Stimulating TSH receptor antibiodies increased DII activities via their nongenomic effects using sera of hyperthyroid Graves' ophthalmopathy, but anti-TPO antibodies could influence DII activities via altering FT<sub>4</sub> levels.
Among them, two patients (patient 1 and 4) were hyperthyroid and TSH receptor antibody (TRAb) positive, two patients (patient 3 and 5) were euthyroid and displayed slightly elevated TRAb titres, one patient (patient 2) was euthyroid and TRAb negative.
Expert opinion: Those agents that can interrupt the TSHR and IGF-IR pathways possess the potential for offering more specific and better tolerated treatments of both hyperthyroidism and TAO.
Previously, in an induced mouse model, injecting TSHR A-subunit protein attenuated hyperthyroidism by diverting pathogenic TSHR Abs to a nonfunctional variety.
Graves' disease is an autoimmune disorder that causes hyperthyroidism because of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyroid gland, triggering thyroid hormone release.
Graves' disease (GD) is an autoimmune thyroid disease defined by the production of stimulating autoantibodies to the thyroid-stimulating hormone receptor (TSHR) (TSAbs) that induce a sustained state of hyperthyroidism in patients.
Based on a literature search regarding all published TSHR mutations, this review covers several mutations which are clearly associated with a hyperthyroidism-phenotype, but interestingly show a lack of constitutive activity determined by in vitro characterization.
Thyroid-infiltrating activated T cells may lead to cell-mediated immunity, thyroid injury and eventually hypothyroidism, whereas humoral immunity via TSHR-stimulating antibodies may give rise to hyperthyroidism.
However, all affected patients with a TSH receptor mutation showed persistent hyperthyroidism regardless of subclinical or overt hyperthyroidism throughout the follow-up.
Hepatoprotective effect of satureja khuzestanica essential oil and vitamin e in experimental hyperthyroid rats: evidence for role of antioxidant effect.
In adults, autonomous adenomas of the thyroid causing hyperthyroidism are relatively common and are most often due to somatic mutations that increase the constitutive activity of the thyroid-stimulating hormone receptor (TSHR).
Curcumin differentially regulates the expression of superoxide dismutase in cerebral cortex and cerebellum of L-thyroxine (T₄)-induced hyperthyroid rat brain.
We report here that TSH and the pathogenic anti-TSHR antibodies that drive hyperthyroidism in GD induce IL-6 expression in fibrocytes and orbital fibroblasts.
Several lines of evidence indicate that the shed A-subunit rather than the full-length thyrotropin receptor (TSHR) is the autoantigen that triggers autoimmunity and leads to hyperthyroidism.
Because of the diffuse (99 m)Tc uptake and the negative TPO, TSHR, and thyroglobulin antibodies, genetic analysis of her TSHR gene was performed, in spite of her negative family history for hyperthyroidism.
Graves' disease, the production of thyroid-stimulating hormone receptor-stimulating antibodies leading to hyperthyroidism, is one of the most common forms of human autoimmune disease.
However, the comparison of the LRA values of sporadic TSHR mutations with LRA values of familial TSHR mutations does show a significantly higher median LRA value for sporadic as compared to familial autosomal dominant hyperthyroidism.
Although hereditary nonautoimmune overt hyperthyroidism is very rare, TSHR activating mutations as a cause of subclinical hyperthyroidism may be more common and should be considered in the differential diagnosis, especially if familial.