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Background The role of the peripheral airways in asthma is increasingly being recognized as a potential target for the achievement of optimal control of the disease. We postulated that the inflammatory changes of the small airways are implicated in the lack of asthma control in mild asthma. Objective To test this hypothesis, we measured the alveolar fraction of exhaled NO (C alv NO) in patients with mild asthma with different levels of control of symptoms. Methods Seventy-eight patients with asthma (35 men, age, 37 ± 15 years; FEV 1 percentage of predicted, 100% ± 9%) were studied. Asthma control was assessed by using the Asthma Control Test (ACT). Measurements of exhaled NO at multiple constant flows were performed. Results Bronchial NO concentrations were 27.1 ± 20 ppb, and C alv NO levels were 5.7 ± 3.4 ppb. The ACT score was 20 ± 4.2. The level of asthma control was not associated with bronchial NO concentrations ( r s = 0.16, P = .15). However, a significant correlation was found between the ACT score and C alv NO ( r s = 0.25, P = .03). Moreover, C alv NO was significantly higher in patients with uncontrolled asthma than in patients with controlled/partially controlled asthma (6.7 ± 2.6 ppb vs 4.9 ± 2.6 ppb, respectively, P = .02). In the subgroup of patients with asthma who underwent extrafine inhaled corticosteroid treatment, the magnitude of the inhaled corticosteroid–induced improvement in asthma control positively correlated with baseline C alv NO at 1 month ( r s = 0.39, P = .003) and at 3 months ( r s = 0.49, P Conclusions The alveolar component of exhaled NO is associated with the lack of asthma control in patients with mild, untreated asthma. This observation supports the notion that abnormalities of the peripheral airways are implicated in the mildest forms of asthma.

The "New Table indicating the percentage of disability resulting from injury and disabling diseases" approved by the Italian Ministerial Decree dated February 5, 1992 gives a superficial, highly disorganized handling of laryngeal pathologies. This Table only considers phonatory function disorders which are included in a special section; it totally neglects dyspnea and dysphagia of laryngeal origin. This omission cannot even be overcome on the basis of similarities since there are no analogous items listed for reference. In fact, the parameters applied to evaluate dyspnea (CV, VEMS, O2 consumption) apply to ventilation disorders of a pulmonary nature and cannot, therefore, be used in cases of laryngeal dyspnea. Moreover, the Table does not deal with dysphagia at all. In addition, the basis for the Table--the concept of permanent functional damage--is not always adhered to in giving indications for evaluation of phonatory tract damage. The purpose of the present work is not, however, to propose a different way to determine the percentages for the individual items in the tables; rather, the aim is to suggest a different, highly standardized procedure for evaluating laryngeal dysfunctions which is easy to apply.