Ultimobranchial origin of calcitonin. Hypocalcemic effect of extracts from chicken glands.
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Animals↗
Biomedical subjects
D W Cockcroft
Publications and source records attributed to D W Cockcroft.
Constrictive bronchiolitis and ulcerative colitis.
Pulmonary complications occur in an estimated 0.21% of patients with inflammatory bowel disease. The most common presentation of pulmonary manifestations is large airway disease, such as tracheobronchitis, chronic bronchitis or bronchiectasis. Small airway disease, such as constrictive bronchiolitis or bronchiolitis obliterans with organizing pneumonia, is less frequently reported, and is described as occurring in isolation from large airway disease. A case of a postcolectomy ulcerative colitis in a patient who has both large airway involvement, tracheobronchitis and bronchiectasis, and constrictive bronchiolitis is presented.
Adult↗
Protease inhibitor phenotype BsaskatoonM is not associated with emphysema - a 20-year follow-up study.
OBJECTIVE: To investigate the association between the PiBsaskatoon variant of alpha-1 protease inhibitor (a1 Pi), present in the heterozygous state, and the development of emphysema. DESIGN: Twenty-year follow-up in the third generation of a family with the variant, naturally controlled with regard to both environmental influences and other genetic factors. SETTING: University teaching hospital. POPULATION STUDIED: Ten siblings, five with PiBsaskatoonM phenotype and five with PiM phenotype, 33 to 46 years of age. INTERVENTIONS: Respiratory symptoms and smoking histories; pulmonary function tests, including static lung volumes, dynamic lung volumes before and after salbutamol 200 mg, and diffusing capacity; allergen prick skin tests; serum a1 Pi level, chest radiographs and high resolution computerized tomography lung scans MAIN RESULTS: The two groups of siblings had similar mean ages, smoking histories and prevalence of current mild respiratory symptoms. Pulmonary function data showed normal mean values and no statistically significant differences for all the variables between the two groups. Chest radiographs were normal in all subjects. High resolution computerized tomography scans were normal in eight subjects, and demonstrated mild and very mild centrilobular emphysema in the two subjects with greatest smoking histories (approximately 30 pack-year each); both of these were PiBsaskatoonM phenotype. CONCLUSION: There is no evidence of an association between a1 Pi phenotype PiBsaskatoonM and the development of emphysema.
Adult↗
Asthma management in the emergency department.
OBJECTIVES: To evaluate various aspects of the management of adult patients who present to the emergency department with acute exacerbations of asthma and who are discharged from the emergency department without hospital admission. Further, to compare the results with accepted management guidelines for the emergency department treatment of asthma. DESIGN: A retrospective chart collection and review until each site contributed 50 patients to the survey. SETTING: Three tertiary care hospitals in the Saskatoon Health District, Saskatoon, Saskatchewan. The study period was from July 1, 1997 to November 18, 1997. POPULATION: Patients aged 17 years or older, who were discharged from the emergency department with the diagnosis of asthma. METHODS: Data were collected on 130 patients from 147 emergency department visits. RESULTS: A number of important physical examination findings were frequently not documented. In contrast to management guidelines, peak expiratory flow rates (44%) and spirometry (1%) were not commonly used in patient assessments. Only 59% of patients received treatment in the emergency departments with inhaled or systemic corticosteroids. Furthermore, specific follow-up plans were infrequently documented in the emergency department charts (37%). CONCLUSIONS: Adherence with published Canadian guidelines for the emergency department management of acute asthma exacerbations was suboptimal. Corticosteroid use in the emergency department was significantly less than recommended. Increased emphasis on education and implementation of accepted asthma management guidelines is necessary.
Administration, Inhalation↗
Respirology manpower in Canada--A report for the Canadian Thoracic Society Education Committee.
A report on adult and pediatric respirology manpower in Canada was prepared from data supplied by the Royal College of Physicians and Surgeons of Canada (RCPSC), and from program directors (and other colleagues) at universities across Canada. The data support a significant deficiency of adult respirologists in Canada, which is estimated to be from 10%, based on a 10-year-old outdated RCPSC recommendation, to 20%, based on equalization with the 'best' province, to as high as 50%, based on long waiting lists, particularly for respiratory sleep problems, and estimates obtained from academic centres across Canada. Although there are less data available for pediatric respirology, a similar approach suggests a 50% to 100% shortfall in pediatric respirologists. Output from Canadian training programs in adult and pediatric respirology is not likely to meet this need. We recommend that steps be taken urgently to provide sufficient resources for training adult and pediatric respirologists, and to ensure that funding is provided for subspecialist positions in the community.
Canada↗
Allergen-induced increase in nonallergic airway responsiveness: a citation classic revisited.
BACKGROUND: The present paper revisits the 1977 paper by DW Cockcroft, RE Ruffin, the late J Dolovich and FE Hargreave entitled "Allergen-induced increase in nonallergic bronchial reactivity" (Clin Allergy 1977;7:503-13) that became a citation classic. Although clinical types of asthma were recognized at the time, there was a poor understanding regarding the role of allergic reactions in causing increases in airway hyperresponsiveness. The objective was to study formally Dr Altounyan's observation that patients with asthma showed increases in airway responsiveness at the times of natural allergen exposure during pollen season. Thirteen atopic patients with asthma were studied over two days, following inhalation of diluent (control) and following doubling amounts of an allergen solution at 10-min intervals until forced expiration volume in 1 s fell by 20%. Methacholine and histamine challenges were performed before, at 8 h, at 32 h and seven days following the inhalations. A significant reduction (reduction of at least one doubling concentration) in the provocative concentration that causes a 20% fall in forced expiration volume in 1 s occurred in seven of 13 patients, and more often in subjects with a late bronchoconstrictor response to allergen challenge. IMPORTANCE: The study showed that large changes in airway responsiveness could occur in patients with asthma and suggested that allergens could cause, rather than trigger, asthma. The study also led to the concept of asthma inducers and inciters - inducers causing airway inflammation and inciters provoking bronchospasm. The results led to a series of observations that have now implicated immunoglobulin E-mediated airway inflammation as perhaps the most important cause of airway hyperresponsiveness in asthma.
Allergens↗
Cytokine expression on cross-linking of human tissue Fc epsilon RI.
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Cytokines↗
Clinical concerns with inhaled beta2-agonists: adult asthma.
Inhaled beta2-agonists, when used regularly, cause subtle but significant worsening of asthma control. Overuse of inhaled beta2-agonists is associated with increased risk of death from asthma in a dose-response fashion. beta2-Agonists enhance airway responses to allergens, including induced airway hyperresponsiveness and induced airway inflammation. This is a plausible explanation for beta2-agonist-worsened asthma control. These direct effects of inhaled beta2-agonists, including increased airway response to allergen, tolerance, etc., may partially explain the association of overuse with asthma death. However, it is probable that the major reason for the association of beta2-agonists overuse and asthma mortality is an indirect effect. Inhaled beta2-agonists are effective relievers and preventers of bronchoconstriction and asthma symptoms but fail to treat the underlying pathogenesis, namely the airway inflammation. Thus, overuse may mask the true asthma severity and result in both an underappreciation and undertreatment of the disease. This would provide a rational explanation for the relationship of inhaled beta2-agonist use and mortality and also would fit the dose-response pattern. Inhaled beta2-agonists should be used exclusively as needed for relief of symptoms and their requirement should be infrequent: the need for excessive doses of beta2-agonists provides a useful marker of asthma (lack of) control.
Administration, Inhalation↗
Allergen-induced late asthmatic responses and increased airway responsiveness.
Our understanding of the airway response to inhaled allergens has increased substantially over the past several years. In addition to the long-recognized immediate or early asthmatic response, allergens also cause late asthmatic responses and allergen-induced increase in airway responsiveness to nonsensitizing stimuli such as exercise, cold air, histamine, and methacholine. These late sequelae are most likely due to airway inflammation and appear to be more clinically relevant than is the early response in the pathogenesis of clinical atopic allergic asthma.
Allergens↗
Airway responses to inhaled allergens.
The understanding of how inhaled allergens affect the asthmatic patient has changed significantly over the years. Allergen inhalation was first recognized as a cause of asthma in 1873, and the clinically important late asthmatic response (LAR) was demonstrated, albeit crudely, in 1952. Immunopathogenesis of the LAR was controversial until the 1970s when it was demonstrated conclusively that allergen-induced late cutaneous response and LAR are immunoglobulin E dependent. Hargreave and colleagues were first to identify nonallergic airway hyper-responsiveness, a consistent feature of all types of asthma, as one important determinant of airway response to inhaled allergens. More important, airway responsiveness was shown to increase following an allergen exposure, primarily in association with the LAR. Inhaled allergens could now be recognized not as one of numerous stimuli triggering symptoms in asthmatics, but as a fundamentally more important stimulus that causes airway responsiveness and, as subsequent investigations showed, airway inflammation. This led to the important recognition that allergens are actually 'causes' of asthma.
Administration, Inhalation↗