Graves Disease?

Question

Any one out here have Graves Disease? I do, mildly, and I struggle with it. I've been to all the Dr.'s and basically there is nothing that can be done. I'm ok in the mornings but as the day progresses it gets worse, but not too bad. I have to tilt my head to the right to see clearly, watch tv, etc. If you have it too, how do you deal with it?

Answer 1

I know people with this disease. For those who dont know what it is. Graves' Disease is a type of autoimmune disease that causes over-activity of the thyroid gland, causing hyperthyroidism. This over-activity is also sometimes called "toxic diffuse goiter." The thyroid gland helps set the rate of metabolism, which is the rate at which the body uses energy. When the thyroid is too active, it makes more thyroid hormones than the body needs. High levels of thyroid hormones can cause side effects such as weight loss, rapid heart rate and nervousness. This is an uncommon disease that affects 2 percent of all women at some time in their lives. Graves’ Disease also tends to affect women between the ages of 20 and 40, although it occurs in infants, children, and the elderly.

Dealing with this takes a lot of effort and continued visits to the doctors, medication, treatments and even surgury. The extreme cases may require removal of the thyroidn gland and hormone replacement therapy for the rest of your life. My suggestion is to eat diets rich in calcium, milk, cheese, yogurt, as well as reviewing natural cures for diseases.

Answer 2

1

Answer 3

I do not have it but i have a very close friend who has it.
She was the same way. She got some steriods and it use make her feel good most of the time except for when she doesn't take it.
She got glasses to see better because he eye sight got worst, and she also had it so people wouldn't stare at how glaring her seys were.
I do not know what part of the world you are in but if you looking for real good medical attention, hope on a plan and go to Cuba.
They have some of the best doctors there.
Make calls and find out if they would be able to tell you anything different from what your doctors have told you.
Keep well!

Answer 4

i be attentive to precisely what you're dealing with. i grew to become into clinically determined with Graves approximately 3 months in the past, and that i could quite go through with an overactive thyroid than have the iodine remedy and finally end up with an underactive one. start up out on the medicine, i'm taking Neo-Mercazole two times an afternoon on the 2d. this is going to take a minimum of a few months for them to locate the nicely suited dose which you would be able to take long term. in case you will get it under administration with drugs, do it. it extremely is a a lot greater effective determination interior the long-term. My medical doctors are predicting 18 months of drugs then I could desire to have the skill to regulate it myself. the concern with Graves is that your physique is generating thyroid antibodies. In one million/2 of all Graves sufferers, those antibodies attack your thyroid and finally end up damaging it besides. there is not any thank you to grant up this happening, no rely once you get remedy. you have a 50% danger of having an underactive thyroid as quickly as the Graves burns itself out. good success, i'm hoping you get it under administration quickly.

Answer 5

What do you mean there is nothing that can be done? Sure, there is no cure, but it can be very easily treated. I think you need a new doctor if your doctor told you that nothing can be done. Here is what you do: get a prescription for methimizole. It's that simple!

Answer 6

Graves-Basedow disease, also known simply as Graves' disease, is a medical disorder that may manifest several different conditions, including goitre and hyperthyroidism (over-activity of thyroid hormone production), infiltrative exophthalmos (protuberance of one or both eyes and associated problems) and infiltrative dermopathy (a skin condition usually of the lower extremities). This disorder is the most common cause of hyperthyroidism. It is known to be related to an antibody mediated type of auto-immunity, but the trigger for the reaction is unknown.

Incidence and epidemiology
The disease occurs most frequently in women (8:1 compared to men). It occurs most often in middle age (most commonly in the third to fifth decades of life), but is not uncommon in adolescents, during pregnancy, at the time of menopause and in people over age 50. There is a marked family preponderance, which has led to speculation that there may be a genetic component. To date, no clear genetic defect has been found that would point at a monogenic cause.


[edit] Etiology
The causes of this disease are unknown, but it is generally felt that genetic and environmental factors contribute to its development.[1] With this being an autoimmune disease which appears suddenly, often quite late in life, a cross reaction by the body to a viral disease is one suspected cause (this is a similar mechanism to that postulated for some cases of type I diabetes).

One possible candidate is infection with yersinia enterocolitica (a cousin of the plague bacteria), but whilst there is indirect evidence for the structural similarity between the bacteria and the human thyrotropin receptor, direct causative evidence is limited.[1] Yersinia seems not to be a major cause of this disease, although it may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.[2] It has also been suggested that yersinia enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility.[3] More recently the role for yersinia enterocolitica has been disputed.[4]


[edit] Signs and symptoms
Graves-Basedow disease is a disorder characterized by a triad of hyperthyroidism, goitre, and exophthalmos (bulging eyeballs).

Due to the many physiological actions of thyroid hormone, many symptoms and signs are linked to Graves' disease:

Cardiac: cardiac arrhythmias (especially atrial fibrillation), tachycardia (increased heart rate), collapsing pulse and widened pulse pressure (difference between systolic and diastolic BP) and congestive cardiac failure with peripheral edema, ascites, anasarca.
Endocrine: weight loss in the presence of increased appetite, intolerance to heat, elevated basal metabolic rate. In premenopausal women, there may be a reduction in the amount of menses (oligomenorrhea).
Dermatological: profuse sweating, thyroid acropachy (clubbing) of the fingernails, onycholysis (fingernail destruction), palmar erythema, pretibial myxedema (3 to 5% of Graves' patients, not to be confused with the myxedema of hypothyroidism)
Neurological: tremor (especially noticeable on extending the arms), apprehension, weakness, headache, proximal myopathy (difficulty rising from a chair or squatting position), restlessness, and hyperactive deep tendon reflexes
Gastrointestinal: diarrhea (common), vomiting (rare)
Ophthalmological: thyroid eye disease (TED) characteristic of Graves' disease include lid retraction (Dalrymple sign) above the superior corneoscleral limbus, lid lag (von Graefe's sign), exophthalmos (forward displacement of the globes), periorbital swelling and chemosis. Visual field defects may be present if periorbital swelling puts pressure on the optic nerve. The patient may complain of dry eye due to incomplete lid closure.
Stomatological: multiple dental caries, parodontitis (rare).
Graves disease can lead to extreme hyperthyroidism which is life-threatening. This is called thyroid storm.

Because similar antibodies to those stimulating the thyroid may also react with the eye muscles, patients may develop an enlargement of the ocular muscles with resultant forward movement of the eyeball (proptosis, also called exopthalmos) and inflammation of the tissues around the eye. Enlargement of the eye muscles may result in difficulty with proper movement and coordination of the eyes, and cause double vision and an obvious disparity in the relative position of both eyes. Difficulty in closing the eyelids may lead to eye dryness and occasionally corneal ulceration.

The ocular manifestations of Graves-Basedow disease are more common in smokers and tend to worsen (or develop for the first time) following radioiodine treatment of the thyroid condition. Thus, they are not caused by hyperthyroidism per se; this common misperception may result from the fact that hyperthyroidism from other causes may cause eyelid retraction or eyelid lag (so-called hyperthyroid stare) which can be confused with the general appearance of proptosis/exopthalmos, despite the fact that the globes do not actually protrude in other causes of hyperthyroidism. Also, both conditions (globe protrusion and hyperthyroid lid retraction) may exist at the same time in the hyperthyroid patient with Graves-Basedow disease.


[edit] Diagnosis
On the basis of the signs and symptoms, thyroid hormone (thyroxine or T4, triiodothyronine or T3) and thyroid-stimulating hormone (TSH) are determined in the medical laboratory. Free T4 and Free T3 is markedly elevated, while TSH is suppressed due to negative feedback. An elevated protein-bound iodine level may be detected. A large goiter is sometimes seen on X-rays.

Thyroid-stimulating antibodies may be detected serologically.


[edit] Pathophysiology
Grave's disease is an example of a type II hypersensitivity autoimmune disorder. Most features are due to the production of autoantibodies that bind to the TSH receptor, which is present on the follicular cells of the thyroid (the cells that produce thryoid hormone). These antibodies activate the cells in the same fashion as TSH itself, leading to an elevated production of thyroid hormone.

The infiltrative opthalmopathy (thyroid eye disease) that is frequently encountered has been explained by the expression of the TSH receptor on retroorbital tissue.

The exact cause of antibody production is not known. Viral infection may trigger antibodies against its epitopes, which cross-react with the human TSH receptor. There appears to be a genetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.


[edit] Treatment
Medical treatment of Graves' disease includes antithyroid drugs, radioactive iodine and thyroidectomy (surgical excision of the gland).

Treatment of the hyperthyroidism of Graves-Basedow disease may be with medications such as methimazole or propylthiouracil (PTU), which reduce the production of thyroid hormone, or with radioactive iodine. Surgical removal of the thyroid is another option, but still requires preoperative treatment with methimazole or PTU. This is done to render the patient "euthyroid" (i.e. normothyroid) before the surgery since operating on a frankly hyperthyroid patient is dangerous. Therapy with radioactive iodine (I-131) is the most common treatment in the United States and in many other parts of the world. Thyroid blocking drugs and/or surgical thyroid removal is used more often than radioactive iodine as definitive treatment in Japan, perhaps because of general fear of radioactivity among many Japanese.

The development of radioactive iodine (I-131) in the early 1940s and its widespread adoption as treatment for Graves' Disease has led to a progressive reduction in the use of surgical thyroidectomy for this problem. In general, RAI therapy is effective, less expensive, and avoids the small but definite risks of surgery. Treatment with antithyroid medications must be given for six months to two years, in order to be effective. Even then, upon cessation of the drugs, the hyperthyroid state may recur. Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood cells.


[edit] Antithyroid drugs
The main antithyroid drugs are methimazole (US), carbimazole (UK) and propylthiouracil (PTU). These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous side-effect is agranulocytosis (1/250, more in PTU); this is an idiosyncratic reaction which does not stop on cessation of drug). Others include granulocytopenia (dose dependent, which improves on cessation of the drug) and aplastic anemia. Patients on these medications should see a doctor if they develop sore throat or fever. The most common side effects are rash and peripheral neuritis. These drugs also cross the placenta and are secreted in breast milk.


[edit] Radioiodine
This modality is suitable for most patients, although some prefer to use it mainly for older patients. Indications for radioiodine are: failed medical therapy or surgery and where medical or surgical therapy are contraindicated.

Contraindications to RAI are pregnancy (absolute), ophthalmopathy (relative- it can aggravate thyroid eye disease), solitary nodules. Disadvantages of this treatment are a high incidence of hypothyroidism (up to 80%) requiring hormone suppletion. It acts slowly and has a relapse rate that depends on the dose administered.


[edit] Surgery
This modality is suitable for young patients and pregnant patients. Indications are: a large goitre (especially when compressing the trachea), suspicious nodules or suspected cancer (to pathologically examine the thyroid) and patients with opthalmopathy.

Both bilateral subtotal thyroidectomy and the Hartley-Dunhill procedure (hemithyroidectomy on 1 side and partial lobectomy on other side) are possible.

Advantages are: immediate cure and potential removal of carcinoma. Its risks are injury of the recurrent laryngeal nerve, hypoparathyroidism (due to removal of the parathyroid glands), hematoma (which can be life-threatening if it compresses the trachea) and scarring.


[edit] Eye disease
For mild disease - artificial tears, steroid eyedrops, oral steroids (to reduce chemosis)
For moderate disease - lateral tarsorrhaphy
For severe disease - orbital decompression or retro-orbital radiation

[edit] If left untreated
If left untreated, more serious complications could result, including birth defects in pregnancy, increased risk of a miscarriage, and in extreme cases, death. Graves-Basedow disease is often accompanied by an increase in heart rate, which may lead to further heart complications. If the eyes are proptotic (bulging) severely enough that the lids do not close completely at night, severe dryness will occur with a very high risk of a secondary corneal infection which could lead to blindness. Pressure on the optic nerve behind the globe can lead to visual field defects and vision loss as well.


[edit] History
Ljunggren (1983) suggests that the Persian physician Sayyid Ismail Al-Jurjani should be credited with recognising the disease, having noted the association of goitre and exophthalmos, in "Thesaurus of the Shah of Khwarazm", the most famous of his five books, and the major medical dictionary of its time.

Caleb Hillier Parry (1755-1822) first noted the clinical picture in 1786, and it is reported in his posthumous collection of unpublished writings in 1825. It was also described by the Italians Giuseppe Flajani (1741-1808) in 1802 and Antonio Giuseppe Testa (1756-1814) in 1810. Robert James Graves (1797-1853) of Ireland in 1835, and Karl Adolph von Basedow of Germany in 1840, independently reported the constellation of symptoms. On the European Continent the term Basedow's disease is the more common, while it is known as Graves' disease in the English-speaking world.


[edit] Noted sufferers
United States President George H. W. Bush developed new atrial fibrillation and was diagnosed in 1991 with hyperthyroidism due to the disease and was treated at Walter Reed Army Medical Center with radioactive iodine. By coincidence (or so it is presumed, since the ultimate cause of this disease remains unknown), the president's wife Barbara Bush also developed the disease about the same time, which in her case produced severe infiltrative exopthalmos and a cosmetic change in the appearance of her eyes.
Canadian Minister of Human Resources and Social Development Diane Finley announced in the House of Commons that she was suffering from the disease. She now wears sunglasses to protect her eyes from the bright lighting in the chamber.
Nadezhda Krupskaya (1869-1939), wife of Vladimir Lenin was believed to have suffered from the disease, which caused her eyes to bulge and her neck to tighten. This was the reason that her Bolshevik codename was 'Fish'. Since Graves' Disease disrupts the menstrual cycle, it is believed that this is why the couple never had children.
Bobby Engram, NFL wide receiver with the Seattle Seahawks, formerly of the Chicago Bears, Penn State Nittany Lions, and Camden High School Bulldogs (diagnosed October 2006)