21 Energy-Saving Tips to Ease Life With Chronic Illness

By Lynda Shrager

Published Jul 28, 2014

Sometimes, even the simplest of tasks may seem daunting.
Especially for people living with a chronic illness, or those just coming home after hospitalization, weakness, limited joint motion, compromised breathing, and decreased endurance are common.
As an occupational therapist, my focus is to teach my patients how to combat fatigue so they can participate in more activities within their physical limits. One method I like uses energy conservation and work simplification techniques to fight fatigue.

Conserve Your Energy for the Important Things in Life

The first thing you need to learn is how to pace yourself.  You can do this by planning ahead and organizing your daily schedule with a balance of strenuous and easy tasks. Leave ample time to complete your tasks so you don’t feel rushed and under pressure.
For example, I suggest to my patients that they avoid early-morning doctor’s appointments as the pressure of getting up, bathing, eating breakfast and getting to the doctor on time can create a stressful scenario. Rather, try to get the first appointment following the staff’s lunch break as they won’t be running behind schedule yet. This gives you plenty of time in the morning to get everything done and still get there on time.

Work Simplification: Sit Wisely, Prioritize, Delegate

The principles of work simplification include sitting to work as much as possible.  When you’re sitting, choose a firm surface with arm rests.  Soft couches and chairs, although tempting, are hard to get out of.  Organize work areas so the bulk of activity occurs at waist height and close to your body, so you can avoid bending, over-reaching, and stooping.  Instead of lifting heavy objects, slide them.  Avoid strenuous arm motions.  If you must pick up objects, bend your knees or squat rather than bending from your back.
Prioritize important tasks, and delegate to others whenever possible.  Remember to save your energy for things you most want to do.  Get to know your own activity tolerance, and stop if you feel symptoms of fatigue such as muscle stiffness, weakness, and shortness of breath.

Try These Strategies to Save Time and Energy

Use the following organizing tips to conserve energy and complete daily tasks and self-care in the most effective way:
Self-care activities in the bathroom:

1. Sit in front of the sink for hair care, makeup, and shaving.
2. Use a long-handled bath brush for your back and feet.
3. Wrap yourself in a terrycloth robe rather than using towels to dry yourself.
4. Sit on a shower bench and use a hand-held shower hose.
5. Keep your hair in an easy-to-care-for style.
6. Use a raised toilet seat and/or toilet safety rails.

When you’re dressing:

1. Gather all of your clothes before you start getting dressed.
2. Sit on a bed or a chair to dress.
3. Dress your lower body first as this takes more energy.
4. Put your underwear on, then pull it up to your knees; put your pants on, then pull them up to your knees; stand once and pull both up at the same time.
5. Choose front-opening, loose-fitting clothes.
6. Choose clothes with elastic waistbands because they’re easiest to manage.
7. If you can’t use slip-on shoes, consider elastic shoe laces.  Bring your feet up to your tie laces; footstools are helpful for this.  Use long-handled shoe horns to avoid bending.
8. If a limb is sore, weak, or otherwise compromised, put that arm or leg into the shirt or pants first and take it out second when you’re undressing.

In the kitchen:

1. Store items according to use, putting most-used items at waist level or above and less-used items below waist level.
2. Consider leaving your most-used items out on the counter.
3. Plan one-dish meals, consider using a Crockpot or other slow cooker, and try prepared mixes and frozen foods.
4. Use a wheeled cart for carrying food from the kitchen to the table and cleaning up after.
5. Slide filled pots, mugs, and other containers along countertops or the stove rather than lifting them.
6. Ease food prep using electric appliances.
7. Use disposable paper goods and utensils to minimize clean-up.

Top Detox Foods To Help The Immune System Help Myasthenia Gravis October 2, 2015 In category Womens Health

Myasthenia gravis is a chronic autoimmune neuromuscular disease, with symptoms of weakness and fatigue of the skeletal (voluntary) muscles of the body, in particular, the eye muscles, the face and throat muscles, as well as muscles in the arms and legs. Oddly enough, after periods of rest, some of the symptoms may improve. Having said that, myasthenia gravis affects the way of everyday living, such as vision, facial expression (facial muscles), breathing, talking, chewing and swallowing, as well as body movements.

Myasthenia gravis is only one of the many autoimmune diseases affecting humans. At present, the medical community is still very much uncertain about how an autoimmune disease may develop in an individual, although there is increasing evidence linking environmental agents to autoimmune diseases. These environmental agents include infectious agents, such as viruses, pharmaceutical and chemical agents, heavy metals, dietary factors, as well as a number of biological agents, including the genetic factor.

The human immune system is complicated, and, as such, affects the whole body system in many different ways. A healthy immune system protects the body, while an impaired immune system opens the door to diseases and viruses. It is, therefore, important to have a healthy immune system, without which the body’s own innate self-healing mechanism may become dysfunctional. It is believed that an autoimmune disease is caused by a dysfunctional immune system attacking the body system, instead of attacking external invaders into the body.

The first step to protect the immune system is to detox the body. You may have a toxic body when you often experience fatigue, headache, insomnia, indigestion, and all types of physical pain. Even if you do not have those symptoms, strengthening the immune system will reduce many of the symptoms of myasthenia gravis.

Some of the top detox foods to help the immune system help myasthenia gravis are as follows:

Seaweed: It contains high doses of minerals, such as calcium, iodine, iron, and magnesium, which bind with radioactive wastes from polluted soils and waters, according to research at McGill University in Canada. Seaweed is an inexpensive sea vegetable. Use seaweed in soup.

Avocado: It is rich in glutathione antioxidant, which is effective in removing toxins from too much alcohol consumption. Eat an avocado for breakfast; it is filling and saves you time.

Kiwi fruit: Like avocado, kiwi fruit is loaded with glutathione. In addition, it is rich in vitamin C. It is a powerful antioxidant to protect the immune system.

Apple: An apple a day keeps the doctor away. There is truth in that: apple is a powerful antioxidant and toxin remover due to its vitamin C and its fiber, pectin. Eat an apple everyday to keep your immune system healthy.

Beet: It contains methionine, which purifies natural waste products from the body. Beet has been used for centuries to purify blood. Make beet juice with carrot, or eat it raw in a salad.

Garlic: It contains allicin, which is a potent purifier of mercury and other toxic chemicals found in food additives. In addition, garlic alkalizes the body, making it more efficient in resisting disease. Put crushed garlic in all your cooking. If you wish to remove the odor from the breath due to garlic, chew some fresh parsley for a fresher breath.

Artichoke: It increases bile production to facilitate bowel movement. Steam artichoke and serve with meted butter.

Watercress: It increases detox enzymes. Watercress is especially effective in removing carcinogens from smokers, according to a UK study. Steam or put watercress in soup.

Cruciferous vegetable: Brussels sprouts, cabbage, cauliflower, and spinach are all effective in enhancing the liver in its production of enzymes for digestion and elimination. Eat them as much and as often as you can, either cooked or raw.

Strengthening the immune system is better than taking medications to deal with a compromised immune system.

Myasthenia Gravis Fact Sheet October 11, 2015 Lussy williams

What is myasthenia gravis?

Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means “grave muscle weakness.” With current therapies, however, most cases of myasthenia gravis are not as “grave” as the name implies. In fact, most individuals with myasthenia gravis have a normal life expectancy.
The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected.
 

What causes myasthenia gravis?

Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction—the place where nerve cells connect with the muscles they control. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travels from the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. These antibodies are produced by the body’s own immune system. Myasthenia gravis is an autoimmune disease because the immune system—which normally protects the body from foreign organisms—mistakenly attacks itself.

What is the role of the thymus gland in myasthenia gravis?

The thymus gland, which lies in the chest area beneath the breastbone, plays an important role in the development of the immune system in early life. Its cells form a part of the body’s normal immune system. The gland is somewhat large in infants, grows gradually until puberty, and then gets smaller and is replaced by fat with age. In adults with myasthenia gravis, the thymus gland remains large and is abnormal. It contains certain clusters of immune cells indicative of lymphoid hyperplasia—a condition usually found only in the spleen and lymph nodes during an active immune response. Some individuals with myasthenia gravis develop thymomas (tumors of the thymus gland). Thymomas are generally benign, but they can become malignant.
The relationship between the thymus gland and myasthenia gravis is not yet fully understood. Scientists believe the thymus gland may give incorrect instructions to developing immune cells, ultimately resulting in autoimmunity and the production of the acetylcholine receptor antibodies, thereby setting the stage for the attack on neuromuscular transmission.

What are the symptoms of myasthenia gravis?

Although myasthenia gravis may affect any voluntary muscle, muscles that control eye and eyelid movement, facial expression, and swallowing are most frequently affected. The onset of the disorder may be sudden and symptoms often are not immediately recognized as myasthenia gravis.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among individuals, ranging from a localized form limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles—sometimes including those that control breathing—are affected. Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, a change in facial expression, difficulty in swallowing, shortness of breath, impaired speech (dysarthria), and weakness in the arms, hands, fingers, legs, and neck.

Who gets myasthenia gravis?

Myasthenia gravis occurs in all ethnic groups and both genders. It most commonly affects young adult women (under 40) and older men (over 60), but it can occur at any age.
In neonatal myasthenia, the fetus may acquire immune proteins (antibodies) from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia gravis are temporary and the child’s symptoms usually disappear within 2-3 months after birth. Other children develop myasthenia gravis indistinguishable from adults. Myasthenia gravis in juveniles is uncommon.
Myasthenia gravis is not directly inherited nor is it contagious. Occasionally, the disease may occur in more than one member of the same family.
Rarely, children may show signs of congenital myasthenia or congenital myasthenic syndrome. These are not autoimmune disorders, but are caused by defective genes that produce abnormal proteins instead of those which normally would produce acetylcholine, acetylcholinesterase (the enzyme that breaks down acetylcholine), or the acetylcholine receptor and other proteins present along the muscle membrane.

How is myasthenia gravis diagnosed?

Because weakness is a common symptom of many other disorders, the diagnosis of myasthenia gravis is often missed or delayed (sometimes up to two years) in people who experience mild weakness or in those individuals whose weakness is restricted to only a few muscles.
The first steps of diagnosing myasthenia gravis include a review of the individual’s medical history, and physical and neurological examinations. The physician looks for impairment of eye movements or muscle weakness without any changes in the individual’s ability to feel things. If the doctor suspects myasthenia gravis, several tests are available to confirm the diagnosis.
A special blood test can detect the presence of immune molecules or acetylcholine receptor antibodies. Most patients with myasthenia gravis have abnormally elevated levels of these antibodies. Recently, a second antibody—called the anti-MuSK antibody—has been found in about 30 to 40 percent of individuals with myasthenia gravis who do not have acetylcholine receptor antibodies. This antibody can also be tested for in the blood. However, neither of these antibodies is present in some individuals with myasthenia gravis, most often in those with ocular myasthenia gravis.
The edrophonium test uses intravenous administration of edrophonium chloride to very briefly relieve weakness in people with myasthenia gravis. The drug blocks the degradation (breakdown) of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. Other methods to confirm the diagnosis include a version of nerve conduction study which tests for specific muscle “fatigue” by repetitive nerve stimulation. This test records weakening muscle responses when the nerves are repetitively stimulated by small pulses of electricity. Repetitive stimulation of a nerve during a nerve conduction study may demonstrate gradual decreases of the muscle action potential due to impaired nerve-to-muscle transmission.
Single fiber electromyography (EMG) can also detect impaired nerve-to-muscle transmission. EMG measures the electrical potential of muscle cells when single muscle fibers are stimulated by electrical impulses. Muscle fibers in myasthenia gravis, as well as other neuromuscular disorders, do not respond as well to repeated electrical stimulation compared to muscles from normal individuals.
Diagnostic imaging of the chest, using computed tomography (CT) or magnetic resonance imaging (MRI), may be used to identify the presence of a thymoma.
Pulmonary function testing, which generally call for immediate medical attention—may be triggered by infection, fever, or an adverse reaction to medication.

What are myasthenic crises?

A myasthenic crisis occurs when the muscles that control breathing weaken to the point that ventilation is inadequate, creating a medical emergency and requiring a respirator for assisted ventilation. In individuals whose respiratory muscles are weak, crises—which generally call for immediate medical attention—may be triggered by infection, fever, or an adverse reaction to medication.

h measures breathing strength, helps to predict whether respiration may fail and lead to a myasthenic crisis.

How is myasthenia gravis treated?

Today, myasthenia gravis can generally be controlled. There are several therapies available to help reduce and improve muscle weakness. Medications used to treat the disorder include anticholinesterase agents such as neostigmine and pyridostigmine, which help improve neuromuscular transmission and increase muscle strength. Immunosuppressive drugs such as prednisone, azathioprine, cyclosporin, mycophenolate mofetil, and tacrolimus may also be used. These medications improve muscle strength by suppressing the production of abnormal antibodies. Their use must be carefully monitored by a physician because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is abnormal in individuals with myasthenia gravis), reduces symptoms in some individuals without thymoma and may cure some people, possibly by re-balancing the immune system. Thymectomy is recommended for individuals with thymoma. Other therapies used to treat myasthenia gravis include plasmapheresis, a procedure in which serum containing the abnormal antibodies is removed from the blood while cells are replaced, and high-dose intravenous immune globulin, which temporarily modifies the immune system by infusing antibodies from donated blood. These therapies may be used to help individuals during especially difficult periods of weakness. A neurologist will determine which treatment option is best for each individual depending on the severity of the weakness, which muscles are affected, and the individual’s age and other associated medical problems.

What is the prognosis?

With treatment, most individuals with myasthenia can significantly improve their muscle weakness and lead normal or nearly normal lives. Some cases of myasthenia gravis may go into remission—either temporarily or permanently—and muscle weakness may disappear completely so that medications can be discontinued. Stable, long-lasting complete remissions are the goal of thymectomy and may occur in about 50 percent of individuals who undergo this procedure. In a few cases, the severe weakness of myasthenia gravis may cause respiratory failure, which requires immediate emergency medical care

What research is being done?

Within the Federal government, the National Institute of Neurological Disorders and Stroke (NINDS), one of the National Institutes of Health (NIH), has primary responsibility for conducting and supporting research on brain and nervous system disorders, including myasthenia gravis.
Much has been learned about myasthenia gravis in recent years. Technological advances have led to more timely and accurate diagnosis, and new and enhanced therapies have improved management of the disorder. There is a greater understanding about the structure and function of the neuromuscular junction, the fundamental aspects of the thymus gland and of autoimmunity, and the disorder itself. Despite these advances, however, there is still much to learn. Researchers are seeking to learn what causes the autoimmune response in myasthenia gravis, and to better define the relationship between the thymus gland and myasthenia gravis.
Different drugs are being tested, either alone or in combination with existing drug therapies, to see if they are effective in treating myasthenia gravis. One study is examining the use of methotrexate therapy in individuals who develop symptoms and signs of the disease while on prednisone therapy. The drug suppresses blood cell activity that causes inflammation. Another study is investigating the use of rituximab, a monoclonal antibody against B cells which make antibodies, to see if it decreases certain antibodies that cause the immune system to attack the nervous system. Investigators are also determining if eculizumab is safe and effective in treating individuals with generalized myasthenia gravis who also receive various immunosuppressant drugs.
Another study seeks further understanding of the molecular basis of synaptic transmission in the nervous system. The objective of this study is to expand current knowledge of the function of receptors and to apply this knowledge to the treatment of myasthenia gravis.
Thymectomy is also being studied in myasthenia gravis patients who do not have thymoma to assess long-term benefit the surgical procedure may have over medical therapy alone.
One study involves blood sampling to see if the immune system is making antibodies against components of the nerves and muscle. Researchers also hope to learn if these antibodies contribute to the development or worsening of myasthenia gravis and other illnesses of the nervous system.
Investigators are also examining the safety and efficacy of autologous hematopoietic stem cell transplantation to treat refractory and severe myasthenia gravis. Participants in this study will receive several days of treatment using the immumosuppressant drugs cyclophosphamide and antithymocyte globulin before having some of their peripheral blood cells harvested and frozen. The blood cells will later be thawed and infused intravenously into the respective individuals, whose symptoms will be monitored for five years.

Myasthenia Gravis Overview, Types, Incidence and Prevalence October 13, 2015 Lussy williams

Overview of Myasthenia Gravis

Myasthenia gravis (MG) is a chronic autoimmune disorder that results in progressive skeletal muscle weakness. Skeletal muscles are primarily muscle fibers that contain bands or striations (striated muscles) that are connected to bone. MG causes rapid fatigue (fatigability) and loss of strength upon exertion that improves after rest.

In early stages, myasthenia gravis primarily affects muscles that control eye movement (extraocular muscles) and those that control facial expression, chewing, and swallowing. If untreated, the disorder may affect muscles that control breathing (respiration), causing acute respiratory failure.

Types of Myasthenia Gravis

pr> Myasthenia gravis can be classified according to which skeletal muscles are affected. Within a year of onset, approximately 85–90 percent of patients develop generalized myasthenia gravis, which is characterized by weakness in the trunk, arms, and legs.

About 10–15 percent of patients have weakness only in muscles that control eye movement. This type is called ocular myasthenia gravis.

Other types of MG include congenital, which is an inherited condition caused by genetic defect, and transient neonatal, which occurs in infants born to mothers who have MG. Congenital MG develops at or shortly after birth and causes generalized symptoms.

Transient neonatal MG is a temporary condition that develops in 10–20 percent of infants born to mothers who have MG. Transient neonatal MG is caused by circulation of the mother’s antibodies through the placenta and it lasts as long as the mother’s antibodies remain in the infant (usually a few weeks after birth).

Incidence and Prevalence of Myasthenia Gravis

Myasthenia gravis affects approximately 2 out of every 100,000 people and can occur at any age. It is most common in women between the ages of 18 and 25. In men, the condition usually develops between 60 and 80 years of age.

 

Why Myasthenia Gravis An Autoimmune Disorder?

Artem is a doctor of veterinary medicine and has taught science and medicine at the college level.

This lesson will go over a condition called myasthenia gravis. We’ll talk about why it occurs, how your immune system is involved, how it can be treated, if it’s curable, and what typical signs it produces in a person.October 15, 2015 Smith

 

Autoimmune Disease

Most every one of us has played a game called ‘monkey in the middle’, or something along those lines. It’s basically where at least one person stands in between at least two other people who throw or kick an object like a ball to one another. The role of the monkey in the middle is to block the ball from getting through to the other person. Typically, as was the case when I was the monkey in the middle, the person in the middle has a hard time intercepting the ball.

But in some cases of autoimmune diseases, diseases where your own body attacks itself, the monkey in the middle is devastatingly effective. So effective, in fact, that it causes serious problems, as this lesson will address.

What is Myasthenia Gravis?

The terrible game that our body plays with us isn’t called monkey in the middle, it’s called myasthenia gravis. This is an incurable autoimmune disease that leads a person to develop severe muscle weakness and fatigue.

Although, as with many diseases, myasthenia gravis can occur at almost any age, it seems to affect more women under 40 and more men over 60 years of age, and in the United States affects about 20 individuals for every 100,000 members of the population.

Some of the most famous people in the world have suffered from this terrible disease, such as Aristotle Onassis, the billionaire Greek shipping magnate who married Jackie Kennedy after JFK’s assassination.

Why Does Myasthenia Gravis Occur?

Scientists are still working out the details of why myasthenia gravis may occur. We know that everything from genetics to immune reactions to drugs may increase the likelihood of developing this condition. Some researchers also believe the thymus , an organ located underneath your breastbone that is responsible for the proper development of the immune system, may play a role in the aberrations that occur in this disease. It has been noted that certain individuals with myasthenia gravis have a thymoma, or a tumor of the thymus.

What we do understand a bit better is the end result of most cases of myasthenia gravis. In this condition, your own body produces little proteins called autoantibodies, which are antibodies that target an individual’s own body, organs, cells, and receptors for destruction or inactivation.

Normally, antibodies are supposed to target foreign invaders such as bacteria and viruses for destruction or inactivation. But in an autoimmune condition such as myasthenia gravis, the antibodies become directed against auto, or self.

Specifically, these autoantibodies attach themselves to the receptors on the skeletal muscles of your body; these are the muscles responsible for locomotion. By doing so, the antibodies prohibit the receptors on the muscles from receiving a specific signal or destroy the receptors outright. Namely, this signal comes from nerves innervating the skeletal muscles. These nerves release a neurotransmitter that activates muscles of locomotion, called acetylcholine.

Under normal conditions, the nerves release this acetylcholine and it lands on its receptor on the muscle the nerve innervates. Once it lands on the receptor on this muscle, the muscle gets all excited, contracts, and allows you to move. The release of acetylcholine occurs at the neuromuscular junction, the place where nerves meet the muscles they innervate. The space between the nerve ending and the muscle it controls is known as the synaptic cleft.

That’s what happens normally. However, in people with myasthenia gravis the autoantibodies bind to the receptors on the muscle cells and thereby destroy or inactivate them.

You can liken the autoantibodies to our monkey in the middle, the nerve and muscle to our two players, the space between the two players as the synaptic cleft, the acetylcholine to our ball, and the receptors on the muscle cells to the hands of our player called ‘the muscle.’

The nerve player wants to pass the ball to the muscle player, but the monkey latches onto the hands of the muscle player and blocks the muscle player from ever catching the ball. If the ball can’t pass from one end to the other and can’t land in the muscle’s hands because those hands are blocked by the monkey, then the muscle player cannot become all excited about catching the ball, becomes depressed instead, and refuses to move because the game is no fun anymore.

Clinical Signs, Symptoms, and Diagnostics

Since the muscles are no longer excited to move, you shouldn’t be shocked by the typical signs and symptoms associated with myasthenia gravis, which means ‘grave muscle weakness’ through its ancient Latin and Greek roots. These signs include:

• Difficulty walking, eating, speaking, smiling, and swallowing
• Droopy eyelids and double vision
• In serious cases, respiratory failure, when the muscles of respiration can no longer work.

What is it like to have Myasthenia Gravis?

What is Myasthenia Gravis?

Myasthenia gravis is a neuromuscular disorder characterized by variable weakness of voluntary muscles, which often improves with rest and worsens with activity. The condition is caused by an abnormal immune response.

What is it like to have Myasthenia Gravis?

Common symptoms		What people are taking for it
Pain		Pregabalin, Hydrocodone-Acetaminophen, Codeine-Acetaminophen
Insomnia		Zolpidem, Clonazepam, Gabapentin
Fatigue		Amphetamine-Dextroamphetamine, Wheelchair (powered), Amantadine
Anxious mood		Alprazolam, Paroxetine, Lorazepam
Depressed mood		Bupropion, Diet and exercise, Escitalopram

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What do patients take to treat Myasthenia Gravis and its symptoms?

Treatments reported by members
Pyridostigmine (Kalymin 60N, Mestinon)
Prednisone (Pulmison, Pronizon, Deltasone, Encorton)
Intravenous Immuno Globulin IVIg (Carimune, Privigen, Pentaglobin, Sandoglobuline)
Azathioprine (Imurek, Azasan, Azapress, Imurel)
Plasmapheresis

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These charts show data from Myasthenia Gravis patients’ latest treatment evaluations

Last updated: June 20, 2014

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• Major
• Moderate
• Slight
• None
• Can't tell

• Severe
• Moderate
• Mild
• None

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Who has Myasthenia Gravis on PatientsLikeMe?

• 266 patients have this condition
• 3 new patients joined this month
• 192 say Myasthenia Gravis is their primary condition

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Age

Age	Proportion	# of patients
<20	3	3
20s	12	12
30s	36	36
40s	58	58
50s	75	75
60s	34	34
70+	15	15

Gender

Distribution of females vs. males

74%	Females
26%	Males

Age at first symptom

Age at first symptom	Proportion	# of patients
0-19 years	17	17
20-29

Genetic Research Reveals Possible New Targets For Treatment Of Myasthenia Gravis October 15, 2015 Smith

NEW YORK – A new genome-wide association study suggests that immunomodulating drugs already approved by the U.S. Food and Drug Administration (FDA) could benefit patients with myasthenia gravis.

Dr. Bryan Traynor, chief of the Neuromuscular Diseases Research Section at the National Institutes of Health in Bethesda, Maryland, and colleagues, found three different disease-associated loci in myasthenia gravis patients. One locus was at CTLA4, and the FDA has approved two CTLA4-targeting treatments, abatacept and belatacept, for treating rheumatoid arthritis and renal transplant patients, respectively.

The findings also showed two distinct, but overlapping, disease-associated loci for the early- and late-onset forms of the illness
 

“The discovery of a genetic locus is always an exciting thing, but often times it can take 10 to 15 years between the discovery of a particular locus and a first-in-humans clinical trial,” Dr. Traynor told Reuters Health in a telephone interview. The fact that drugs targeting CTLA4 are already FDA approved should accelerate that timeline, he added.

In their study, published online February 2 in JAMA Neurology, Dr. Traynor and his colleagues looked at DNA from more than 1,000 white, North American patients with acetylcholine-receptor antibody positive myasthenia gravis and nearly 2,000 controls.

They investigated associations between more than 8 million variants and myasthenia gravis risk. Significant association signals were found at CTLA4 (odds ratio, 1.37); HLA-DQA1 (OR, 2.31) and TNFRSF11A (OR, 1.31).

The CTLA4 and HLA-DQA1 associations were replicated in a cohort of 423 myasthenia gravis patients and 467 controls from Italy.

The analysis also confirmed past observations that myasthenia gravis strikes younger patients, who are usually female, as well as patients 60 and older who are usually male.

We were able to find different genetic loci that drive genetic susceptibility in each case,” Dr. Traynor said. “We genetically proved that they are two fundamentally different conditions, but overlapping conditions as well.”

The CTLA4 associations were seen in both early- and late-onset patients, the researcher noted. It’s likely, he added, that clinical trials testing CTLA4-targeting drugs in myasthenia gravis would enroll all patients with the illness, regardless of their genotype.

Even in patients who don’t have the CTLA4 variants he and his colleagues identified, Dr. Traynor noted, “it’s possible that in the other patients there are other variants in that region that are altering CTLA4 function, but we are not powered to pick it up.”

While effective therapy for myasthenia gravis is available, the researcher added, some patients with the disease do wind up having significant problems. “I think there is considerable room to grow new treatments,” Dr. Traynor said.

Dr. Robert Lisak of Wayne State University School of Medicine in Detroit co-authored an editorial accompanying the study.

“As in other complex immune-mediated disorders, there is an important influence of minor changes in multiple genes, likely interacting with the environment and with one another and their protein products, in the pathogenesis of myasthenia gravis,” Dr. Lisak told Reuters Health by email. “And in an autoimmune disease it is not surprising that the minor changes occur in genes for proteins that are critical in the immune response.”

“Identifying changes in genes in patients with different types of myasthenia gravis has the potential to help us understand which molecules and pathways in the immune system are the most important in development of disease,” he added. “In theory that might help in development of more-focused treatments for patients with myasthenia gravis. Only time will tell if this ultimately happens.”