"Is there anything that can be done for relapses in MS?"
Actually, yes, there are drug treatments which reduce both the severity and duration of relapses in multiple sclerosis. There are two types of drug which have this effect, steroids which are routinely prescribed by some neurologists, and immunosuppressants which can still be viewed as somewhat experimental. Both types of drug have serious side effects although, on balance, those of immunosuppressants are the more serious and their use is generally confined to treating progressive forms of MS. In this section, I shall discuss the benefits and drawbacks of steroids and the hormone, ACTH, that induces the body to increase production of its own natural steroids. In the next section I shall deal with immunosuppressants.
"Ok then, tell me about steroids."
Steroids are naturally occuring hormones in the human body. There are a variety of steroids including glucocorticosteroids, mineralcorticosteroids, androgens and progestins. Of these, only the glucocorticosteroids (often simply called glucocorticoids) are regularly prescribed to treat relapses in multiple sclerosis. However both androgens (the sex hormones, oestrogen and testosterone) and progestins (the sex hormone, progesterone) are now thought to have potential in treating MS and their use is now being researched. I shall discuss the use of androgens in my section on multiple sclerosis research.
Glucocorticosteroids occur naturally in the body as cortisone and hydrocortisone. These hormones are produced by a pair of organs called the adrenal glands which are situated next to the kidneys. The adrenal glands are organised into two discreet tissue types, somewhat confusingly called the medulla and cortex. These have nothing to do with their namesakes in the brain. The cortisones are produced in the adrenal cortex in response to the release of a regulatory hormone called adrenocorticotrophic hormone (ACTH) which is manufactured in both the pituitary gland in the brain as well as in the adrenal cortex. ACTH is naturally secreted in response to a variey of stress factors including fear, anxiety, pain, exercise, infection and very low levels of blood glucose (hypoglycaemia).
Cortisone is also present in an inactive, bound-up state throughout the body. It is rapidly unbound and therefore activated through a number of mechanisms including certain types of white blood cell activity and high body temperature - i.e. the signs of infection. Cortisones have an immunosuppressive effect by deactivating white blood cells specifically T-cells by inhibiting their release of messanger molecules called cytokines and effector molecules. This form of immuno-regulation is known as "lymphocytopenia" which is not to be confused with the disease of the same name that results in immuno-deficiency in people unlucky enough to have it. Cortisones also induce a degree of white blood cell death and is also believed that they reduce the "leakiness" of the blood-brain barrier.
"You're just blinding me with science - what has all this got to do with MS?"
For whatever reason, white blood cells, the cells of the immune system, appear to be responsible for the damage done by multiple sclerosis. One would therefore expect that glucocorticoids, which reduce white blood cell counts, would reduce the severity of MS relapses. This is what is observed. Glucorticsteroids and ACTH reduce both the severity and duration of relapses.
ACTH was used first to release natural cortisone into the body but, since then, it has been found that synthetic glucorticsteroids are much more effective and have longer half-lives than the naturally occuring cortisones and they have gradually replaced it.
Synthetic glucorticosteroids are chemically derived from cortisone and hydrocortisone, with just slight changes to their composition. They include fluorohydrocortisone (derived from cortisone), prednisolone (from hydrocortisone), prednisone (from cortisone), methylprednisolone (from prednisolone), dexamethosone (from prednisolone) and betamethasone (from prednisolone). Perhaps the best known synthetic brand is Solu-Medrol which is IV methylprednisolone but there are many other brands.
"This all sounds great - what's the catch?"
It seems to me that the use of steroids to treat MS relapses is not as contraversial as it should be. While glucocorticoids are certainly effective at reducing the immediate impact of relapses, they have been found to have no effect at all on the overall progress of the disease. I would like to reiterate this: steroid use does nothing at all to delay the progression of multiple sclerosis. Seen this way their use is merely palliative much as taking an aspirin to treat a headache reduces the pain but does nothing to address the cause. This would be fine if steroids didn't have such significant side-effects.
Since so many of the cells in the human body have receptors for glucocorticosteroids, it's not surprising that they have such a range of side-effects. These can (but by no means always) include: acne, weight-gain, seizures, psychosis, depression, headaches, fatigue, facial hair, nausea, vomitting, adrenal insufficency and many more some of which can be very serious. Long-term use of glucocorticoids is not advised nor is it effective in MS.
Potential severe side-effects are part and parcel of all drug use and we all have to make a decision on whether the benefits of a particular drug outweigh it's disadvantages. I tend to be rather conservative - as far as disease progression goes, I like the idea of drugs that slow down the rate of progression but I'm also not adverse to taking a drug that mitigates against severe symptoms. As far as glucocorticosteroids are concerned, I would need the relapse to be pretty severe to consider their use. Relapses tend to remit within four to six weeks and steroids don't affect the amount nor severity of the residual deficits. You have to make up you're own mind with your own neurologist to advise you.
"Do steroids work with progressive forms of MS?"
The short answer is, probably not, corticosteroids do not appear to have a beneficial effect on progressive forms of the disease. Trials have been done on low-dose methylprenisolone use with secondary progressive MS and, although the results were equivocal, the degree of disability was not affected [Goodkin et al, 1998]. However this study concluded that more work needed to be done to determine whether corticosteroids might have a place in treating SPMS.
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