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Wise et al.

Page 159

The study however did find that 33.5% of patients were diagnosed with combinations of respiratory disease; the most frequent was asthma and AR 1987,1988 (Table X.H).

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While patients with AR that have concomitant chest symptoms such as cough often do have asthma, seasonal asthma, and/or a nonspecific bronchial hyperreactivity, many studies show generalized inflammation of the upper airways extending to the lower airways. There is a complex interplay between cells and inflammatory cytokines and hence one should consider the upper and lower airways as a single unique functional unit. 1986 The key pathogenic mechanism is the inflammation of the upper airways with extension to the lower airways and the induction of a systemic dysregulation via a complex interaction between cells and inflammatory cytokines. 1986 Many patients with AR and cough do not have the diagnostic airflow obstruction or the reversibility of forced expiratory volume in 1 second (FEV1) following bronchodilator administration to make a diagnosis of asthma. 1167 Krzych-Falta et al. 1989 performed a nasal challenge in 30 patients with AR. Extranasal symptoms were noted, including a cough and breathlessness, especially in those with PAR. In 2000, Chakir et al. 1990 performed histochemical tests on bronchial biopsies of patients with AR but without current or history of asthma. They demonstrated increased numbers of lymphocytes, eosinophil recruitment and IL-5 expression in the bronchial mucosa after exposure with natural pollen. 1990 This 2000 study followed a prior investigation of deposition of type I and III collagens and fibronectin by bronchial myofibroblasts in AR patients. 1991 This is suggestive of an active structural remodeling of the lower airways in AR patients that is similar to asthma patients but less severe. In addition, Buday et al. 1992 demonstrated that guinea pigs sensitized to HDM had a significantly enhanced cough response compared to those that were not sensitized; however, airway resistances did not change. This study is relevant to humans, since the neurophysiology of the vagus nerve in the guinea pig is thought to be closest to humans. These studies demonstrate that AR, unrelated to asthma, can indeed result in bronchial inflammation, possible lower airway remodeling and ultimately a symptom of cough. A large-scale cross-sectional, multinational observational study set out to determine the symptom of cough as it relates to respiratory diseases in the Asia-Pacific region. With over 5250 patients enrolled, the study found that 47% of patients with AR frequently reported cough as a symptom; however, only 11% of these patients had cough as the main reason for seeking medical care. 1993 The numbers were 61% and 33%, respectively, for patients with asthma and cough. In a prospective study with 2713 AR patients, He et al. 1994 found the occurrence of comorbidities, including cough, to gradually increase from mild intermittent, to mild persistent, to moderate-severe intermittent, and moderate-severe persistent AR. There is low level evidence that associates AR with cough or, more commonly, cough as a comorbidity of AR. 1990-1992 The severity of AR may affect its manifestation toward upper airway cough syndrome. 1994 AR is often a comorbidity with asthma which also has an increased correlation with cough. The exact pathways and mechanisms by which the unified airway functions continue to unfold.

Int Forum Allergy Rhinol . Author manuscript; available in PMC 2020 June 10.