The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade that leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications such as NSAIDs or<unk>  block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with<unk> -induced asthma, this results in the overproduction of pro-inflammatory leukotrienes, which can cause severe exacerbations of asthma and allergy-like symptoms. The underlying cause of the disorder is not fully understood, but there have been several important findings: * Abnormally low levels of prostaglandin E2 (PGE2), which is protective for the lungs, has been found in patients with<unk> -induced asthma and may worsen their lung inflammation. * In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with<unk> ; certain of these products may help promote the inflammatory response. * Overexpression of both the cysteinyl leukotriene receptor 1 and the leukotriene C4 synthase enzyme has been shown in<unk>  tissue from patients with<unk> -induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder. * The attachment of platelets to certain leukocytes in the blood of patients with<unk> -sensitive asthma also has been shown to contribute to the overproduction of leukotrienes. * There may be a relationship between<unk> -induced asthma and TBX21, PTGER2, and LTC4S. * Eosinophils isolated from the blood of<unk> -induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects;<unk>  treatment of eosinophils from<unk>  intolerant subjects causes the cells to mount a further increase in eoxin production. These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, is contributing to<unk> -induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.
Aspirin exacerbated respiratory disease
Severe cutaneous adverse reactions
Aluminium toxicity in people on dialysis
complications of Bronchiolitis
Acute severe asthma
Effects of high altitude on humans
Medications used in dentistry and periodontics
Myocardial infarction complications