Graves’ is a disease of thyroid autoimmunity. The cause of thyroid autoimmunity remains unclear. See "basic ideas on immunology" here.
There are three diseases of thyroid autoimmunity:
Hashimoto's thyroiditis (thyroid enlarges and is often underactive).
Idiopathic hypothyroidism, (the result of Hashimoto's).
All three are closely associated, and in fact, overlapping syndromes. Patients can move from one to the other.
They all share immune reactivity to specific thyroid antigens and histological changes in the thyroid gland.
So, Graves' disease is not a disease of the thyroid, but an immune disease where an "attack" to the thyroid gland is present, leading to its dysfunction.
Graves' disease is an organ specific autoimmune disease, the same as diabetes.
It is a syndrome that includes two major categories of signs and symptoms:
Those that can be considered specific for Graves' disease, and induced by the autoimmunity:
-thyroid stimulation (hyperthyroidism)
-eye disease (ophthalmopathy, aka TED, TAO, GO, AGO)
-thyroid enlargement (goitre)
-dermal changes (pretibial myxedema)
Those that are caused by the excess thyroid hormone (thyrotoxicosis, or hyperthyroidism) and do not differ from those induced by any other cause of excess thyroid hormone.
Antibodies in Graves' disease
Can be classified into three general types -more details here-:
-TSAb - thyroid stimulating antibodies interact with the TSH receptor causing all aspects of thyroid stimulation, probably identical to the effects induced by TSH itself. If they predominate, the patient is said to have Graves' disease. Formerly known as LATS. Currently also known as TSI (thyroid stimulating immunoglobulin). Up to 90% to 95% of patients with Graves' disease have them, and newer assays shows nearly 100%.
The presence of TSAb is thought to be characteristic of Graves.
However, TSAb are typically associated with other antibodies, and cell-mediated immunity, which damages the thyroid or develops blocking antibodies, and the patient may become hypothyroid.
-TSBAb - Antibodies blocking the binding of TSH to the receptor, while not having stimulating function, they may induce hyopothyroidism, and the patient is said to have Hashimoto's thyroiditis or idiopathic myxedema.
-TBII - thyrotrophin binding inhibitory immunoglobulins, neither stimulate nor inhibit its function, but interfere with the binding of TSH to the receptor.
Probably all patients with Graves' disease have a mixture of all of these antibodies.
This is what happens to these antibodies under the three conventional therapies:
During antithyroid therapy TSAb tend to decline. It's also thought that anti-thyroid drugs have an immuno-modulator action, and the stimulant antibodies are replaced by others which have binding or blocking activity
After surgery, TSAb tend to decline too, if euthyroidism is achieved.
After radioiodine therapy, TSAb are raised during several months or a year, probably because of release of antigens. TSAbs gradually return to lower levels during the subsequent years.
Below an abstract of a paper published in the N Engl J Med 1994 Jun 16;330(24):1731-8. Published erratum appears in N Engl J Med 1994 Aug 25;331(8):559
The management of hyperthyroidism.
Franklyn JA, Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, United Kingdom.
Although effective treatments for hyperthyroidism are available, none is perfect.
Particularly with respect to Graves' disease, what is needed is a therapy directed at modulating the disease process itself rather than merely reducing the synthesis and secretion of thyroid hormones in the hope that the underlying Graves' disease will remit.
Greater understanding of the pathogenesis of Graves' disease, resulting from cloning of the thyrotropin receptor and better knowledge of the interactions between these receptors or other thyroid antigens and the immune system, may lead to such treatment.
Broad-spectrum immuno-suppression, with all its side effects, is not the answer; more focused therapies to inhibit the immune response to specific thyroid antigens may represent the treatment of the future.
Meanwhile, radioiodine therapy is the most effective and convenient method of achieving long-term control of hyperthyroidism, although at the cost of hypothyroidism in many patients.
PMID: 7910662, UI: 94247461
While we agree with what is said about addressing the immune response to thyroid antigens may represent the treatment of the future, we think that calling RAI an "effective and convenient" treatment can only be said by someone who did not undertake it.
So, the first (but not last!) Atomic Women observations:
If we consider that:
- Graves' is a disease of autoimmunity.
- Acting antibodies have been identified.
- Anti-thyroid drugs decrease them, and modulate them.
- Surgery also decreases them.
- On the contrary, RAI, raises them, hence eye disease is triggered in many cases.
Why, then, is RAI (radio-iodine, I-131) so rapidly and frequently pushed, even to young people, thus totally or partially destroying a gland which is of foremost importance for the body properly function?
Using antithyroid drugs, as done in other countries, preserving the organs intact, and giving the patient the opportunity of going into remission by correcting nutritional imbalances and adopting healthier habits would be pretty much medically correct, in terms of health for us (and specially U.S.) patients.
Rheumatoid arthritis is also an autoimmune disease. But, fortunately, limbs are not being amputated nor radiated.
Diabetes mellitus is also an autoimmune disease. And, fortunately, the pancreas is not being removed or radiated.
What is the point of irradiating and killing thyroid glands, which are fundamental for life?.