Genetic factors appear to influence the incidence of thyrotoxicosis. Autoimmune thyroid disease, including Hashimoto hypothyroidism and Graves disease, often occurs in multiple members of a family. Show
Several genetic syndromes have been associated with hyperthyroidism, especially autoimmune thyroid disease. McCune-Albright syndrome is caused by mutations in the GNAS gene. This gene encodes the stimulatory G-protein alpha subunit, which is a key component of many signal transduction pathways. Patients present with the classic triad of polyostotic fibrous dysplasia, irregular café-au-lait spots, and precocious puberty. The syndrome may also include facial asymmetry, Cushing syndrome, hyperthyroidism, and acromegaly. [8] A number of disorders of thyroid function have been found to be caused by mutations in the TSHR gene, which encodes the TSH receptor protein. These disorders include the following:
Type II autoimmune polyendocrine syndrome is associated with hyperthyroidism and hypothyroidism, as well as type 1 diabetes mellitus and adrenal insufficiency. Patients may also have immune deficiency, as manifested by chronic mucosal candidiasis. [9] Autoimmune thyroid disease has a higher prevalence in patients with human leukocyte antigen (HLA)-DRw3 and HLA-B89. Graves disease is felt to be an HLA-related, organ-specific defect in suppressor T-cell function. Similarly, subacute painful or granulomatous thyroiditis occurs more frequently in patients with HLA-Bw35. Like other immune diseases, these thyroid conditions occur more frequently in women than in men. With the availability of genome-wide association studies, more than a dozen genes and gene regions have been found to be associated with an increased risk for development of thyrotoxicosis, particularly Graves disease. [10, 11, 12, 13, 14, 15] Unsurprisingly, these studies have shown associations between these same genes and the development of other endocrine autoimmune disorders, such as type 1 diabetes mellitus. The loci for which specific function can be deduced appear to involve genes related to HLA, non-HLA immune function, and thyroid function. [14] However, the odds ratios that have been determined generally indicate only a mildly increased risk for Graves disease. Most of the genome-wide association studies have focused on diffuse toxic goiter (ie, Graves disease). One study, however, found an association between development of toxic multinodular goiter (Plummer disease) and a single-nucleotide polymorphism (SNP) in the TSHR gene. [16] . This SNP was seen in 9.6% of normal patients, 16.3% of patients with Graves disease, and 33.3% of patients with toxic multinodular goiter. Iodine intakeIodine intake also appears to influence the occurrence of thyrotoxicosis. Clearly, patients in borderline iodine-deficient areas of the world develop nodular goiter, often with areas of thyroid autonomy. When members of this population move to areas of sufficient iodine intake, thyrotoxicosis occurs. Evidence exists that iodine can act as an immune stimulator, precipitating autoimmune thyroid disease and acting as a substrate for additional thyroid hormone synthesis. Graves diseaseThe most common cause of thyrotoxicosis is Graves disease (50-60% of cases). Graves disease is an organ-specific autoimmune disorder characterized by a variety of circulating antibodies, including common autoimmune antibodies, as well as anti-TPO and anti-TG antibodies. The most important autoantibody is thyroid-stimulating antibody (TSab; also called TSI, LATS, or TRab), which is directed toward epitopes of the TSH receptor and acts as a TSH-receptor agonist. Like TSH, TSab binds to the TSH receptor on the thyroid follicular cells to activate thyroid hormone synthesis and release and thyroid gland growth (hypertrophy). This results in the characteristic picture of Graves thyrotoxicosis, with a diffusely enlarged thyroid, very high radioactive iodine uptake, and excessive thyroid hormone levels compared with a healthy thyroid (see the images below).  Thyroid hormone levels can be highly elevated in Graves disease. Clinical findings specific to Graves disease include thyroid ophthalmopathy (periorbital edema, chemosis [conjunctival edema], injection, or proptosis) and, rarely, dermopathy over the lower extremities. This autoimmune condition may be associated with other autoimmune diseases, such as pernicious anemia, myasthenia gravis, vitiligo, adrenal insufficiency, celiac disease, and type 1 diabetes mellitus. In pregnant women with Graves disease, fetal or neonatal thyrotoxicosis can result from maternal TSH-receptor antibodies (TRabs) crossing the placenta. A literature review by van Dijk et al indicated that during pregnancy, neonatal thyrotoxicosis is a risk when the concentration of maternal TRabs reaches 4.4 U/L, a level 3.7 times the upper limit of normal. [17] Subacute thyroiditisThe next most common cause of thyrotoxicosis is subacute thyroiditis (approximately 15-20% of cases), a destructive release of preformed thyroid hormone. A typical nuclear scintigraphy scan shows no radioactive iodine uptake (RAIU) in the thyrotoxic phase of the disease (see the images below). Thyroid hormone levels can be highly elevated in this condition. Toxic multinodular goiterToxic multinodular goiter (Plummer disease) accounts for 15-20% of thyrotoxicosis cases (see the image below). It occurs more commonly in elderly individuals, especially those with a long-standing goiter. Thyroid hormone excess develops very slowly over time and often is only mildly elevated at the time of diagnosis. Symptoms of thyrotoxicosis are mild, often because only a slight elevation of thyroid hormone levels is present, and the signs and symptoms of thyrotoxicosis often are blunted (apathetic hyperthyroidism) in older patients. However, very high thyroid hormone levels may occur in this condition after high iodine intake (eg, with iodinated radiocontrast or amiodarone exposure). Toxic adenomaToxic adenoma is caused by a single hyperfunctioning follicular thyroid adenoma. This disorder accounts for approximately 3-5% of thyrotoxicosis cases. The excess secretion of thyroid hormone occurs from a benign monoclonal tumor that usually is larger than 2.5 cm in diameter. The excess thyroid hormone suppresses TSH levels. RAIU usually is normal, and the radioactive iodine scan shows only the hot nodule, with the remainder of the normal thyroid gland suppressed because the TSH level is low. Other causes of thyrotoxicosisSeveral rare causes of thyrotoxicosis exist that deserve mention. Struma ovarii is ectopic thyroid tissue associated with dermoid tumors or ovarian teratomas that can secrete excessive amounts of thyroid hormone and produce thyrotoxicosis. [18] Iodide-induced thyrotoxicosis (Jod-Basedow syndrome) occurs in patients with excessive iodine intake (eg, from an iodinated radiocontrast study). The antiarrhythmic drug amiodarone, which is rich in iodine and bears some structural similarity to T4, may cause thyrotoxicosis (see Thyroid Dysfunction Induced by Amiodarone Therapy). Iodide-induced thyrotoxicosis also occurs in patients with areas of thyroid autonomy, such as a multinodular goiter or autonomous nodule. Iodide-induced thyrotoxicosis appears to result from loss of the normal adaptation of the thyroid to iodide excess. It is treated with cessation of the excess iodine intake and with administration of antithyroid medication. Usually, after depletion of the excess iodine, thyroid functions return to preexposure levels. Patients with a molar hydatidiform pregnancy or choriocarcinoma have extremely high levels of beta human chorionic gonadotropin (β-hCG), which can weakly activate the TSH receptor. At very high levels of β-hCG, activation of the TSH receptors is sufficient to cause thyrotoxicosis. Metastatic follicular thyroid carcinoma may also result in thyrotoxicosis. These lesions maintain the ability to make thyroid hormone, and in patients with bulky tumors, production may be high enough to cause thyrotoxicosis. What symptoms are associated with hyperthyroidism and hypothyroidism?Common symptoms. nervousness, anxiety and irritability.. hyperactivity – you may find it hard to stay still and have a lot of nervous energy.. mood swings.. difficulty sleeping.. feeling tired all the time.. sensitivity to heat.. muscle weakness.. diarrhoea.. What do hyperthyroidism and hypothyroidism have in common?Thyroid nodules are common in both hypothyroidism and hyperthyroidism. More often than not, these nodules are benign. In hyperthyroidism, these nodules can lead to an increase in your thyroid's size or produce too much T4 thyroid hormone. Doctors don't always know why this happens.
Which condition is associated with hypothyroidism?The most common cause of hypothyroidism is an autoimmune disorder known as Hashimoto's thyroiditis. Autoimmune disorders occur when your immune system produces antibodies that attack your own tissues.
What condition is associated with hyperthyroidism?Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism). Although a number of disorders may result in hyperthyroidism, Graves' disease is a common cause. Thyroid hormones affect many body systems, so signs and symptoms of Graves' disease can be wide ranging.
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Which of the following conditions is associated with hyperthyroidism and hypothyroidism?
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