP. Her labs though showed continued peripheral eosinophilia of 8% and high IgE level. Her prednisone taper was prolonged with eventual normalization of her eosinophilia and IgE level. Pulmonary function tests were normal and repeat CT chest showed minimal residual ground glass infiltrates. DISCUSSION: AEP and CEP don’t have clear diagnostic criteria but there is an overlap between their symptoms, different radiologic findings and eosinophils on BAL being the cornerstone for diagnosis.[2] In AEP, symptoms usually resolve in less than 4 weeks, with higher incidence and severity of respiratory failure and lower incidence of peripheral eosinophilia. Our case shows an overlap between AEP and CEP with peripheral eosinophilia and high IgE levels despite steroid therapy and the resolution of symptoms. Carmi Barta, et al, propose that AEP and CEP may be a spectrum of the same underlying pathological pathway with a difference in clinical presentation.[3] It appears that duration of symptoms may be a discriminating factor between the two entities, but the diagnosis is less clear when symptoms resolve with persistence of lab abnormalities. Our case demonstrates such clinical and laboratory discordance; thus, we suggest that AEP and CEP may in some cases be the same disease process with AEP being an exacerbation or an inciting event. CONCLUSIONS: Our case highlights the need for additional investigations and understanding of eosinophilic lung diseases. Reference #1: Evans R., et al. Eosinophilic lung diseases. Med Clin North Am 2011;95:1163–118. Reference #2: Yuzo Suzuki, Takafumi Suda, Eosinophilic pneumonia: A review of the previous literature, causes, diagnosis, and management, Allergology International, Volume 68, Issue 4, 2019, Pages 413-419. Reference #3: Bartal, Carmi et al. “Drug-induced eosinophilic pneumonia: A review of 196 case reports.” Medicine vol. 97,4 (2018): e9688. DISCLOSURES: No relevant relationships by Youssef Abouleish, source=Web Response No relevant relationships by Elise Stephenson, source=Web Response No relevant relationships by Sami Tahhan, source=Web Response