Background-Airway wall thickening has been observed in post mortem studies of patients with asthma. Assessment of airway wall thickening by high resolution computed tomographic (HRCT) scanning has been reported in experimental studies. We have used HRCT scanning to measure airway wall thickness at the segmental and subsegmental levels in 40 patients with asthma and 14 normal controls. Methods-The subjects were prospectively divided into four age and sex matched groups: 14 patients with a history of near fatal attack of asthma (NFA; group 1), 12 patients with moderate asthma (group 2), 13 patients with mild asthma (group 3), and 14 normal controls (group 4). All subjects were non-smokers. High resolution (1 mm collimation) CT scans of the chest were done at five diVerent levels. Results-The mean (SD) forced expiratory volume in one second (FEV 1 ) was 68 (20)% of predicted for group 1, 73 (12)% for group 2, 102 (12)% for group 3, and 103 (12)% for group 4. The ratio of airway wall thickness to outer diameter (T/D) and the percentage wall area (WA%) defined as (wall area/total airway area) × 100 were used to compare airway wall thickness between the groups. The mean (SD) T/D and WA% were 0.27 (0.05) and 78.0 (9.2)% for group 1, 0.27 (0.05) and 78.8 (9.2)% for group 2, 0.25 (0.04) and 74.2 (7.5)% for group 3, and 0.23 (0.04) and 70.9 (8.2)% for group 4. T/D and WA% were not significantly diVerent between groups 1 and 2. However, both groups 1 and 2 had higher T/D and WA% than either group 3 or 4 (p < 0.001) and group 3 had a higher T/D and WA% than group 4 (p < 0.03).The diVerences (95% CI) between the groups in WA% were 7.1% (0 to 14.4) for groups 1 and 4, 3.8% (-3.4 to 10) for groups 1 and 3, and 3.3% (-4.4 to 10) for groups 3 and 4. The diVerences between the groups in T/D and WA% were noted both for those with airways with a luminal diameter of >2 mm and those with a luminal diameter of <2 mm. Conclusions-All the patient groups had greater airway wall thickening than the normal subjects as assessed by HRCT scanning, but patients with more severe asthma had greater airway wall thickening than those with mild asthma. The methodology described in this study may be useful in assessing airway calibre in early intervention studies with antiinflammatory therapy. (Thorax 1998;53:248-253)

AAT replacement therapy has not been proven definitively to be clinically effective in reducing the progression of disease in AAT-deficient patients, but there is a possible benefit to selected patients. A placebo controlled, randomized clinical trial of AAT replacement therapy is required. The authors recommend reserving AAT replacement therapy for AAT-deficient patients with impaired FEV1 of 35% to 50% predicted who have quit smoking and are on optimal medical therapy but continue to show a rapid decline in FEV1, and participation of all AAT-deficient subjects in the Canadian AAT Registry.

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