Asthma attack precipitation

Asthma, a disease featuring sudden and dramatic variations in respiratory symptoms and pulmonary function, is well known to be related to environmental factors in many cases. Many other factors, however, may play a significant role in the precipitation of asthma attacks, including meteorologic factors, emotional factors, infection, allergy, and physical activity. It has also been demonstrated that there is a significant ethnic variation in factors associated with acute asthma attacks. Nevertheless, between 2 and 5% of the population is subject to asthma attacks, so it has been examined as an indicator of health effects of photochemical-oxidant pollution. 

Note Synthetic adrenalin can be emptied into a vessel, from those Primatine Mist type inhalers that asthma attacks are treated with, and extracted and precipitated (water and ammonia respectively) as described above. 

However, there is usually a price to pay for extensive alteration in autonomic processes in the body. For instance, adverse effects include precipitation of asthma attacks. Similarly, the blood flow in the extremities will often be reduced, so patients may well complain of cold feet or hands. It may be possible to gain some selectivity of drug action, with consequent minimization of side-effects, by using receptor-subtype-selective p-blockers. Thus, Pi-adrenoceptor antagonists have a higher affinity for the pj-adrenoceptor of the heart, and thus they may have some preferential action there, since P2-adrenoceptors are found at most other sites in the body, including the airways and blood vessels. 

Emotions and stress rarely can precipitate attacks of asthma but more commonly worsen an attack in progress. Bronchoconstriction from psychological factors appears to be mediated primarily through excess parasympathetic input. Atropine has been shown to block experimental psychogenic bronchoconstriction. It is most important to emphasize to patients and to parents of asthmatic children that asthma is not an emotional disease however, calming influences and relaxation techniques may benefit the patient who becomes severely emotionally distraught during an asthma attack. 

B. Inhalation of these compounds may precipitate wheezing in asthmatics. An 11 -year-old girl had a fatal asthma attack after applying a pyrethrin-containing shampoo to her dog. Inhalation or pulmonary aspiration may also cause a hypersensitivity pneumonitis. 

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. 

A non-allergic mechanism imderlying precipitation of asthmatic attacks by aspirin in hypersensitive patients was proposed over 30 years ago [4]. It was founded on pharmacological inhibition of COX of arachidonic acid and explained a cross-reactivity between different NSAIDs varying in chemical structure. This COX theory was confirmed by several studies [11] and was further refined following discovery of the second COX isoenzyme - COX-2. At least two COX isoenzymes, COX-1 and COX-2, are coded by separate genes. Their role in inflammation, asthma and anaphylaxis has been reviewed previously [12]. 

Salbutamol is a selective beta2-receptor agonist indicated in the management of asthma as a bronchodilator relieving acute attacks. It may be used in combination with inhaled corticosteroids such as beclometasone. Salbutamol acts within a few minutes and tends to be short-acting, unlike salmeterol. Side-effects of salbutamol include tachycardia and palpitations. It does not cause drowsiness and does not precipitate oral candidiasis. Inhaled corticosteroids may precipitate oral candidiasis. 

Extensive studies have been done on a clearly defined asthma syndrome produced by exposure to western red cedar. ° Plicatic acid has been identified as the etiologic agent. The western red cedar asthma syndrome includes rhinitis, conjunctivitis, wheezing, cough, and nocturnal attacks of breathlessness characterized by a precipitous decline in FEVi. There is no apparent relation between skin sensitivity and respiratory changes. No precipitating IgG antibodies are found in the serum of sensitized individuals, and circulating IgE antibodies are present in about one-third of affected individuals. 

In respect of persons who were in ill health previous to exposure, we have paid particular attention to cases of asthma, chronic bronchitis and emphysema. We believe that it must be accepted in principle that exposure to CS may precipitate an acute asthmatic attack, but we found no evidence that such attacks differed in kind or degrees from those attributable to natural causes and, in the cases that we either saw or heard of, we were unable to exclude the possibility that the attacks in mid-August were due to such causes. 

Non-steroidal anti-inflammatory drugs (NSAIDs) (e.g. aspirin), which can precipitate an attack in 5% of people with asthma. 

Codeine and morphine should be used with caution in hypotension, hypothyroidism, asthma (avoid during an attack) and decreased respiratory reserve, shock, prostatic hypertrophy, obstructive or inflammatory bowel disorders, diseases of the biliary tract, pregnancy and breastfeeding. They may precipitate coma in patients with hepatic impairment and as such, they should be avoided or a reduced dose used. In patients with renal impairment, the dose should be reduced or they should be avoided. If used in the elderly and debilitated, the dose should be reduced. 

When sulphur dioxide dissolves, the disulphide chemical bonds which result destroy the vitamin B or thiamine in foods by breaking up the protein molecules. Sulphurous acid, produced when sulphur dioxide is dissolved, may cause gastric irritation. Healthy people have no problem metabolising sulphur dioxide the kidneys and liver both produce enzymes which oxidise sulphites, but those with impaired kidney and liver may need to avoid sulphites. Foods containing sulphites may precipitate an asthmatic attack in asthma sufferers, who are very sensitive to the irritant effects of sulphur dioxide gas which may be liberated from the foods containing it and inhaled as the food is swallowed. It is one of the additives which the Hyperactive Children s Support Group recommends is eliminated from the diets of the children it represents. ... 

There is no evidence that CS causes permanent lung damage after one or several exposures to field concentrations (Blain, 2003). Inhalation of an irritant might be expected to exacerbate underlying pulmonary disease such as asthma, emphysema, or bronchitis. Histories of asthma and chronic obstructive pulmonary disease may exacerbate effects from CS (Worthington and Nee, 1999) or CN (Thorbum, 1982). CS may exacerbate ehronic bronchitis or precipitate an attack in known asthmatics (Anonymous, 1971). 

Most people tolerate aspirin well, but not patients with asthma, of whom there is a subgroup in whom aspirin precipitates asthmatic attacks (61,62). This is a distinct clinical syndrome, called aspirin-induced asthma, which affects about 10% of adults with asthma (63). Aspirin-induced asthma is usually accompanied by naso-ocular symptoms and can be triggered not only by aspirin, but by several NSAIDs, a fact that makes immunological cross-reactivity most unlikely. The propensity of an NSAID to precipitate an attack of asthma is probably related to inhibition of COX (63). There is evidence that potent inhibitors of COX-1 (such as ibuprofen, indometacin, and naproxen) are more likely to precipitate bronchoconstriction than NSAIDs that inhibit COX-2 preferentially (such as meloxicam and nime-sulide) (64,65). A widely accepted hjrpothesis is that in patients with asthma and aspirin intolerance, NSAJD-induced COX inhibition results in increased products from the 5-lipoxygenase pathway, the leukotrienes, which are both potent bronchoconstrictors and also inducers of... 

Aspirin and other nonsteroidal anti-inflammatory drugs can precipitate an attack in up to 20% of adults with asthma. The mechanism is related to cyclooxygenase inhibition, and 5-hpoxygenase inhibition can prevent the symptoms. The prevalence increases with age. The greatest frequency occurs in severe corticosteroid-dependent asthmatics in their fourth and fifth decades who also have perennial rhinitis and nasal polyposis (presence of several polyps). Other drugs that do not precipitate bronchospasm but which prevent its reversal are the 8-blocking agents. ... 

In some patients with asthma, aspirin and several other NSAID precipitate asthmatic attacks. This is a distinct clinical syndrome. It is called aspirin-induced asthma (AIA). 

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