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                                  Graves Disease Page

     

              Grave DISEASE and  syndromes are autoimmune and easily and permanently treatable please read our e-book for permanent cures.

GRAVES' DISEASE

What is Graves’ disease?
What is an autoimmune disease?
What are the symptoms of Graves' Disease?
How do I know if I have this disease?
What is the treatment for this disease?
What could happen if this disease is left untreated?

See also . . .

What is Graves’ disease?

Graves' Disease is a type of autoimmune disease in which the immune system over stimulates the thyroid gland, causing hyperthyroidism. Over-activity of the thyroid gland is also sometimes called "diffuse toxic goiter." The thyroid gland helps set the rate of metabolism (the rate at which the body uses energy), and when it is over-stimulated, it produces more thyroid hormones than the body needs. High levels of thyroid hormones can cause difficult side effects. This is an extremely rare disease that tends to affect women over the age of 20. The incidence is about 5 in 10,000 people.

What is an autoimmune disease?

An autoimmune disease occurs when the body's immune system becomes misdirected and attacks the very organs, cells, or tissues that it was designed to protect. About 75% of autoimmune diseases occur in women, most frequently during their childbearing years.

What are the symptoms of Graves' Disease?

The most common symptoms of Grave’s Disease, or thyroid over-stimulation include insomnia, irritability, weight loss without dieting, heat sensitivity, increased perspiration, fine or brittle hair, muscular weakness, eye changes, lighter menstrual flow, rapid heart beat, and hand tremors. Grave’s Disease is the only kind of hyperthyroidism that is associated with inflammation of the eyes, swelling of the tissue around the eyes, and protrusion, or bulging, of the eyes. Some patients will develop lumpy reddish thickening of the skin in front of the shins called pretibial myxedema. This skin condition is usually painless. The symptoms of this disease can occur gradually or very suddenly and are sometimes confused with other medical problems. Women can have Grave’s Disease and have no obvious symptoms at all.

How do I know if I have this disease?

The only way to positively know if you have Graves' Disease is to visit your doctor. Your doctor will perform a simple blood test that will be able to tell if your body has the correct amount of thyroid hormones.

What is the treatment for this disease?

There are many treatments for Graves' Disease.

  • Medications: There are some prescription medications that can lower the amount of thyroid hormones produced by the body, regulating them to normal levels.

  • Surgery: Part or all of the thyroid gland will be removed. In most cases, people who have surgery for Graves' Disease will develop an under-active thyroid (hypothyroidism), and will have to take thyroid replacement hormones for the rest of their lives.

  • Radioactive iodine: The iodine damages thyroid cells to shrink the thyroid gland, to reduce hormone levels. Like surgery, this condition usually leads to hypothyroidism, requiring medication for the rest of the patient's life.

After a diagnosis is made and a treatment is selected, you should return to your health care provider annually to make sure that your thyroid levels are normal and do not need to be adjusted.

What could happen if this disease is left untreated?

If left untreated, Grave's Disease can lead to more serious complications, including birth defects in pregnancy, increased risk of a miscarriage, and in extreme cases, death. Graves’ Disease is often accompanied by an increase in heart rate, which may lead to further heart complications.

 

 
Harefuah. 2001 May;140(5):392-4, 455, 454. Related Articles, Links

[Intravenous immunoglobulins treatment of patients with Graves' ophthalmopathy]

[Article in Hebrew]

Leibe A, Levy Y, Shoenfeld Y.

Department of Medicine B and Research Unit of Autoimmune Diseases, Chaim Sheba Medical Center, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University.

Graves' ophthalmopathy is an autoimmune disease manifested as exophthalmus, lid lag and diplopia. As in the accompanying autoimmune thyroid disease, there is an autoimmune homonal and cellular attack on the orbita, mainly the retro-orbital tissues. Steroids are the cornerstone of therapy. We reviewed the evidence for a similar therapeutic effect of i.v., immunoglobulins (IVIGs) and their better side affect profile as compared to steroids. We also described an impressive therapeutic success with IVIG given to a patient with resistant ophthalmopathy. The clinical picture of Graves' ophthalmopathy is attributed to a pathologic hyper--activation of orbital fibroblasts, deposition of collagen and glycosaminoglycans in the extra-cellular matrix and eventually fibrosis. These are mediated by leucoregulin, IL-1, IFN-gamma, and TGF-beta--all secreted by lymphocytes and mast cells in the retorbital space. Another mode of cell activation is by binding of autoantibodies (presumably thyroid stimulating Ab's) to an antigenic determinant on the surface of fibroblasts. I.v. immunoglobulins, known today to be active in a variety of autoimmune processes, exert their effect on autoantibodies, complement, phagocytic cells etc. IVIGs also inhibit orbital lymphocytes and fibroblasts through inhibition of IL-1 or/and TGF-beta.

Publication Types:
  • Case Reports

PMID: 11419058 [PubMed - indexed for MEDLINE]
 
Thyroid. 1997 Aug;7(4):579-85. Related Articles, Links

Intravenous immunoglobulin versus corticosteroid in treatment of Graves' ophthalmopathy.

Baschieri L, Antonelli A, Nardi S, Alberti B, Lepri A, Canapicchi R, Fallahi P.

Institute of Clinical Medicine II, University of Pisa, Italy.

We compared the effectiveness of systemic corticosteroids with the use of high-dose intravenous immunoglobulin (IVIG) in the treatment of Graves' ophthalmopathy. This was performed as a prospective, nonrandomized study including a blinded ophthalmological and orbital computed tomographic (CT) evaluation. The two groups of patients were not significantly different in relation to sex composition, age distribution, duration of Graves' disease, and ophthalmopathy and previous hyperthyroidism. All patients were followed up by endocrinologic evaluation and blinded ophthalmological (before therapy = B, at the end of therapy = E, and 6 months after the end = 6M) and orbital CT (B and E) evaluations. Twenty-seven patients treated with IVIG were followed up after the end of treatment for an average of 21 months (range 12 to 48 months). Soft tissue involvement (NOSPECS) improved or disappeared in 32 of 35 (90%) patients treated with IVIG and in 25 of 27 (92.5%) patients treated with corticosteroids. Diplopia improved or disappeared in 22 of 29 (75%) patients treated with IVIG and in 16 of 20 (80%) patients treated with corticosteroids. The results observed by clinical evaluation were confirmed with orbital CT score in 30 IVIG patients and in the corticosteroid-treated patients; a significant reduction of extraocular muscle thickness was observed after treatment in both groups. Proptosis improved or disappeared in 20 of 31 (65%) patients treated with IVIG and in 15 of 24 (62%) patients treated with corticosteroids. Mean values of proptosis evaluated by Hertel's exophthalmometer showed a slight reduction both in IVIG as well as in corticosteroid-treated patients. It is interesting to observe that in 28 IVIG-treated patients in whom it was possible to evaluate soft tissue involvement, proptosis and diplopia in the period between the fifth and sixth month from the start of therapy, the most important part of the amelioration (if responders) was already obtained at that time. Responder patients were defined in relation to the decrease in the highest NOSPECS class or grade. Among IVIG-treated patients 26 of 34 (76%) responded; while in the corticosteroid group 18 of 27 (66%) responded to treatment. The prevalences of patients who responded to the treatments were not significantly different in the two groups (Chi-square). The initial values of the subjective eye score were similar in the two groups, and a significant reduction was observed in both. Major side effects requiring discontinuation of the corticosteroid therapy were observed in two patients with hemorrhagic gastritis and in one patient with manic-depressive psychosis. Among 15 patients submitted to the evaluation of bone mineral content before and after corti-costeroid therapy, 4 presented signs of osteoporosis and 3 a reduction of bone mineral content. Moderate and minor side effects were more frequently noted in steroid-treated patients than in the IVIG group. These data suggest that IVIG is safe and effective in reducing the eye changes in patients with Graves' ophthalmopathy.

PMID: 9292946 [PubMed - indexed for MEDLINE]

 

 

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