|Year : 2006 | Volume
| Issue : 1 | Page : 1-2
Eosinophilic bronchitis: Clearing confusion
Department of Pulmonary Medicine, Postgraduate Insitutute of Medical Education and Research, Chandigarh, India
Department of Pulmonary Medicine, Postgraduate Insitutute of Medical Education and Research, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta D. Eosinophilic bronchitis: Clearing confusion. Lung India 2006;23:1-2
Ever since the description of eosinophils in late 19th century it has been believed to play an important role in the pathogenesis of asthma.  Lately esoniphilic inflammation of the airways has also been shown in several other conditions like cough variant asthma, atopic cough, isolated chronic cough, respiratory symptoms without asthma, allergic rhinitis, and chronic obstructive pulmonary disease (COPD). Gibson et al (1989) described seven patients presenting with chronic dry cough, who had normal lung function studies and did not demonstrate bronchial hyper-responsiveness (BHR) on bronhco-provocation testing. These patients had sputum eosinophilia, there by suggesting eosinophilic inflammation of the airways and were given a label of eosinophilic bronchitis (EB)  . EB has increasingly been recognized as a common cause for chronic unexplained cough, with various studies reporting its prevalence in the range of 1030% in subjects with chronic cough. , There are several confusions about E.B. such as: What is EB? Is it different from asthma ? Is it early asthma? Is it early COPD?
Eosinophilic bronchitis is defined as eosinophilic inflammation of the airways (defined as presence of >2.5 eosinophils in induced sputum). Although EB is a feature of many conditions as listed above the term in itself is generally used to describe patients who have only isolated chronic cough and EB. Diagnosis of EB is made by demonstrating eosinophilic inflammation of airways by sputum eosinophilia (>25%) or in bronchial biopsies (not mandatory) in patients with chronic cough in the absence of any other demonstrable cause of cough, such as sinusitis, post nasal drip syndrome, GERD and drug (ACE inhibitors) intake. Peripheral blood eosinophilia is not seen in EB. Also by definition there should be no pulmonary parenchymal disease and spirometry is normal.
Pathophysiologically EB is different from asthma.  Though the level of eosinophilic inflammation in the bronchial epithelium, sub-epithelium and bronchoalveolar lavage is similar in two conditions, EB is distinct by the absence of BHR. Absence of BHR in EB also differentiates it from cough variant asthma, where BHR is present, even though the spirometry may be normal like in EB. Also, there are important differences in other cellular and cytokine profiles seen in asthma and EB.  Mast cell infiltration into the bronchial smooth muscles, expression of vascular endothelial growth factor and increased airway permeability are seen in asthma and are not present in EB. Prostaglandin D and histamine levels are increased in EB, compared to asthma.
Treatment is by inhaled steroids and response is good. Nearly 75% patients will resolve in two months and 100% by four months. Long terms prognosis is variable. Many patients may continue to have recurrent symptoms and/or sputum eosinophilia, less than 10% patients develop asthma and about 15% patients have progressive decline in FEV 1 , thereby raising the possibility that EB may be precursor of asthma or COPD. ,
To summarize, it is important to recognize EB as a cause of chronic cough, since it responds well to inhaled steroids. The exact nature and significance of EB is yet not clear, however it has definitely raised a debate on the role of eosinohils in the pathogenesis of asthma, since many patients with EB never develop asthma.
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