[Diagnostic values of the clinical characteristics of chronic cough].

OBJECTIVE: To evaluate whether the clinical characteristics of chronic cough were helpful in determining its specific causes. METHODS: Patients with chronic cough were evaluated by a validated systematic diagnostic protocol. The patients with identified single cause were divided into 4 groups accordingly: cough-variant asthma (CVA), upper airway cough syndrome (UACS) or post-nasal drip syndrome (PNDS), eosinophilic bronchitis (EB), gastroesophageal reflux related cough (GERC), and the characteristics of the timing, character, onset and associated manifestations of chronic cough in different causes were compared. RESULTS: A total of 196 patients met the inclusion criteria, including 55 with EB, 45 with UACS, 50 with CVA and 46 with GERC. No significant difference was found in age, gender and course among EB, UACS, CVA and GERC. The incidence of nocturnal cough in CVA was 26.0% (13/44), significantly higher than in EB (9.1% (5/55), chi2 = 5.272, P<0.05), UACS (2.2% (1/45), chi2 = 10.657, P<0.01) and GERC (0% (0/46), chi2 = 13.833, P<0.01). The specificity of nocturnal cough for CVA was 95.9%. The sensitivity and specificity of cough associated with meals in GERC was 52.2% (24/46) and 83.3%, and regurgitation associated symptom in GERC were 69.6% (32/46) and 80.0%, which were significantly higher than other groups. The incidence of postnasal drip, rhinitis associated symptom and case history of nasal diseases in UACS were 66.7% (30/45), 88.9% (40/45) and 82.2% (37/45), and the specificity of them were 89.4%, 65.6% and 63.6% respectively. CONCLUSION: The timing character and some associated symptoms of chronic cough are useful in predicting a single cause.

[The role of airway neurogenic inflammation in gastro-esophageal reflux induced cough].

OBJECTIVE: To investigate the role of airway neurogenic inflammation in the pathogenesis of gastro-esophageal reflux induced cough (GERC). METHODS: Sputum was induced by hypertonic saline aerosol inhalation in 20 patients with GERC (GERC group), 10 healthy subjects (normal control group) and 8 patients with chronic cough due to other causes but complicated with gastro-esophageal reflux diseases (GERD, GERD group). Airway mucosal biopsy was performed in 6 patients with GERC and 4 patients with GERD using flexible fiberoptic bronchoscopy. The expression of substance P (SP), neurokinin 1 receptor and neurokinin A (NKA) in sputum cells and airway mucosa were detected by immunohistochemistry, and was assessed semi-quantitatively. SP, NKA, and NKB in the supernatant of induced sputum were measured with enzyme linked immunosorbent assay. Calcitonin gene-related peptide (CGRP) was measured with radioimmunoassay. RESULTS: The concentration of SP in the supernatant of induced sputum was significantly higher in GERC group [(266 +/- 207) ng/L] than those in normal control group [(143 +/- 36) ng/L, P < 0.05] and GERD group [(130 +/- 11) ng/L, P < 0.05], and the sputum supernatant concentration of CGRP in GERC group [(180 +/- 83) ng/L] was significantly higher than those in normal control group [(105 +/- 64) ng/L, P < 0.01] and GERD group [(89 +/- 16) ng/L, P < 0.01]. The expression of SP, NK-1 receptor and NKA in induced sputum cells in GERC group were significantly higher than those in normal control group (P < 0.01, < 0.05, < 0.05) and GERD group (all P < 0.05); Expressions of SP in airway mucosa was significantly higher in GERC group than in GERD group (P < 0.01). After treatment, the concentration of CGRP in the supernatant of sputum in GERC patients was significantly lower than that before treatment (P < 0.05); the expression of SP, NK-1 and NKA in the induced sputum cells were significantly lower than that before treatment (P < 0.01, P < 0.01 or P < 0.05). CONCLUSION: There is airway neurogenic inflammation in GERC patients, which maybe closely related to the development of GERC.

[Characteristics of airway inflammatory cells and mediators in eosinophilic bronchitis patients].

OBJECTIVE: To investigate the features of airway inflammation in patients with eosinophilic bronchitis (EB) by analyzing the inflammatory cells and mediators in induced sputum and bronchoalveolar lavage fluid (BALF). METHODS: Sputum induced by hypertonic saline aerosol inhalation was collected in 43 patients with EB (EB group), 20 patients with cough variant asthma (CVA, CVA group), 16 patients with bronchial asthma (asthma group) and 21 healthy controls (healthy group). Bronchoalveolar lavage was also performed in 11 patients with EB and 10 patients with CVA. Differential cell count was carried out in sputum and BALF. Levels of eosinophilic cationic protein (ECP), leukotriene C(4) (LTC(4)) and histamine in sputum and BALF were measured. RESULTS: The percentage of sputum eosinophils (EOS) showed significant difference among the four groups; healthy group 0.0020 +/- 0.0050, EB group 0.1130 +/- 0.1470, CVA group 0.1900 +/- 0.1800, asthma group 0.3860 +/- 0.2670 (P < 0.01). The difference between asthma group and CVA group, and the difference between CVA group and EB group were significant (P < 0.05). The percentage of EOS in BALF was (0.011 +/- 0.016) in EB group, (0.053 +/- 0.040) in CVA group, the difference being significant (P < 0.05). The concentration of sputum ECP was (0.62 +/- 0.66) mg/L in EB group, (1.27 +/- 1.74) mg/L in CVA group, (0.07 +/- 0.10) mg/L in healthy group, the difference among the three groups being significant (P < 0.01). The difference of LTC(4) level was also significant when CVA group (0.65 +/- 0.62) microg/L was compared with EB group (0.39 +/- 0.61) microg/L (P < 0.05) and healthy group (0.15 +/- 0.11) microg/L (P < 0.01). The difference of histamine level in the supernatant of BALF was significant between CVA group (3.4 +/- 1.4) microg/L and EB group (1.6 +/- 1.5) microg/L (P < 0.05). CONCLUSIONS: EOS infiltration is mainly localized to the central airway in EB, with lower airway levels of LTC(4) and histamine as compared to CVA. These inflammatory features may partly explain the absence of non-specific airway hyperresponsiveness in patients with EB.