Subjective and objective markers of treatment response in patients with seasonal allergic rhinitis.
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Biomedical subjects
Publications and source records attributed to R A Tan.
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BACKGROUND: Occupational asthma may often be a challenge to diagnose as the relationship between work and symptoms may not be immediately clear. The potential consequences for the worker's career make an accurate diagnosis essential. A history of work-associated asthma symptoms that recede when the patient is not at work is the first clue. METHODS: A nonspecific bronchial challenge, most commonly with methacholine, can help confirm the diagnosis of asthma. Specific IgE to suspected agents can be tested for, preferably with skin testing. Serial monitoring of peak expiratory flow rate (PEFR) or forced expiratory volume in 1 second (FEV1) at work and outside of work can determine if the asthma is occupational in nature. CONCLUSION: Specific bronchial challenge to suspected occupational agents is the gold standard for diagnosis of occupational asthma.
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The antileukotriene agents are the first new category of asthma medications introduced in the past two decades. Leukotriene synthesis inhibitors block the production of leukotrienes whereas leukotriene receptor antagonists block the effects of leukotrienes at the receptor level. Leukotriene synthesis inhibitors are further classified as either 5-lipoxygenase inhibitors or 5-lipoxygenase-activating protein inhibitors. Zafirlukast, montelukast, and pranlukast are leukotriene receptor antagonists whereas zileuton is a 5-lipoxygenase inhibitor. Antileukotrienes have been shown to be relatively safe and effective in chronic mild to moderate asthma. Studies are ongoing to determine how they compare with inhaled steroids, which remain the drug of choice for anti-inflammatory therapy.
Exercise-induced asthma (EIA) is characterised by transient airway obstruction occurring after strenuous exertion. A fall of 10% or more in the FEV1 after exercise is diagnostic. Inhalation of large volumes of dry, cold air during exercise leads to loss of heat and water from the bronchial mucosa and airway cooling and drying. Proposed mechanisms for bronchoconstriction include: (i) mucosal drying and increased osmolarity stimulating mast cell degranulation; and (ii) rapid airway rewarming after exercise causing vascular congestion, increased permeability and oedema leading to obstruction. EIA symptoms start after exercise, peak 8 to 15 minutes after exercise and spontaneously resolve in about 60 minutes. A refractory period of up to 3 hours after recovery, during which repeat exercise causes less bronchospasm, has been observed. The amount of ventilation and the temperature of inspired air are important factors in determining the severity of EIA. Greater ventilation and cold, dry air increase the risk for EIA. Education regarding the nature and management of EIA is important not only for asthmatics but also for their families and coaches. With the proper precautions and workout techniques, there is no limit to what individuals with asthma can achieve in sports. Prevention is the main objective in managing EIA. Nonpharmacological measures include warming up before vigorous exertion, covering the mouth and nose in cold weather, exercising in warm, humidified environments if possible and warming down after exercise. Aerobic fitness and good control of baseline bronchial reactivity also help to diminish the effects of EIA. Inhaled beta-agonists are the medications of choice in EIA prophylaxis. Inhaled sodium cromoglycate (cromolyn sodium) or nedocromil may also be used. Agents that may be added if inhaled beta-agonists or sodium cromoglycate are not adequate include anticholinergic agents (such as ipratropium bromide), theophylline, calcium channel blockers, alpha-agonists, antihistamines and oral beta-agonists. Newer agents include antileukotriene agents, inhaled heparin and inhaled furosemide (frusemide).
The antileukotriene agents, the first new class of asthma medications introduced in two decades, represent a promising new alternative in the continuing search for effective and safe therapy for chronic inflammation in asthma. The leukotrienes are inflammatory mediators whose effects on asthma include bronchoconstriction, increased vascular permeability, and increased mucus production. In chronic asthma, regular use of either leukotriene synthesis inhibitors or leukotriene receptor antagonists has improved pulmonary function and clinical symptoms significantly. Antileukotriene agents appear to be safe and well tolerated, although long-term studies will be needed to confirm this.
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