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Biomedical subjects

Donald W Cockcroft

Publications and source records attributed to Donald W Cockcroft.

8 recordsLinked to original sources

Sex differences in asthma, atopy, and airway hyperresponsiveness in a university population.

BACKGROUND: A male predominance in atopy, a preadolescent male predominance in asthma, and a female predominance in airway hyperresponsiveness (AHR) have been previously documented, mostly in separate populations. OBJECTIVE: We examined gender differences in a single population of 500 randomly selected university students from a previous publication which addressed sensitivity and specificity of histamine bronchoprovocation (Cockcroft et al. J Allergy Clin Immunol. 1992;89:23-30). METHODS: In these 500 subjects (age 21.8 +/- 1.5 years) we assessed gender differences in asthma, atopy, and AHR. We compared our findings with those in the literature from a PUBMED search using the keywords gender, asthma, atopy, AHR, and bronchial reactivity. RESULTS: A diagnosis of asthma made by another physician was seen in 31, a male-to-female ratio of 2.9:1 (P = 0.004). Our definition of asthma increased the total to 52 and reduced the male-to-female ratio to 1.2:1. Atopy was seen in 190, male-to-female ratio of 1.5:1 (P = 0.001). Borderline to mild AHR had a female predominance with a male-to-female ratio of 1:1.5 (P = 0.02), whereas moderate AHR had a marked predominance with a male-to-female ratio of 7:1 (P = 0.03). CONCLUSIONS: In our population, the associations among gender and asthma, atopy, and AHR were similar to those seen in the literature with the exception of males having more severe AHR. This may be the one factor contributing to the higher prevalence of asthma (including previous doctor-diagnosed asthma in our population) in boys and young men.

Adult↗

A case report of wegener granulomatosis treated only with corticosteroids for 30 years.

BACKGROUND: Wegener granulomatosis is a systemic vasculitis classically described as involving the upper and lower respiratory tracts together with glomerulonephritis. Its poor prognosis was marginally improved with the use of corticosteroids, and long-term remission was not achieved until the introduction of cytotoxic agents. Generalized or systemic Wegener granulomatosis has a worse prognosis than those limited to the respiratory tracts. OBJECTIVE: To report the case of an individual who we suspect has a 30-year history of Wegener granulomatosis treated only with prednisone. METHODS: A literature search was performed with PubMed using the keywords Wegener granulomatosis, survival, prognosis, and treatment. RESULTS: Our patient is alive 32 years after her initial symptoms of vasculitis. She has been taking daily prednisone only for the majority of this time. Our clinical diagnosis of Wegener granulomatosis is based on the history and very high antineutrophil cytoplasmic antibody with the cytoplasmic pattern. CONCLUSIONS: There may be variants of generalized Wegener granulomatosis that survive with less aggressive treatment.

Aged↗

The effects of an anti-CD11a mAb, efalizumab, on allergen-induced airway responses and airway inflammation in subjects with atopic asthma.

BACKGROUND: Efalizumab is a humanized IgG(1) mAb against the lymphocyte function antigen-1 (LFA-1) alpha chain, CD11a. Blocking of LFA-1/intercellular adhesion molecule interactions could inhibit asthmatic inflammation by blocking adhesion and activation of LFA-1-positive leukocytes. OBJECTIVE: A randomized, double-blinded, placebo-controlled, parallel group, multicenter study investigated the effects of efalizumab on allergen-induced airway responsiveness and airway inflammation. METHODS: Thirty-five nonsmoking subjects with mild allergic asthma were randomized to receive efalizumab (n = 24) or placebo (n = 11) in 8 weekly subcutaneous doses (0.7 mg/kg conditioning dose followed by 7 weekly doses of 2.0 mg/kg). Allergen challenges were performed at screening and after 4 and 8 weeks of treatment. Samples of sputum (n = 18 subjects) and blood (n = 35 subjects) were collected the day before challenges, and sputum was collected again at 7 and 24 hours after each challenge. Nonparametric tests were used to compare allergen-induced differences between efalizumab and placebo groups. RESULTS: Subjects receiving efalizumab developed headache (48%) and flu syndrome (28%) compared to subjects receiving placebo (0%). After 8 weeks of efalizumab, the maximum late percent fall in FEV(1) (late asthmatic response) was inhibited by 50%, but neither the late response nor the late area under the curve was statistically different than placebo (P =.098 and.062, respectively). Efalizumab had no effect on the maximum early percent fall in FEV(1) (early asthmatic response) or early area under the curve compared to placebo (P >.59). Efalizu-mab significantly reduced the postallergen increase in sputum EG2-positive cells and metachromatic cells (P <.05). No other comparisons were statistically different. CONCLUSIONS: Blocking of LFA-1/intercellular adhesion module interactions by efalizumab inhibits the development of allergen-induced cellular inflammatory responses measured in induced sputum and might attenuate the late asthmatic response. Larger studies are needed to confirm this.

Adult↗

Bronchoprovocation methods: direct challenges.

Inhalation challenges with direct-acting stimuli histamine and methacholine are widely used to measure airway responsiveness. Three widely used methods (2-min tidal breathing method, breath-activated dosimeter method, hand-held manual nebulizer) are described. Careful standardization is important so as to best differentiate normal from increased airway responsiveness and to permit comparison between methods. With current methods standardized as suggested by the ATS, a methacholine (or histamine) PC(20) > 16 mg/mL is considered normal. A PC(20) < 16 mg/mL is highly sensitive for current symptoms of asthma. Interpretation of methacholine or histamine inhalation test requires that symptoms be current (within a few days) and that FEV(1) be normal.

Administration, Inhalation↗

Microscopic pulmonary tumour embolism: an unusual presentation of thymic carcinoma.

The present report describes the first reported case of microscopic pulmonary tumour embolism (MPTE) from thymic carcinoma. The carcinoma was discovered during an autopsy in a 55-year-old man who had undergone surgery for a pilonidal sinus two weeks before presentation. Pulmonary thromboembolism was suspected. This case was unusual because MPTE has never before been associated with thymic carcinoma, MPTE was the first clinical indication of an occult malignancy, and the clinical presentation was that of sudden onset of dyspnea associated with acute cor pulmonale. The cause of death was determined to be hypoxia secondary to extrinsic compression of the right pulmonary artery and extensive tumour emboli in the small arteries, arterioles and venules of the pulmonary parenchyma. A review of the clinical presentation and diagnosis of MPTE is included.

Fatal Outcome↗

Formoterol thrice weekly does not result in the development of tolerance to bronchoprotection.

BACKGROUND: Loss of bronchoprotection routinely follows regular treatment with beta2-agonists. There are no data on the effects on bronchoprotection for thrice weekly use of a beta2-agonist. METHODS: A double-blind, randomized, placebo controlled crossover trial was conducted to investigate the effects of thrice weekly administration of 12 microg of formoterol versus placebo on bronchoprotection against methacholine. As an expected positive control, formoterol 12 microg once daily was also evaluated. RESULTS: There was no significant difference versus placebo in the bronchoprotective effects of 12 microg of formoterol administered on day 8, following daily treatment for seven days or treatment every other day (analysis of variance P=0.34). However, a nonsignificant trend towards lower concentration of methacholine that caused a 20% fall in forced expiratory volume in 1 s developed only following the daily formoterol dosing. CONCLUSIONS: Thrice weekly dosing does not result in the development of tolerance to bronchoprotection against the direct acting stimulus methacholine.

Administration, Oral↗