Eosinophilic pneumonias in children: A review of the epidemiology, diagnosis, and treatment

Abstract

Pediatric eosinophilic pneumonias (EPs) are characterized by a significant infiltration of the alveolar spaces and lung interstitium by eosinophils, with conservation of the lung structure. In developed countries, EPs constitute exceptional entities in pediatric care. Clinical symptoms may be transient (Löffler syndrome), acute (<1 month and mostly <7 days), or chronic (>1 month). Diagnosis relies on demonstration of alveolar eosinophilia on bronchoalveolar lavage, whether or not associated with blood eosinophilia. EPs are a heterogeneous group of disorders divided into: (i) secondary forms (seen mainly in parasitic infections, allergic bronchopulmonary aspergillosis, and drug reactions); and (ii) primary forms (eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, idiopathic chronic eosinophilic pneumonia, and idiopathic acute eosinophilic pneumonia). Despite their rarity, the etiological approach to EP must be well-defined as some causes can be rapidly life-threatening without initiation of the proper treatment. This approach (i) eliminates secondary forms, with comprehensive history taking and minimal biological assessment, (ii) is oriented in primary forms by the acute or chronic setting, and the existence of extrapulmonary symptoms. Treatment of primary forms has traditionally relied on corticosteroids, usually with a dramatic response. Specific treatments or the adjunction of corticosteroid-sparing treatment or immunosuppressors are currently being evaluated in order to improve the prognosis and the side effects associated with corticosteroid treatment in a pediatric setting.

IL-35 Suppresses Lipopolysaccharide-Induced Airway Eosinophilia in EBI3-Deficient Mice

“…In conclusion, our findings suggest that IL-35 negatively regulates airway eosinophilia, at least in part by reducing the production of eosinophil-attracting chemokines CCL11 and CCL24. Given that increased accumulation of eosinophils is known to be pathogenic in various diseases, such as allergic asthma, eosinophilic pneumonias, and eosinophil-associated gastrointestinal disorders (35)(36)(37)(38)(39), IL-35 may provide a new therapeutic tool to reduce tissue recruitment of eosinophils in such diseases. Furthermore, the suppressive effect of IL-35 on stimulus-induced production of chemokines may not be limited to CCL11 and CCL24; it may well extend to other chemokines targeting different types of leukocyte.…”

Drug-induced eosinophilic pneumonia

“…As the disease progresses, the eosinophil count increases. [ 3 , 33 ] In this study, only 20.7% of patients with AEP had eosinophil counts >500 cells/μL and the average among those with initial peripheral blood eosinophilia was 1390 cells/μL.…”

Interleukin‐35 in immune‐related diseases: protection or destruction

“…64 Increased eosinophils could be pathogenic in various diseases, such as eosinophilic pneumonias, allergic asthma, and eosinophil-associated gastrointestinal disorders. 65,66 Recent findings suggest that IL-35 decreases airway eosinophilia by reducing the production of the eosinophil-attracting chemokines CCL11 and CCL24, which demonstrates that IL-35 may provide a new therapeutic strategy to reduce tissue recruitment of eosinophils in such diseases. 67 In addition, studies have shown that the expression of IL-35 is down-regulated in chronic obstructive pulmonary disease, a chronic bronchitis and emphysema characterized by airflow obstruction.…”