Bronchial hyperresponsiveness in patients with sarcoidosis.

OBJECTIVE: To study bronchial hyperresponsiveness (BHR) in patients with sarcoidosis. METHODS: Twenty freshly diagnosed patients with sarcoidosis were evaluated. Progressively increasing concentrations of methacholine were administered using a standard five-breath dosimeter protocol, and spirometry performed after each challenge. BHR was expressed as PC20 (provocating concentration of methacholine resulting in 20% fall in forced expiratory volume in first second). All patients were nonsmokers, had no other concurrent cardiopulmonary disease, and were not on any specific treatment for sarcoidosis. RESULTS: Borderline (PC20 4.0-16.0 mg/mL), mild (PC20 1.0-4.0 mg/mL) and moderate to severe (PC20 <1.0 mg/mL) BHR was documented in three (15%), one (5%) and five (25%) patients respectively. Patients with BHR were similar to those having normal reactivity in terms of age, gender, disease duration and results of pulmonary function testing. All patients with endobronchial disease had BHR. CONCLUSION: BHR may be seen in several patients of sarcoidosis and could possibly contribute to decline in lung function.

Methacholine inhalation challenge in patients with post-Mycoplasma pneumoniae pneumonia.

We studied methacholine bronchial inhalation challenge in 12 patients at 4th week and 12th week after recovered from Mycoplasma pneumoniae pneumonia, compared with 12 healthy subjects as controls. The aerosolized methacholine was produced by an atomized nebulizer of the Provocationtest I, Pari-Starnberg, Germany and the aerosol was kept into a reservoir bag. Then, it was inhaled slowly by a subject. Increasing concentration of methacholine solutions (0, 0.5, 1, 5, 10, and 25 mg/ml) were used. The results revealed that 67% of the patients had bronchial reactivity to methacholine at the first time of challenge with a mean concentration of methacholine producing a fall in FEV1 of 20% from baseline (PC20) of 12.3 +/- 6.44 mg/ml. Fifty percent of the patients were still positive to the test on the second time of challenge with a mean PC20 of 20.1 +/- 6.89 mg/ml. None of the healthy subjects had bronchial hyperreactivity (PC20 > 25 mg/ml). Two patients experienced wheezing and asthmatic attacks requiring bronchodilator therapy during acute phase pneumonia. They were also diagnosed as having bronchial asthma for the first time. Many patients had prolonged coughing during the recovery phase lasting more than 4 weeks. This prolonged coughing seemed to have a correlation with the development of bronchial hyperresponsiveness (BHR). We concluded that M. pneumoniae could induce BHR which may be transient or persistent. The effect of mycoplasma respiratory tract infection may result in airway inflammations and asthmatic attacks.

Airway response to acid instillation in esophagus in bronchial asthma.

OBJECTIVE: An increased incidence of gastroesophageal reflux has been reported in patients with bronchial asthma. We studied the pulmonary effects of acid instillation in the esophagus. METHODS: Fifteen patients with bronchial asthma and 15 healthy adults in the age group 15-50 years were studied. The control subjects were first screened for bronchial hyperreactivity by a methacholine challenge test. Patients and controls were both subjected to modified Bernstein test. Spirometry was done at baseline and after each instillation of either acid or saline. Respiratory and reflux symptoms were noted after each infusion and antacid administration. RESULTS: Five patients and one control subject had history of reflux symptoms (p < 0.05) and six patients had nocturnal asthma. There was a significant fall in FEV1/FVC after acid infusion patients; this improved significantly after antacid administration. All six patients with nocturnal asthma had respiratory signs or symptoms and had more than 20% fall in FEV1 on acid instillation in the esophagus, while none in the control group developed the same. CONCLUSIONS: Gastroesophageal reflux occurs more frequently in patients with bronchial asthma and acid instillation in the esophagus triggers bronchoconstriction.

Effect of calcium channel antagonists on cholinergic bronchial responsiveness in asthma.

Bronchial responsiveness to methacholine was studied in 23 stable asthmatics before and after nifedipine and diltiazem. There was no significant bronchodilatory effect of either calcium channel antagonists. The mean provocative dose of methacholine required to produce a 20% fall in FEV1 (PC20 = 0.157 +/- 0.74 mg) was not altered by nifedipine (PC20 = 0.159 +/- 0.61). However, diltiazem offered significant protection. The mean ratio of PC20 after diltiazem over baseline was 3.27 +/- 3.55. The results suggest that although both calcium channel antagonists have no influence on normal basal bronchomotor tone, diltiazem does significantly protect against cholinergic stimulation.