A recent review looked at 2 types of eosinophilic pneumonia: acute eosinophilic pneumonia and chronic eosinophilic pneumonia.
A recent review examined the etiology, clinical manifestation, and treatment of 2 types of a rare disorder called eosinophilic pneumonia: acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP).
Both types are characterized by marked accumulation of eosinophils in lung tissues and/or bronchoalveolar lavage fluid. Eosinophilic lung disease is made up of a rare group of heterogeneous diffuse parenchymal lung diseases, which are characterized by marked accumulations of infiltrating eosinophils in the alveolar space and the interstitium.
The epidemiology of AEP is not clearly understood. Most patients with AEP are about 20 years of age, current smokers, and male. It has been hypothesized that AEP involves an acute hypersensitivity reaction in an otherwise healthy individual to an inhaled antigen, such as tobacco smoke, or an unusual environmental trigger. AEP has been found in military personnel working in the Middle East; a firefighter after the collapse of the World Trade Center towers on September 11, 2001; people who inhaled smoke from fireworks; and those who were exposed to environmental factors at home.
A history of allergic disease such as bronchial asthma, dermatitis, and rhinitis is uncommon.
Alveolar or epithelial damage can trigger an inflammatory signal, leading to secretion of interleukin-33, interleukin-25, and thymic stromal lymphoprotein, and a subsequent cascade of other cytokines and chemokines.
Clinically, AEP is characterized by dyspnea accompanied by cough and fever/chills. Symptoms of chest pain and myalgia occur up to 50% of the time. Most symptoms can develop within several days after an acute onset.
Systematic corticosteroid therapy usually reverses respiratory failure; in severe cases, intravenous administration of high-dose corticosteroids are used.
In contrast to AEP, smokers with CEP are uncommon, and most patients with CEP have never smoked. As with AEP, CEP is rare. Unlike AEP, CEP can develop at any age, with women being twice as likely to develop this disease. Most patients are in their 30s to 50s.
The incidence of CEP among the interstitial lung diseases (ILDs) was reported to be 0% to 2.7% in an ILD registry in Europe and 0.5% to 1.2% in an ILD registry in the United States.
There is an association between CEP and allergic diseases, such as bronchial asthma, atopic dermatitis, and allergic rhinitis; these can develop both prior to and after the onset of CEP.
CEP has no common set of specific symptoms. While prolonged respiratory symptoms such as cough (60% to 90%) and shortness of breath/dyspnea (20% to 50%) are the most common, fever, sputum, and wheezing are often found. Patients with CEP may also show appetite loss and/or weight loss and occasionally present with chest pain. They rarely develop respiratory failure and usually show normal or mild hypoxemia.
Patients with CEP usually respond well to corticosteroids. Intravenous high-dose corticosteroid therapy is also used in severe cases.
Although AEP can cause life-threatening severe acute respiratory failure, relapse is rare and corticosteroid therapy can be discontinued with complete recovery.
However, more than half of patients with CEP experience relapse, and prolonged corticosteroid treatment is needed in about half of these patients. Additionally, there is a risk of persistent impairment of pulmonary function.
Reference
Suzuki Y, Suda T. Eosinophilic pneumonia: A review of the previous literature, causes, diagnosis, and management [published online June 25, 2019]. Allergol Int. doi: 10.1016/j.alit.2019.05.006.
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