The question whether eosinophilic esophagitis (EoE) might be an 'asthma of the esophagus' is reasonable. There are a number of similarities between the two diseases: EoE and asthma, as well as other atopic diseases, are frequently associated and have a number of similarities in their pathogenesis. Thus, investigating differences and similarities between the diseases might be a worthwhile endeavor.

Both EoE and asthma are chronic immune-mediated conditions characterized by inflammatory changes in the mucosa and submucosa with a characteristic and diagnostic infiltration of eosinophils. They result in organ dysfunction with considerable morbidity and (in the case of asthma) even mortality. Asthma and EoE affect all ages, but frequently start in childhood or adolescence.

While asthma has seen a large increase in its prevalence in the past 50 years, EoE was first described in the 1970s. Since then the frequency of the diagnosis of EoE has increased significantly. The prevalence for both diseases seems to be highest in the Western world. In contrast to asthma, where females are more often affected, EoE is more frequent in males. Asthma in children, however, is also more common in boys, but this changes after puberty. EoE is frequently associated with asthma, and up to 80% of patients with EoE are atopic, similar to childhood asthma. Adult-onset asthma is not necessarily associated with atopy (termed intrinsic asthma) and similar observations have been made for EoE. Endoscopically, asthmatic airway mucosa as well as esophageal mucosa in EoE can appear normal, and biopsies are required for diagnosis. Long-standing disease in asthma has been associated with 'remodeling' compared to predominantly reversible inflammatory changes early in the course of the disease. Similar observations have been made in EoE. Toxic proteins derived from eosinophils such as major basic protein, eosinophil-derived neurotoxin and eosinophil cationic protein can be found in the mucosa of both diseases, which are also characterized by a thickening of the lamina propria or basement membrane, respectively. Despite these histologic and immunochemistry findings, asthma as well as EoE remain clinical diagnoses, and diagnosing either condition can be challenging. Therapeutically, both diseases respond well to corticosteroids. Ironically, corticosteroids for inhalation are deliberately swallowed in EoE to reach the esophageal mucosa. Allergen/food avoidance can improve symptoms in asthma and EoE.

Taken together, allergic asthma and EoE have a number of common features which make a common pathogenesis manifested in different organs for reasons not yet fully understood likely. Combining allergological research with gastroenterologic and pneumologic expertise with a focus on similarities between these diseases might be a way forward. © 2014 S. Karger AG, Basel.

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This consensus statement provides practical recommendations for specific inhalation challenge (SIC) in the diagnosis of occupational asthma. They are derived from a systematic literature search, a census of active European centres, a Delphi conference and expert consensus.

This article details each step of a SIC, including safety requirements, techniques for delivering agents, and methods for assessing and interpreting bronchial responses. The limitations of the procedure are also discussed.Testing should only be carried out in hospitals where physicians and healthcare professionals have appropriate expertise. Tests should always include a control challenge, a gradual increase of exposure to the suspected agent, and close monitoring of the patient during the challenge and for at least 6 h afterwards. In expert centres, excessive reactions provoked by SIC are rare.A positive response is defined by a fall in forced expiratory volume in 1 s ≥15% from baseline. Equivocal reactions can sometimes be clarified by finding changes in nonspecific bronchial responsiveness, sputum eosinophils or exhaled nitric oxide.

The sensitivity and specificity of SIC are high but not easily quantified, as the method is usually used as the reference standard for the diagnosis of occupational asthma.

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With the childhood prevalence of obesity and asthma increasing, it is important for pediatric professionals to appreciate that obesity modifies the diagnosis and management of asthma. These disease modifications present challenges to clinical management, including decreased responsiveness to controller therapy and decreased quality of life compared with normal-weight asthmatic children.

While consensus guidelines do not currently suggest specific changes in asthma management for obese patients, management of some patients may be improved with consideration of the latest evidence. This article briefly summarizes what is known regarding the complex relationship between obesity and asthma in children, and discusses practical issues associated with the diagnosis and effective clinical management of asthma in obese children. On average, obese patients with asthma do not respond as well to inhaled corticosteroid therapy. Management approaches including weight loss and routine exercise are safe, and may improve important asthma outcomes.

Asthma providers should learn to facilitate weight loss for their obese patients. In addition, pharmacologic interventions for weight loss in obese asthma, though not currently recommended, may soon be considered.

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A 41-year-old man with a smoking history of 30 pack-years presented with chronic chest pain, dyspnea, and cough. His vital signs were normal, and laboratory studies were unremarkable, including his level of α₁-antitrypsin, which was normal. Physical examination revealed cachexia, with decreased apical breath sounds and hyperresonance to percussion in both lungs. Chest radiography showed extensive bullous lung disease in the apex and upper lobes of both lungs, which was suggestive of vanishing lung syndrome; air–liquid levels were seen in the left lung. Computed tomography of the chest confirmed these findings.

Vanishing lung syndrome, otherwise known as idiopathic giant bullous emphysema, typically occurs in young, thin male smokers. The radiographic criteria for vanishing lung syndrome were proposed in 1987, and they include giant bullae in one or both upper lobes occupying at least one third of the hemithorax and compressing surrounding parenchyma. Air–liquid levels within bullae are uncommon and raise the question of bacterial superinfection. Lung-volume–reduction surgery is considered for selected patients with vanishing lung syndrome after assessment of exercise capacity, pulmonary-function testing, and smoking cessation.

This patient underwent successful lung-volume–reduction surgery and is currently without residual symptoms.

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