Thyrotoxicosis is the term used to describe the collection of symptoms that result from an excess of thyroid hormone, from any source. The disease that is responsible for 50–80% of all cases of thyrotoxicosis was first described in 1825 by Parry but has come to be known in the English-speaking world as Graves’ disease after the eminent 19th century physician, Robert Graves. Its prevalence in women is 1–2%, about 5–10 times the occurrence in men. There is a strong heredity component to this polygenic disorder, with at least eight genes implicated in the propensity for its development.

Graves’ disease is an autoimmune disease in which circulating antibodies directed against the TSH receptor are produced. These antibodies stimulate the TSHR, activating both Gsα and Gq signaling cascades. Thus the thyroid gland responds as if under continual stimulation by TSH (Table1). Since there is no feedback regulation of these antibodies, the result of their production is the unrestrained synthesis and secretion of T4 (and some T3) as well as growth of the thyroid tissue. The latter process leads to an enlarged thyroid gland, referred to as goiter.

Table1. Thyroid Responses to TSH

Treatment of Graves’ disease is focused on decreasing the high amounts of T4 being secreted by the overstimulated gland. This can be achieved chemically by inhibiting one or more of the steps of T4 synthesis and secretion with thionamides such as methimazole or propylthiouracil or iodide uptake by perchlorate, for example (see Figure 1). An additional approach to treating hyperthyroidism is destruction of the excessive thyroid tissue through surgery or administration of radioactive iodide.

Fig2. 3-iodothyronamine.

The occurrence of ophthalmopathy, the disorder associated with the eye orbital area, depends on the diagnostic procedure used and ranges from 10–25% (clinically evident) up to 70% (computed tomography scans) of individuals with Graves’ disease. The symptoms can range from mild enlargement of the extraocular muscles to vision-threatening disfigurement, with fewer than 5% exhibiting these severe symptoms. While the anti gen(s) involved in this part of the autoimmune response in Graves’ disease has not yet been definitively identified, the TSH receptor is a likely candidate. TSHR is expressed by orbital adipocytes, fibroblasts, and lymphocytes. Ocular fibroblasts participate in the softening and enlargement of the muscles and fat surrounding the eyeball causing its forward protrusion or exopthalmia. However, there is still much that is unknown about the genetic and immunological relationship between Graves’ disease and the ophthalmopathy associated with it.

There are other causes of hyperthyroidism besides the autoimmune disorder described here. They include: mutation in the TSHR gene resulting in increased activity; a functioning thyroid adenoma (toxic adenoma); a pituitary tumor secreting excess TSH.

اخر الاخبار

اخبار العتبة العباسية المقدسة

المجمع العلمي يقيم مهرجانًا بذكرى الولادات الشعبانية في بغداد

معهد القرآن الكريم النسوي يباشر استعداداته لإقامة مهرجان السقاء القرآني السنوي الخامس

بالتعاون مع جامعة ستانفورد.. جامعة الكفيل تعتمد منهجًا متطورًا لطب الطوارئ

سماحة السيد الصافي يستقبل وفد شركة (سيتي فارما) الباكستانية المختصة في الأدوية

المزيد

الآخبار الصحية

اللحظات الأخيرة قبل الموت.. هذا هو تسلسل "فقدان الحواس"

وخز الأطراف وضعف الذاكرة.. علامات على نقص فيتامين هام

عادة صباحية بسيطة.. تأثيرها قد يحسن ضغط الدم

عادات يومية تدمر قلبك بصمت.. خبراء يطلقون التحذير

المزيد

الآخبار التكنلوجية

الذكاء الاصطناعي يفك لغز آثار أقدام الديناصورات

القمر أولا.."سبيس إكس" تؤجل خططها الخاصة بالرحلات إلى المريخ

الذكور أم الإناث؟ دراسة "تنسف الشائع" بشأن التوحد

خبير يكشف عن اقتراب العلماء من فك شفرات "لغات الحيوانات" !

المزيد

مواضيع ذات صلة

Clinical Features of Hyper- and Hypothyroidism

Clinical Associations of Aplastic Anemia

Typical and Atypical Presentations of Aplastic Anemia

Pathophysiologic Pathways Leading to Aplastic anemia

Epidemiology of Aplastic anemia

Pneumonia

Bronchitis

Pathogenesis of the respiratory tract: Microorganism Factors

Pathogenesis of the respiratory tract: Host Factors

Clinical Manifestations of Bloodstream Infections

Definition of Sepsis

Types of Bloodstream Infections