BASEDOW-GRAVES HASTAL PDF

Graves hastal ve gebelik graves hastal genellikle gebeliin 2. Basedow graves hastal nda %50 sklkla rastlanan ve %2 kadarnda ise ar olarak nitelenebilen. Graves-Basedow disease (GBd) since late fifties has been considered to be autoimmune thyroid disorder where the presence of thyroid. Graves Hastal›¤›nda ve Graves Oftalmopatisinde Tiroid Otoantikor Düzeyleri .. treatment on circulating thyrotropin-receptor antibodies in Basedow’s disease.

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Graves-Basedow disease GBd since late fifties has been considered to be autoimmune thyroid disorder where the presence of thyroid stimulating antibodies TSAb may lead to hyperthyroidism, thyroid orbitopathy and thyroid dermopathy.

During last years it was generally accepted that development of Graves-Basedow disease is dependent on the presence of two or three groups of factors – genetic and environmental or genetic, environmental and endogenous. Familial clustering of GBd, familial presence of hasyal autoantibodies and high concordance in the incidence and clinical course of the disease in monozygotic siblings all suggested that several genes decide about susceptibility to this disorder and likely its phenotypes.

On the other hand environmental agents and endogenous factors served as triggers important to the development of the disease, its clinical course and response to given therapy. It was believed that finally, development of GBd and other autoimmune disorders is a consequence of lack of balance between the formation of self reactive T cells and central and peripheral tolerance. As a result thyroid was infiltrated by self reactive T cells that in turn affected B cells and led to the production of thyroid stimulating antibodies.

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Graves’ disease – Wikipedia

Most recently hastwl of GBd became further complicated by both clinical and molecular findings. First, GBd can be clinically presented as a hypothyroidism depending on the switch of TSAb production to thyroid blocking antibody TBAb production as well as vice versa. Some findings suggest that in prone classically hyperthyroid patient the administration of methimazole can provoke switch off of TSAb generation and start of TBAb followed by block of thyroid hormones biosynthesis and quite rapid morphological damage of thyroid cells.

It is a pity that in other hypothyroid patient administration of thyroxine can switch on the generation of TSAb and switch off the basedow-gravess of TBAb. In addition presence of GBd disease in patients with DTC leads to increased mortality of cancer patients. In addition to these clinical observations, the pathogenesis of GBd during the last baasedow-graves years was strongly affected by studies suggesting that non sufficient peripheral tolerance was a key to autoimmunity in general, including mechanisms leading to development of Graves-Basedow disease.

In a way we returned to Volpe hypothesis developed in the ies of the previous century that pointed out the role of T-suppressor cells. At present the name suppressor cells was postponed and we know that control of self reactive T cells is a function of T regulatory cells Tregs.

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It has been proven basedow-grave block of activation of Tregs both in experimental animals and humans led to the development of generalized fatal autoimmunity. The progress in our knowledge concerning autoimmunity as a whole and GBd as a thyroid autoimmune disorder clearly shows that pathogenesis of this disorder is more complex than previously expected and that personalized approach to given patient based on clinical and molecular findings is more important than the hope that single finding light in corridor brings a positive solution for all patients with Graves-Basedow disease.

National Center basedow-gaves Biotechnology InformationU.

Etiopathogenesis of Graves-Basedow disease; where we are and where we are going

bsaedow-graves Journal List Thyroid Res v. Published online Apr 5. Author information Article notes Copyright and License information Disclaimer. Supplement 4th Congress of the Polish Thyroid Association Publication of this supplement was funded by the Polish Thyroid Association.

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