Myasthenia Gravis Society of the Philippines

Compiled by Rory Esperanza, MGS President

MGA BAGAY NA DAPAT MALAMAN TUNGKOL SA MYASTHENIA GRAVIS PARA SA MGA PASYENTE AT KANILANG PAMILYA

Ang Myasthenia Gravis o MG ay nagbuhat sa mga salitang Griyego at Latin na ang ibig sabihin ay malalang panghihina ng kalamnan. Ito ay isang nagpapatuloy na sakit ng nerbiyos-kalamnan (chronic neuro-muscular disease) na kinatatampukan ng panghihina ng mga voluntary muscles ng katawan.  Ang sakit na ito ay napag-alamang nagsimula noon pang ikalabing-siyam na siglo. 

Mga Klinikal na Katangian at Sintomas

DIAGNOSTIC PROCEDURES
The Edrophonium Chloride (Tensilon) Test
Weakness caused by abnormal neuromuscular transmission characteristically improves after intravenous administration of edrophonium chloride. Some patients who don't respond to intravenous edrophonium chloride may respond to intramuscular neostigmine, because of the longer duration of action. Intramuscular neostigmine is particularly useful in infants and children whose response to intravenous edrophonium chloride may be too brief for adequate observation. In some patients, a therapeutic trial of daily oral pyridostigmine may produce improvement that can't be appreciated after a single dose of edrophonium chloride or neostigmine.

Antibodies Against Acetylcholine Receptor (AchR)
Seventy four percent of patients with acquired generalized myasthenia and 54% with ocular myasthenia have serum antibodies that bind human AChR. The serum concentration of AChR antibody varies widely among patients with similar degrees of weakness and cannot predict the severity of disease in individual patients. Approximately 10% of patients who do not have binding antibodies, have other antibodies that modulate the turnover of AChR in tissue culture. The concentration of binding antibodies may be low at symptom onset and become elevated later. AChR binding antibodies concentrations are sometimes increased in patients with systemic lupus erythematosus, inflammatory neuropathy, amyotrophic lateral sclerosis, rheumatoid arthritis taking D-penicillamine, thymoma without myasthenia gravis, and in normal relatives of patients with myasthenia gravis. False positive tests are reported when blood is drawn within 48 hours of a surgical procedure involving the use of general anesthesia and muscle relaxants. In general, an elevated concentration of AChR binding antibodies in a patient with compatible clinical features confirms the diagnosis of myasthenia gravis, but normal antibody concentrations do not exclude the diagnosis.

Electromyography
Repetitive Nerve Stimulation RNS)
The amplitude of the compound muscle action potential (CMAP) elicited by repetitive nerve stimulation is normal or only slightly reduced in patients without MG. The amplitude of the fourth or fifth response to a train of low frequency nerve stimuli falls at least 10% from the initial value in myasthenic patients. This decrementing response to RNS is seen more often in proximal muscles, such as the facial muscles, biceps, deltoid, and trapezius than in hand muscles. A significant decrement to RNS in either a hand or shoulder muscle is found in about 60% of patients with myasthenia gravis.

Single Fiber EMG (SFEMG)
SFEMG is the most sensitive clinical test of neuromuscular transmission and shows increased jitter in some muscles in almost all patients with myasthenia gravis. Jitter is greatest in weak muscles but may be abnormal even in muscles with normal strength. Patients with mild or purely ocular muscle weakness may have increased jitter only in facial muscles. Increased jitter is a nonspecific sign of abnormal neuromuscular transmission and can be seen in other motor unit diseases. Normal jitter in a weak muscle excludes abnormal neuromuscular transmission as the cause of weakness.

Comparison of Diagnostic Techniques
Intravenous edrophonium chloride is often diagnostic in patients with ptosis or ophthalmoparesis, but is less useful when other muscles are weak. Elevated serum concentrations of AChR binding antibodies virtually assures the diagnosis of myasthenia gravis, but normal concentrations do not exclude the diagnosis. Repetitive nerve stimulation confirms impaired neuromuscular transmission but is not specific to myasthenia gravis and is frequently normal in patients with mild or purely ocular disease. The measurement of jitter by SFEMG is the most sensitive clinical test of neuromuscular transmission and is abnormal in almost all patients with myasthenia gravis. A normal test in a weak muscle excludes the diagnosis of myasthenia gravis, but an abnormal test can occur when other motor unit disorders cause defects in neuromuscular transmission.

A controlled clinical trial has never been reported for any medical or surgical modality used to treat myasthenia gravis. All recommended regimens are empirical and experts disagree on treatments of choice. Treatment decisions should be based on knowledge of the natural history of disease in each patient and the predicted response to a specific form of therapy. Treatment goals must be individualized according to the severity of disease, the patient's age and sex, and the degree of functional impairment. The response to any form of treatment is difficult to assess because the severity of symptoms fluctuates. Spontaneous improvement, even remissions, occur without specific therapy, especially during the early stages of the disease.

Cholinesterase Inhibitors
ChE inhibitors retard the enzymatic hydrolysis of ACh at cholinergic synapses, so that ACh accumulates at the neuromuscular junction and its effect is prolonged. ChE inhibitors cause considerable improvement in some patients and little to none in others. Strength rarely returns to normal. Pyridostigmine bromide (Mestinon) and neostigmine bromide (Prostigmin) are the most commonly used ChE inhibitors. No fixed dosage schedule suits all patients. The need for ACh inhibitors varies from day-to-day and during the same day in response to infection, menstruation, emotional stress, and hot weather. Different muscles respond differently; with any dose, certain muscles get stronger, others do not change, and still others become weaker. Adverse effects of ChE inhibitors may result from ACh accumulation at muscarinic receptors on smooth muscle and autonomic glands and at nicotinic receptors of skeletal muscle. Central nervous system side effects are rarely seen with the doses used to treat myasthenia gravis. Gastrointestinal complaints are common; queasiness, loose stools, nausea, vomiting, abdominal cramps, and diarrhea. Increased bronchial and oral secretions are a serious problem in patients with swallowing or respiratory insufficiency. Symptoms of muscarinic overdosage may indicate that nicotinic overdosage (weakness) is also occurring. Excessive nicotinic receptor overdosage results in Myasthenic Crisis characterized by severe generalized weakness and respiratory failure.

Thymectomy
Thymectomy is recommended for most patients with myasthenia gravis. Most reports do not correlate the severity of weakness before surgery and the timing or degree of improvement after thymectomy. The maximal favorable response generally occurs 2 to 5 years after surgery. However, the response is relatively unpredictable and significant impairment may continue for months or years after surgery. Sometimes, improvement is only appreciated in retrospect. The best responses to thymectomy are in young people early in the course of their disease, but improvement can occur even after 30 years of symptoms. Patients with disease onset after the age of 60 rarely show substantial improvement from thymectomy. Patients with thymomas do not respond as well to thymectomy as do patients without thymoma.

Corticosteroids
Marked improvement or complete relief of symptoms occurs in more than 75% of patients treated with prednisone, and some improvement occurs in most of the rest. Much of the improvement occurs in the first 6 to 8 weeks, but strength may increase to total remission in the months that follow. The best responses occur in patients with recent onset of symptoms, but patients with chronic disease may also respond. The severity of disease does not predict the ultimate improvement. Patients with thymoma have an excellent response to prednisone before or after removal of the tumor. The most predictable response to prednisone occurs when treatment begins with a daily dose of 1.5 to 2 mg/kg/day. About one-third of patients become weaker temporarily after starting prednisone, usually within the first 7 to 10 days, and lasting for up to 6 days. Treatment can be started at low dose to minimize exacerbations; the dose is then slowly increased until improvement occurs. Exacerbations may also occur with this approach and the response is less predictable. The major disadvantages of chronic corticosteroid therapy are the side effects.

Immunosuppressant Drugs
Azathioprine reverses symptoms in most patients but the effect is delayed by 4 to 8 months. Once improvement begins, it is maintained for as long as the drug is given, but symptoms recur 2 to 3 months after the drug is discontinued or the dose is reduced below therapeutic levels. Patients who fail corticosteroids may respond to azathioprine and the reverse is also true. Some respond better to treatment with both drugs than to either alone. Because the response to azathioprine is delayed, both drugs may be started simultaneously with the intent of rapidly tapering prednisone when azathioprine becomes effective. Approximately one-third of patients have mild dose-dependent side effects that may require dose reductions but do not require stopping treatment.

Cyclosporine inhibits predominantly T-lymphocyte-dependent immune responses and is sometimes beneficial in treating myasthenia gravis. Most patients with myasthenia gravis improve 1 to 2 months after starting cyclosporine and improvement is maintained as long as therapeutic doses are given. Maximum improvement is achieved 6 months or longer after starting treatment. After achieving the maximal response, the dose is gradually reduced to the minimum that maintains improvement. Renal toxicity and hypertension, the important adverse reactions of cyclosporine. Many drugs interfere with cyclosporine metabolism and should be avoided or used with caution .

Cyclophosphamide has been used intravenously and orally for the treatment of myasthenia gravis. More than half of patients become asymptomatic after one year. Side effects are common. Life-threatening infections are an important risk in immunosuppressed patients, but in our experience, this risk is limited to patients with invasive thymoma. The long-term risk of malignancy is not established, but there are no reports of an increased incidence of malignancy in patients with myasthenia gravis receiving immunosuppression.

Plasma Exchange
Plasma exchange is used as a short-term intervention for patients with sudden worsening of myasthenic symptoms for any reason, to rapidly improve strength before surgery, and as a chronic intermittent treatment for patients who are refractory to all other treatments. The need for plasma exchange, and its frequency of use is determined by the clinical respo࡮se in the individual patient. Almost all patients with acquired myasthenia gravis ࡩmprove temporarily following plasma exchange. Maximum improvement may be reached as early as after the first exchange or as late as the fourteenth. Improvement lasts for weeks or months and then the effect is lost unless the exchange is followed by thymectomy or immunosuppressive therapy. Most patients who respond to the first plasma exchange will respond again to subsequent courses. Repeated exchanges do not have a cumulative benefit.

Intravenous Immune Globulin (IVIG)
Several groups have reported a favorable response to high-dose (2 grams/kg infused over 2 to 5 days) IVIG. Possible mechanisms of action include down-regulation of antibodies directed against AChR and the introduction of anti-idiotypic antibodies. Improvement occurs in 50 to 100% of patients, usually beginning within 1 week and lasting for several weeks or months. The common adverse effects of IVIG are related to the rate of infusion. The mechanism of action is not known but is probably non-specific down regulation of antibody production.

THE FUTURE

The future of Myasthenia Gravis lies in the elucidation of the molecular immunology of the anti-acetylcholine receptor response with the goal of developing a rational treatment for the illness that will cure the abnormality in the immune system that results in the AChR immune response. To this end, six broad categories of theoretical treatment strategies need to be explored. First, those treatments which target the antigen specific B-cells; Second, those treatments which target the antigen specific CD4+ T-cells; Third, those treatments which interfere with co-stimulatory response for antigen presentation, Fourth, treatments aimed at inducing tolerance or anergy of the CD4+ T-cell to the autoantigen or the CD4+ epitopes; Fifth, those treatments designed to stimulate those immunological circuits which activate CD8+ cells specific for the activation antigens expressed by CD4+ cells and Sixth, those treatments which intervene with cytokine function and discourage autoimmune mediated inflammatory responses.

Copyright � 1997 by Myasthenia Gravis Foundation of America and James F. Howard, Jr., M.D.. All rights reserved.
Most recent revision Tuesday, November 11, 1997.  

Myasthenia Gravis Foundation of America
5841 Cedar Lake Road, Suite 204
Minneapolis, MN 55416
Telephone - (952) 545-9438 or (800) 541-5454
Fax:  (952) 545-6073

Drugs which may aggravate MG

by Dr Stanley Freedman

The important word in the title of this article is "may". Just as myasthenics differ widely in the sites and severity of their weakness, so they differ in their susceptibility to the effects of drugs, as, indeed, do non-myasthenics. There are, therefore, no absolute prohibitions, apart possibly from some of the drugs used in anaesthesia, and no need to panic if you are taking, or have taken, one of the drugs listed below without any ill-effects. If your MG is well-controlled, these drugs are very unlikely to have any ill-effects, and it is important not to deny yourself their benefits. Decisions about whether or not to take a drug must be made in consultation with your doctor. It should also be emphasised that while these drugs may make the symptoms of MG worse, none of them affects the basic disease process, apart from penicillamine.

From the doctor's viewpoint, problems arise because information on the drugs, in reference books as well as in the packaging, is often inaccurate. Some drugs, temazepam being a good example, are labelled as being absolutely contra-indicated in MG, when in fact they do not affect it at all, while on the other hand, some drugs which commonly aggravate MG do not carry a warning. Further problems arise for doctor and patient, because of the profusion of available drugs. For example, no fewer than 15 different "beta-blockers" are licensed for use in the UK, and any one of these may be marketed by several companies under different brand names.

In this article, I have listed drugs according to their class, and provided both "official" name, in bold, and trade names, where these are different, in italic. Popular mixtures which contain the offending drug are listed (in brackets). I have attempted a brief outline of how they may affect MG. As well as tablets and injections, I have listed preparations used locally in the eye, as significant amounts of drug can be absorbed into the bloodstream when given by this route.

Also, beware of laxatives, which can impair the absorption, and therefore the effectiveness, of all your drugs, but particularly of pyridostigmine (mestinon).

1. ANTI-ARRHYTHMICS

These are used to treat and prevent irregular heart beat. The ones in this list have largely been superseded by newer, safer, drugs, including beta-blockers (see below).

• Procaine Amide Pronestyl

• Quinidine Kinidin Durules

2. ANTIBIOTICS

These are used to prevent and treat bacterial infections. One group (A), which contains six members, affects transmission between nerve and muscle, and therefore can make MG worse. They are chiefly given by injection, and you are therefore most likely to come across them in hospital. You are more likely to encounter those in groups B, which are usually given as tablets, often for chest infections, but which are much less likely to upset your MG, and C, which are commonly used for bladder and kidney infections. Group D is now used very rarely.

• A.

  • Gentamicin Genticin, Genticin Ear/Eye drops, Cidomycin Injection, Cidomycin Ear/Eye drops/ointment

  • Amikacin Amikin

  • Netilmicin Netillin

  • TobramycinNebcin

  • Streptomycin

  • KanamycinKannasyn

• B.

  • Tetracycline Achromycin, Sustamycin, Tetrabid, Tetrachel, Deteclo, (Mysteclin).

  • Doxycycline Nordox, Vibramycin,

  • Limecycline Tetralysal 300

  • Minocycline Minocin MR

  • Oxytetracycline Terramycin

• C.

  • Ciprofloxacin Ciproxin

  • Acrosoxacin Eradicin

  • Cinoxacin Cinobac

  • Nalidixic Acid Mictral, Negram, Uriben

  • Norfloxacin Utinor

  • Ofloxacin Tarivid

• D.

  • Polymixin B

  • Colistin Colomycin Injection

3. ANTI-MALARIALS

These drugs are sometimes also used to treat rheumatic conditions.

• Chloroquine Avloclor, Nivaquine

• Hydroxychloroquine Plaquenil

4. ANTI-RHEUMATIC DRUGS

• Penicillamine Distamine, Pendramine.

5. ANTI-SPASMODICS

These drugs, which are used to relax and reduce the activity of the bladder and bowels, act by opposing the action of acetylcholine (whereas drugs like mestinon promote it), and therefore carry a warning against their use in patients with MG. In fact, theoretically, they should not interfere with the action of acetyl-choline on muscle, and in practice there have been no reports of adverse effects in MG - perhaps because the warning has been so effective!

• Flavoxate Urispas

• Oxybutinin Cystrin, Ditropan

• Propantheline Probanthine

6. BETA-BLOCKERS

These drugs are used for the treatment of angina and other forms of heart disease, high blood pressure, migraine, and, occasionally, anxiety. They commonly produce a feeling of fatigue or muscle weakness, which tends to improve with continued treatment, and, rarely, have been reported to induce MG.

• Propranolol Inderal, Angilol, Apsolol, Bedranol, Berkolol, Beta-Prograne, Cardinol, Propanix, (Inderetic, Inderex)

• Atenolol Tenormin (Tenif, Tenoretic, Tenoret 50, Co-Tenidone), Atenix, Antipressan, Kalton, Totamol, (Beta-Adalat, Co-Tenidone, Totaretic)

• Acebutolol Sectral (Secadrex)

• Betaxolol Kerlone

• Bisoprolol Emcor, Monocor, (Monozide)

• Carvedilol Eucardic

• Celiprolol Celectol

• Esmolol Brevibloc

• Labetalol Trandate

• Metoprolol Betaloc, Lopresor, (Co-Betaloc)

• Nadolol Corgard

• Oxprenolol Trasicor, (Trasidrex)

• Pindolol Visken, (Viskaldix)

• Sotalol Beta-Cardone, Sotacor, (Sotazide, Tolerzide)

• Timolol Betim, Blocadren, (Moducren, Prestim, Timoptol Eye-drops).

7.DRUGS USED IN EPILEPSY

• Phenytoin Epanutin

This is always listed among drugs which can precipitate MG, but actual reports of problems are rare.

8. DRUGS USED IN PSYCHIATRY

A. Chlorpromazine and related drugs. These drugs are used in a wide variety of conditions. The original members of the group, chlorpromazepine and promazine, were reported to aggravate, or even to precipitate MG, but there are now a lot of newer analogues, and reports of trouble from these are rare. However it is probably still wise to use them cautiously.

• Chlorpromazine Largactil

• Clozapine Clozaril

• Flupenthixol Depixol

• Fluphenazine Moditen

• Loxapine Loxapac

• Methotrimeprazine Nozinan

• Oxypertine

• Pericyazine Neulactil

• Perphenazine Fentazin

• Pimozide Orap

• Prochlorperazine

• Promazine Sparine

• Risperidone Risperdal
• Sulpiride Dolmatil, Sulpitil
• Thioridazine Melleril
• Trifluoroperazine Stelazine
• Zuclopenthixol Clopixol Acuphase

• B. Lithium Camcolit, Liskonum, Li-liquid, Litarex, Priadel.
• C.
  • Phenelzine Nardil,
  • Isocarboxazid Marplan
  • Tranylcypromine Parnate, (Parstelin)

9. MUSCLE RELAXANTS

These drugs are designed to cause muscle paralysis and are used almost exclusively by anaesthetists. For this reason, I consider it unnecessary to list them individually. There are two classes of muscle-relaxants: curare-like drugs, which must not be used in MG, and depolarising relaxants, which can sometimes be used. Both types must be distinguished from drugs such as the minor tranquillisers, which are often called "muscle-relaxants", although their effects are entirely non-specific.

Side effects of some medicines used to treat MG

by Dr Stanley Freedman

All medicines and drugs have some unwanted effects, or side effects, and those commonly used to treat MG are no exceptions to this rule. The frequency and the seriousness of these unwanted effects vary greatly from drug to drug and from patient to patient, and, in deciding whether to use a particular treatment, a doctor has to weigh up the potential benefits and balance these against the risk of unwanted effects. In most cases, the benefits far outweigh the risks, but it is as well to understand the nature of the unwanted effects and the problems they can pose. For simplicity, I am only going to consider three groups of medicines: Pyridostigmine and similar drugs, Azathioprine and Steroids.

Pyridostigmine (a.k.a. Mestinon) and Neostigmine

These act by slowing the normal breakdown of Acetylcholine and therefore building up its concentration at the muscle receptor, which is where it is needed to transmit messages from the nerves to the muscles, and where the defect in MG is located. Unfortunately, Acetylcholine has important actions at numerous other sites in the BODY apart from the muscle receptors, and Pyridostigmine causes a lot of unwanted effects, most of which are not very serious but which are, none the less, very inconvenient. Thus, it may cause over activity of the muscle in the wall of the bladder and the bowel, which in turn may cause frequently of passing urine, or even incontinence, and abdominal discomfort and diarrhoea. The muscle controlling the pupil of the eye is also affected, and there may be difficulty in focusing. There are Acetylcholine receptors in the heart and so Pyridostigmine may cause a very slow heart beat, which can, in turn, cause dizziness. The activity of many glands is increased by Acetylcholine, and patients may notice increased sweating and production of saliva. All these unwanted effects can be prevented by taking another drug, Atropine (or a related drug) at the same time. The only really serious potential unwanted affect of Pyridostigmine is that if the dose is too high, it can make the muscle weakness of MG worse rather than better It is therefore important, when using Pyridostigmine, to emulate the admirable principle which some of the older readers of this article will remember from the adverts for ""Erasmic"" shaving cream" i.e. not too little, not too much, but just right! It is also important to emphasise that all the unwanted effects of Pyridostigmine are short-lasting, and that it does not cause any permanent or long-term problems.

Azathioprine

This drug depresses the immune system including the cells which produce the antibodies which are responsible for MG. It is extremely useful because it allows us to take much smaller doses of steroids than we would otherwise have to. It has to be taken for a least six months, and often for a year or more, before it is fully effective. It has several unwanted effects.

(i) Hypersensitivity

Some people have a hypersensitivity or allergy, to Azathioprine and develop fever, chills, joint and muscle pains, vomiting and dizziness. Usually soon after the start of treatment. It is, of course, important to make sure that the symptoms are due to Azathioprine and not to coincidental flu, but when this unwanted reaction occurs, treatment must be stopped and cannot usually be restarted. It is, unfortunately, impossible to forecast who will react to Azathioprine in this way.

(ii) Effects on the blood

Azathioprine depresses the formation of new blood cells, just as it depresses antiBODY-forming cells. It is therefore necessary to monitor the situation closely by performing frequent blood counts at the start of treatment and three to four times a year once treatment is established. If the count drops significantly, it may be necessary to stop treatment temporarily.

(iii) Susceptibility to Infection

As Azathioprine depresses immunity, it increases susceptibility to infections. Special care must be taken to avoid contact with shingles and chicken pox which are much more severe in patients with lowered immunity.

(iv) Effects on the Liver

Liver function may be upset by Azathioprine. This can be monitored by blood tests. The effects are reversible on stopping treatment or reducing the dose.

(v) Increased incidence of tumours?

This is the most controversial, unwanted effect of Azathioprine. There are reports of an increased frequency of tumours mainly of the lymph glands in patients with rheumatoid arthritis taking Azathioprine. The sort of tumours that occurred in these patients were those that respond well to treatment once Azathioprine is stopped. However, a more recent report in 755 patients taking Azathioprine for bowel disease and who were followed for up to 29 years found no increase in the number of tumours of any sort. There are no comparable figures for MG Patients, but, on the basis of current knowledge, there is little cause for alarm.

 

STEROIDS

These drugs receive a bad press, and yet there is no doubt that there are life-saving in many diseases, including MG and their use has enormously improved the treatment of MG and related diseases. They act in the same way as Azathioprine, by depressing the BODY's immune system.

The first thing to make clear is that these are not the steroids taken by some athletes and about which so much is written. These are more correctly named anabolic steroids, whereas those used for MG are properly known as corticosteriods, although for the sake of complicity I shall refer to them simply as "sterods". They occur naturally in the BODY as part of its defence and messenger systems although the dosage used in medicine are usually much higher than those occurring naturally. The most commonly used drug in this group is prednisolone, but others may be used, including prednisone, hydrocortisone and dexamethasone. They have numerous unwanted effects of varying severity and importance. All of these are less severe if steroids are taken on alternate days, rather than daily.

(i) Weight and Appearance

This is the affect which concerns patients the most and Doctors the least. Sterods alter the distribution of BODY fat, causing more fat on the face and trunk, with less on the legs and arms, giving a general picture which has been graphically described by one of my colleagues as that of a lemon on two matchsticks. Like most of the unwanted effects of steroids, this one varies in severity according to the dose and individual susceptibility. Most patients will notice little alteration in their appearance at maintenance doses of 10-15mg per day. There is also no doubt that many patients gain a lot of weight when taking steroids. This is due not so much to an affect on metabolism as to stimulation of the appetite and can be controlled by careful attention to diet. Another unfortunate affect is the occurrence of a skin rash like acne, which may require treatment to control it.

(ii) Effects on glucose handling

Steroids make the BODY less capable of dealing with glucose and other sugars. They therefore adversely affect diabetic patients, who may require an increase in the dose of their injection or tablets, and they may also induce mild diabetes in patients who didn't previously have it. Again, strict dietary control may be necessary to counter effect this.

(iii) Thinning of bones

This is probably the most serious long-term unwanted affect of steroids. It is part of a generalised effect on BODY tissues that also involves muscle and skin (see below). It results in thinning and consequently in weakening of bones and particularly of the bones in the spine and the pelvis. This may result in fractures which can occur after a mild injury or even spontaneously. The affect is worse in those who are already at risk of thinning of their bones, i.e. older people and women past the age of childbearing. It is most likely to occur at doses of 10mg per day or more, and at maintenance levels of 7.5 mg or less one is pretty safe from this complication. It is now well established that exercise particularly weight-bearing exercise such as walking and aerobics helps to avid or reverse the bone thinning associated with ageing. and it is probable that it will also protect against the effects of steroids. It is also important to have am adequate diet with plenty of calcium, protein and Vitamin D. There are now also available drugs (such as etidronate) which are being used successfully to treat bone thinning.

(iv) Effects on other BODY tissues

Steroids tend to break down BODY tissues, and particularly to deplete them of protein. This results in the bone thinning already discussed, and also in wasting of the muscles and thinning of the skin. Muscle wasting results in weakness. It can be counteracted by exercises, although they have to be quite severe and really stress the muscles, which may be impossible in MG. Thinning of the skin leads to it being easily cut or broken, and also to increased susceptibility to the affects of sunlight.

(v) Salt and Water Retention

Steroids form part of the BODY's natural system of conserving salt and water. Steroid treatment sometimes therefore leads to abnormal retention of salt and water in the BODY, with some puffiness or swelling around the ankles which is not a serious problem.

(vi) Psychological Effects

To those of us who take steroidų, and also our families and friends, the mental effects are striking, especially on alternate day treatment when we can appreciate the contrast between steroid and non-steroid days. Elation, feeling like superman, talkativeness - these and similar feelings will be readily recognised by may of you. Families and friends of MG Patients on steroids will often recognise uncharacteristic irritability on steroid days. Occasionally, more profound and worrying psychological symptoms may occur, and serious depression can result - but usually only if this tendency was present before the start of treatment.

(vii) Insomnia

This is a common accompaniment of steroid therapy, and can be sufficient of a nuisance to require treatment with mild sedatives or tranquillisers taken at night.

(viii) Susceptibility to Infection

The same considerations apply to steroids as were described above for Azathioprine - only more so!

(ix) Effects on the stomach

Steroids irritate the lining of the stomachࠠand gullet ࡡnd often cause quite severe indigestion. Tablets should never be taken on an empty stomach. Less frequently they cause stomach or duodenal ulcers. Fortunately, modern treatment of these problems is safe and effective, and does not adversely affect MG.

(x) Effects on the BODY's reaction to stress

Normally, when we are in a situation of physical or psychological stress, the BODY reacts by increasing its output of steroids. This automatic regulation is lost when we take steroid treatment, and so it is vital, in order to cover unforeseen emergencies, to carry a card or wear a bracelet stating that the bearer is on steroid treatment and giving the current dose and the phone number of a reliable hospital or general practice contact.

(xi) Cataract

There is an increased chance of developing cataracts in the lenses of the eyes when taking sterods and unfortunately there seems to be no way of avoiding this.

This is a pretty frightening list and there are other, rarer, complications of steroid therapy which I have not described. However, I should like to re-emphasise three points I have made already.

* In doses equivalent to 10 mg per day, or less, you are very unlikely to run into serious trouble (and remember the importance of drugs like Azathioprine which enable one to reduce the steroid dose).

* Alternate day dosing reduces the incidence and severity of unwanted effects.

* For most of us, the benefits of steroid treatment far outweigh its risks.

MGA NEWS February 1997

<ņONT color=#ffff00 size=4>MGS Philippines

Rory Esperanza, President (1st from left)

Naty I�igo, Treasurer (2nd from left)

Dr. Carissa Dioquino, Consultant-in-Charge (3rd from left)

Dr. Marita B. Dantes, former Consultant-in-Charge (3rd from right)