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VACCINE FOR ASTHMA BEING DEVELOPED
 



A vaccine against asthma could be ready for trials in just three years. In a major breakthrough, scientists have discovered the active part of the virus that is thought to be behind a third of all asthma cases. The respiratory syncytial virus (RSV) inflames the inside of the lungs, weakens the immune system and produces mucus that obstructs the airways. Scientists at the Imperial College School of Medicine in London and American experts at the National Institute of Health believe they have identified the protein, which causes the inflammation. It was found that only a small amount of the G protein was necessary to damage the immune system of mice.

The National Institute in Washington hopes to develop a vaccine, which could be tested on humans within three years. But it may not all be plain sailing as earlier trials of a vaccine for RSV led to hospitalisation of some children following exposure to the virus.

http://news.bbc.co.uk/1/hi/health.
 
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SALMETEROL IMPROVES PULMONARY FUNCTION IN HEART PATIENTS


Inhaled salmeterol, a long acting 2 agonist used in asthma, has been found to improve pulmonary function in heart patients.

Investigators from the Department of Pharmacy Practice and Internal Medicine at the University of Utah Health Sciences Center, U.S. conducted a prospective, randomised, double-blind, 14-day cross over study to determine the effect of inhaled salmeterol on pulmonary function. Inhaled salmeterol (84 g) was administered every 12 hours for 14 days to 8 symptomatic heart failure patients with left ventricular ejection fraction (LVEF) < 40% and FEV1 < 80%.

Results showed that the therapy led to a significant 6% improvement in FEV1 2.46 litres compared to 2.33 litres with placebo. Rate pressure product also increased by 5% with salmeterol. However, there was no increase in plasma norepinephrine, epinephrine, plasma renin activity or ventricular ectopy. Thus, the study revealed that inhaled salmeterol improved FEV1 without producing measurable effects on neuroactivation or ventricular ectopy. The clinical significance of the minor increase in rate-pressure product remains to be determined.

J. Cardiovasc. Pharmacol 2002; 40(1): 140-145


 
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ROFECOXIB IN ASPIRIN-SENSITIVE ASTHMA


Aspirin-induced asthma (AIA) is an airway mucosa inflammatory disease that combines with the precipitation of asthma and attacks of rhinitis and is triggered by the ingestion of aspirin and most nonsteroidal anti-inflammatory drugs (NSAIDs). AIA affects about 10% of adults with asthma. These asthmatic attacks usually occur within 3 hours after ingestion of aspirin or an NSAID. The attacks are often severe and in many cases life-threatening, requiring emergency mechanical ventilation. AIA is a crucial problem since drugs for the management of common medical conditions such as pain, fever and inflammation are commonly required. Therefore, it is important to choose an alternative anti-inflammatory agent for vulnerable asthma patients. Cyclooxygenase (COX) enzymes, which appear to be central to the mechanism of aspirin sensitivity, exist in at least two isoforms, COX-1 and COX-2. Most NSAIDs inhibit both isoforms, although at different intensities. The anti-inflammatory effects are due to COX-2 inhibition and adverse effects are due to COX-1 inhibition. Rofecoxib is a selective COX-2 inhibitor, used as an analgesic in patients with primary dysmenorrhoea and post-operative dental pain. It has very little or no effect at all on gastric mucosa.

A study was conducted to demonstrate the safety of rofecoxib in asthma patients suffering from AIA or other NSAID- induced asthma. The study covered 40 patients, all of whom experienced asthma induced by at least two different NSAIDs. Out of the 40 patients, 77.5% had moderate asthma and 12.5% had severe asthma. The patients were challenged in a single-blind manner with different doses of rofecoxib on 3 different days (1st day- 6.25 mg, 2nd day - 12.5 mg, 3rd day - 25 mg), until either the therapeutic dose of 25 mg or intolerance was reached. Each patient was again challenged with 25 mg of rofecoxib 7 days later if no evidence of intolerance had been observed before.

At the end of the challenge procedure, all the patients tolerated the 25 mg dose of rofecoxib well, without any signs of immediate or delayed reactions. The mean PEF variation before the provocation test was 11.20% and afterwards 11.38%. There were no significant differences between PEF variations before and after the administration of rofecoxib. Thus the study demonstrated that a 25 mg dose of rofecoxib was well tolerated in all 40 patients with AIA and NSAID- induced asthma.

Chest 2002; 121: 1812-1817
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