In most patients with glandular disease, the thyroid gland is increased to 2 to a few times normal size, with tremendous dysplasia and biological process of the cyst cell lining into the follicles, so the number of cells is increased greatly. Also, each cell increases its rate of secretion severalfold; hot iodine uptake studies indicate that a number of these hyperplastic glands secrete endocrine at rates five to fifteen times traditional. The changes within the endocrine in most instances are almost like those caused by excessive thyrotropic hormone. However, plasma thyrotropic hormone concentrations ar but traditional rather than increased in most patients and sometimes are primarily zero. However, different substances that have actions almost like those of thyrotropic hormone ar found in the blood of virtually of these patients. These substances are immune serum globulin antibodies that bind with the same membrane receptors that bind thyrotropic hormone. They induce continual activation of the cAMP system of the cells, with resultant development of glandular disease.
These antibodies ar known as thyroid-stimulating immune serum globulin and ar selected TSI. they need a chronic stimulating impact on the endocrine, lasting for as long as twelve hours, in distinction to a touch over one hour for TSH. The high level of endocrine secretion caused by TSI successively suppresses anterior pituitary gland formation of thyrotropic hormone. The antibodies that cause glandular disease virtually certainly occur because the results of pathology that has developed against thyroid tissue. Presumably, at some time within the history of the person, AN more than thyroid cell antigens was free from the thyroid cells, and this has resulted within the formation of antibodies against the thyroid gland itself.