Abstract

A pleural effusion is defined to be eosinophilic when 10% or more of the white blood cells in pleural fluid are eosinophils. Despite the multitude of studies enumerating the causes of eosinophilic pleural effusion (EPE), 14%-25% of such cases remain idiopathic even after thorough work-up. We report a case report of a 28-year-old never smoker male from the Rukum district of Nepal who presented to the emergency department (ED) with a chief complaint of shortness of breath associated with a low grade fever, nonproductive cough, and pleuritic right-sided chest pain for two weeks. There was no past medical and surgical history of note. Clinical examination revealed findings suggestive of a right-sided pleural effusion and relevant laboratory and radiological investigations were performed. Symptomatic treatment for the fever was administered. Full blood count showed a leukocytosis of 34 × 109/L with an absolute eosinophil count (AEC) of 7.5 × 109/L (22%). Peripheral blood smear showed normocytic normochromic erythrocytes with eosinophilia (morphologically normal eosinophils). Autoimmune profile was normal, inflammatory markers including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were raised, and an ultrasound and a plain radiograph of the chest confirmed the right-sided pleural effusion. Empirical anti-helminthic coverage was instituted. Subsequent infectious disease work-up was negative. An ultrasound-guided thoracentesis was performed, and the straw-colored pleural fluid showed an exudative picture which was eosinophil-predominant (42%). No malignant cells were detected. Failure of response to anti-helminthic therapy for one week led the team to start oral prednisolone 1 mg/kg once daily with the dose tapered subsequently. The patient responded dramatically. This was continued for one week and a regression of pleural effusion was demonstrated on chest radiography with a normalization of inflammatory parameters (ESR and CRP) and peripheral blood counts. Outpatient follow-up after one month showed no remaining clinical and radiological signs of EPE, and the peripheral eosinophilia resolved. As far as we know, this is the first case report of idiopathic EPE in the context of Asia. There are many causes of EPE, and some of them are still being discovered.

Highlights

  • IL-5 plays a role in stimulating eosinophil production of vascular endothelial growth factor (VEG-F), which increases vascular permeability and is thought to be a major mediator of the formation of exudative pleural effusions [6]

  • The patient responded dramatically to prednisolone therapy. This was continued for one week and a regression of pleural effusion was demonstrated on chest radiography with a normalization of inflammatory parameters (ESR and C-reactive protein (CRP)) and peripheral blood counts (AEC < 0.5 × 108/L; N 86%; L 13%; Rest 1%)

  • This case report features a gentleman who presents with a right-sided pleural effusion found to be eosinophilic in nature

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Summary

Introduction

A pleural effusion is defined to be eosinophilic when 10% or more of the white blood cells are eosinophils [1]. Eosinophilic pleural effusion (EPE) has been attributed to many causes, of which the main broad categories include infectious, inflammatory, malignant, traumatic, and drug-related causes [2]. How to cite this article Shrestha T M, Nepal G, Shing Y K, et al (January 29, 2019) Idiopathic Eosinophilic Pleural Effusion Treated Successfully with Corticosteroid Therapy: A Clinical Case Report. Chest X-ray showed a right-sided pleural effusion, with no associated interstitial infiltrates, apical calcifications, hilar lymphadenopathy, or abnormalities in the pulmonary vasculature observed (see Figure 1). The patient responded dramatically to prednisolone therapy This was continued for one week and a regression of pleural effusion was demonstrated on chest radiography (see Figure 2) with a normalization of inflammatory parameters (ESR and CRP) and peripheral blood counts (AEC < 0.5 × 108/L; N 86%; L 13%; Rest 1%). The test was negative, confirming the absence of the aforementioned suspected infections

Discussion
Conclusions
Disclosures
Zangrilli JG
Findings
World Health Organization

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