Corticosteroids, Part 1 Print E-mail



Caution: Whenever your doctor prescribes a new medication, it's very helpful to ask your doctoror pharmacistif there are any foods that interact with it. Scientists are continuously learning more and more about food-drug interactions. (As an example: grapefruit alters the amount in your blood of certain drugsincreasing some, decreasing others.)


Natural corticosteroidsusually simply called steroidsare hormones produced in the body by the outer layers (the cortex) of the adrenal glands, which are located on the kidneys. These hormones are essential to life. They play a critical role in such diverse bodily processes as energy metabolism, kidney function, and the immune system.

The corticosteroids fall into two groups. One of themcalled the glucocorticoids for their effect on glucose (a kind of sugar) metabolismhas strong anti-inflammatory properties. When we talk about steroids in relation to COPD, we are really referring to this particular group of steroids.

Soon after the glucocorticoid hormones were synthesized in the laboratory and their dramatic anti-inflammatory characteristics identified, they were brought into the treatment of asthma, a chronic respiratory disease. In the early 1950s, steroids revolutionized life for many asthmatics whose symptoms responded poorly to the other drugs then available. Instead of being incapacitated by their disease, their symptoms suddenly disappeared and their dependence on other forms of treatment lessened.

But the unexpectedly high price paid for this miracle soon became obvious. The catalogue of far-ranging side effects included many that were extremely serious: for example: loss of calcium from the bones, psychosis, and stunted growth in children. The use of steroids in asthma was rejected about ten years after they were first introduced.

Now the situation in regard to asthma has changed again. A deeper and more objective understanding of steroids' therapeutic effects has clearly established them as a first-line drug in controlling this respiratory disease. The new inhaled steroids greatly lessen side effects. And advances in our understanding of the body's response to steroids have led to auxiliary techniques that also help in minimizing side effects.

The use of steroids in COPD, however, is unresolved. Those supporting it feel that the same anti-inflammatory properties so important in managing severe asthma can also help chronic bronchitis patients. There are two potential situations for adding steroids to the drug regimen of a COPD patient with a substantial chronic bronchitis component. One involves intravenous steroids during hospitalization for a temporary worsening. The other would add oral or inhaled steroids to the regular medication menu of a stable patient.

The first scenariointravenous steroid use to bring the patient more quickly through acute episodes and minimize the increase in blood gas imbalancehas not yet been adequately examined. But there is a reliable study demonstrating steroids' benefits in bringing patients through the acute respiratory failure that exacerbations can provoke. Although this does not warrant adopting intravenous steroids as a regular therapy for acute episodes, it certainly underscores their value for patients who are not responding to standard therapy.

The use of steroids by stable COPD patients has, by contrast, been thoroughly evaluated. Most reliable studies find steroids effective for only a minority of patients. But the lack of any means for predicting which patients will benefit prevents specific recommendations. The general sense, however, is that steroids should be tried for all patients with very severe airflow obstruction (that is, their FEV1 is only 1 to 1.5 liters).

The following example indicates how a two-week steroid trial should be conducted. For two to three months before starting medication, FEV1 is measured several times. After two weeks of medication, the patient's FEV1 is measured again. If it is not at least 25% larger than the best pre-steroid value, discontinue steroids. But if the patient's airflow is significantly improved, then continue treatment. Taper the dosage to the lowest one that works. Discontinue using steroids periodically to see if the patient still needs them to do his best.

How Steroids Work

Steroid production is controlled by the body's master gland, the pituitary, via its secretion of adrenocorticotrophic hormone (ACTH). The pituitary releases ACTH into the bloodstream, which brings it to the adrenal glands. The arrival of ACTH at the adrenal cortex is its signal to immediately manufacture and release steroids. (Their release then temporarily stops any further release of ACTH.)

Steroids are produced in their greatest amounts shortly after waking up. They are lowest during sleep, with the lowest production of all usually between 2 A.M. and 4 A.M. (As we will see, this diurnal variation must be kept in mind when steroid drugs are prescribed.) The amount of steroids normally produced at any given time of the day or night can be increased by stress.

Steroids work along two different avenues simultaneously. Their action is rapid by one route, and slower by the other. The net effect is that steroids inhibit the release and further formation of the body's inflammatory chemicals.

Steroids also prevent the initial decrease in beta-receptor sensitivity that otherwise happens when beta-stimulating bronchodilators are used. In addition, some investigators feel that steroids directly relax airway muscle, inhibit bronchoconstricting cholinergic mechanisms, increase mucociliary activity, and dectease mucus production.


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