Rhinitis and asthma: nasal provocation test in the diagnosis of asthma.
Our purpose was to determine if the study of rhinitis is useful in the diagnosis of asthma. We formulated the hypothesis that the inflammation of the upper airway reflects the inflammation of the lower airway. It was found that there are allergens that produce rhinitis more frequently than asthma, and vice versa. This can be explained by size. This explanation, however, is questionable as the allergic proteins are extracted from the carrying agent, and through the lymphatic route or the blood, reach the entire human organism. It was also found that with bronchoalveolar lavage in allergic asthma it is possible to obtain the same results for eosinophils as with a nasal wash or using Citospyn. However, the results in the late phase are questionable. In the immediate phase and in the late phase, eosinophil cationic protein (ECP) was detected in the blood (in asthma) and in nasal washes (in rhinitis). In the immediate response tryptase was detected from the mast cells. The role of leukotrienes in asthma and rhinitis is well established in the early and late response. The use of leukotriene inhibitors guarantee their importance in the airway. Platelet-activating factor (PAF) has been demonstrated to increase vascular permeability and the use of antagonists were the best nasal feature. The inhalation of histamine caused bronchospasm, while instillation of histamine in the nasal passages increased resistance. With this information it seems that our hypothesis has been confirmed. Rhinitis and BHR together are equivalent to asthma, although the PFER decreases during the course of nasal provocation test (NPT) in nonasthmatic patients. In pure rhinitis patients, however, we find decreases in PFER due to effort. All this suggests that the study of nasal inflammation is still unclear with regard to bronchial inflammation.
Olivé Pérez
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D001249:Asthma / Q000175:diagnosis* / Q000503:physiopathology; D006801:Humans; D009299:Nasal Provocation Tests; D012220:Rhinitis / Q000503:physiopathology*