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Steroid Drug 'Increases Heart Disease Risk'

Study warns of hazards in treatment used to fight asthma

Mar 24, 2003 | PATIENTS taking a widely-used steroid drug to combat common inflammatory diseases could be increasing their risk of heart disease by up to 50%, Scots researchers will report today.

It is the first time a direct link has been shown between high doses of glucocorticoids and heart disease. The steroid is commonly prescribed to alleviate conditions including asthma, rheumatoid arthritis and inflammatory bowel disease.

It emerged from a population study in Tayside, which will be unveiled today at the annual meeting of the British Endocrine Societies in Glasgow.

More than 164,000 people took part in the study by Dr Li Wei and Professor Tom MacDonald, of Dundee University, and Professor Brian Walker, of Edinburgh University.

The subjects were all over 40 and nearly half had received at least one glucocorticoid prescription between 1993 and 1996. Increased dosage correlated with increase in the incidence of heart disease.

The results showed a decade of glucocorticoid use at the highest doses, taken by about 2% of the group, increased the risk of heart disease in over-40s from approximately 19 people in every 100, to 32.

Professor Walker cautioned yesterday against a panic reaction to the discovery, pointing out that these drugs were very effective in the treatment of certain conditions.

"The overall benefits of treatment with glucocorticoids outweighs the risks for most patients," he said. "However, this study reminds doctors to be cautious when using high doses for extended periods, especially in patients already considered to be at a greater risk of cardiovascular disease."

Other research being presented today will show that raised levels of naturally-occurring glucocorticoids in particular the stress hormone cortisol can run in families and lead to high blood pressure or obesity.

Results from a group at the Western General Hospital in Edinburgh, will also explain why foetal exposure to high levels of cortisol is linked to high blood pressure in adults.

Tests in rats showed that prenatal exposure to cortisol speeds up the body's major blood pressure regulation system.

Natural levels of cortisol, and the activity of an enzyme that regulates it in the placenta and foetus, vary between individuals. If maternal cortisol is high for example because of stress or enzyme activity is low, the foetus will be over-exposed to the hormone, say researchers.

This influences "foetal programming" when adverse events in the uterus permanently alter the physiology of adult offspring causing reduced birth weight and increased chance of high blood pressure in adulthood.

David O'Regan, who will present the results, said: "Our study is the first describing the molecular basis for this example of foetal programming. It provides further evidence that exposure to hormones in the uterus affects adult offspring."

"The mechanism by which cortisol interacts with this system may be a potential target for future prenatal preventative therapy in high risk groups."

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