This study aimed at documenting airway inflammation and subepithelial collagen deposition in patients using only inhaled beta(2)-agonists with either recently diagnosed asthma (RDA: /= 13 yr, n = 16) and at the influence of an intense inhaled corticosteroid (ICS) treatment on these parameters, in relation to changes in airway responsiveness. Patients had a methacholine inhalation test and a bronchoscopy with bronchial biopsies before and after an 8-wk treatment with inhaled fluticasone propionate (FP), 1,000 microgram/day. Baseline FEV(1) (mean +/- SEM) was normal and similar in both groups (RDA: 98.1 +/- 2.7, LSA: 94.5 +/- 4.6%). Geometric mean methacholine PC(20) was lower in LSA than in RDA (0.44 versus 3.37 mg/ml) at baseline and improved similarly by 1.85 and 1.86 double concentrations with FP treatment. PC(20) normalized (>/= 16 mg/ml) in five patients with RDA and two patients with LSA. Baseline mean bronchial cell counts (per mm(2) connective tissue surface) for CD3(+), CD4(+), CD8(+), CD25(+), EG1(+), CD45ro(+), and AA1(+) cells were similar in both groups. With FP, EG1(+) (p < 0.001), EG2(+) (p = 0.018), and AA1(+) counts (p = 0.009) decreased significantly in both groups while CD45ro(+) (p = 0.02) counts decreased only in LSA. Baseline type 1 and type 3 collagen deposition underneath the basement membrane was similar in RDA and LSA and did not change significantly after FP. This study shows that recent compared to long-standing mild asthma is associated with a similar degree of airway inflammation and subepithelial fibrosis, and a similar improvement in airway hyperresponsiveness after 8 wk on high-dose ICS. It also indicates that once asthma becomes symptomatic, airway responsiveness cannot normalize in most subjects over such a time period, even with a high dose of ICS.

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The relations of body weight, height, and Quetelet index to axillary node involvement at diagnosis, estrogen receptor status, and histologic features of the primary tumor were examined in 656 patients with a newly diagnosed infiltrating breast carcinoma first treated in Québec City from July 1982 to December 1984. Node involvement increased with body weight and Quetelet index. This association was more regular and much stronger among patients with estrogen receptor-positive tumors than among those with estrogen receptor-negative breast cancers. Among patients with estrogen receptor-positive tumors, the percentage with involved nodes at diagnosis increased regularly from 32.9% among lean patients (Quetelet index less than 21 kg/m2) to 65.6% among obese women (Quetelet index greater than 27 kg/m2). This trend was seen even after adjustment for age and tumor size. In contrast, among patients with estrogen receptor-negative breast cancers, the association of weight and Quetelet index with node involvement were weak and irregular. The modifying effect of estrogen receptor status on the relation of obesity to node involvement was apparent in pre- and post-menopausal women. Body weight and Quetelet index were not related to estrogen receptor status or to any of the measured histologic features of breast tumors including nuclear grade, histologic grade, tubule formation, mitotic activity, and size of nucleus of cancer cells. These findings suggest that the observed deleterious effect of obesity on breast cancer prognosis is unlikely to be an artifact of delayed diagnosis in overweight patients. It may be due to hormonal changes associated with increases in body weight.

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