Is hyperthyroidism hereditary
Hyperthyroidism: causes & risk factors
Thyroid function is controlled by the pituitary gland thyroid-stimulating hormone (TSH) to ensure normal production of T3 and T4. The concentration of the free hormones (fT3, fT4) is decisive here, with the vast majority of T3 and T4 being bound to a specific protein (TBG = thyroxine-binding globulin) or to albumin.
This form of hyperfunction can typically be accompanied by bulging of the eyeballs and other changes in the eyes, e.g. eyelid edema (Graves disease or Graves disease). Typically lower leg edema (so-called pretibial myxedema) can also occur. Without these specific signs one speaks of an immune hyperthyroidism type Graves. The causes for the development of this autoimmune disease are unclear; hereditary predispositions, psychological stress and smoking are assumed to be favorable factors.
This immune-related hyperthyroidism is caused by the body's own defense substances (so-called antibodies), which are normally supposed to protect the body from infection with pathogens (vaccination principle). In this case, however, the antibodies direct their action against the body's own structures and are therefore called autoantibodies. The stimulating thyroid autoantibodies stimulate the thyroid cells to produce more hormones. Since the thyroid hormones in turn have an inhibitory effect on the control hormone TSH, an overactive thyroid can be detected on the basis of a reduced or non-measurably low TSH level in the blood.
Overfunction through autonomies
So-called autonomy of the thyroid gland can also lead to hyperfunction. A functional autonomy (further terms: thyroid autonomy, unifocal autonomy, multifocal autonomy, disseminated autonomy) describes the fact that parts of the thyroid gland (e.g. individual nodes) or the entire thyroid gland (which is then penetrated by diseased cells) produce thyroid hormone without the central one Control by the brain (control circuit of the hypothalamus, pituitary and thyroid glands) to obey. In the case of autonomy, one or more definable regions or the entire thyroid gland are involved in a TSH-independent excessive production of T3 and T4. You will then produce too much hormone regardless of the actual need. TSH is in turn suppressed or is at least reduced. A chronic iodine deficiency promotes the development of autonomy, even if the reasons for this have not yet been clearly clarified.
If a patient has a predisposition to overactive and receives excessive amounts of iodine over a long period of time, iodine-induced hyperfunction can develop. This is the case in around 15% of all overactive thyroid glands. This is usually done with drugs or foods containing iodine (e.g. seaweed), which are intended to prevent goiter. However, X-ray contrast media, disinfectants or medication (e.g. for the respiratory tract) can also contain large amounts of iodine and thus be triggers.
Excessive dose therapy with thyroid hormones in case of goiter formation (goiter) or due to an underactive thyroid also leads to overactive (Hyperthyreosis factitia).
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