A deficiency of which element causes goitre?
"appearance of cells is viewed to determine whether they resemble normal or cancerous cells. There can be many nodules, which is termed a multinodular goitre, and this can sometimes be a toxic multinodular goitre. An enlarged thyroid gland is called a goitre. Goitres are present in some form in about 5% of people, and are the result of a large number of causes, including iodine deficiency, autoimmune disease (both Grave's disease and Hashimoto's thyroiditis), infection, inflammation, and infltrative disease such as sarcoidosis and amyloidosis. Sometimes no cause can be found, a state called ""simple goitre"". Some forms of goitre are"
"consumption of iodine-rich foodstuffs (e.g. marine products) and the over-consumption of foodstuffs causing goitre, particularly bitter cassava, which is a staple in Central Africa. Anaemia is quite prevalent in Africa especially among young children due mainly to a diet that is low in animal-based foodstuffs and high in fibre-rich cereals, tannins and phytates which inhibit iron absorption. In 2006, about 67.6 per cent of children under 5, and overall 83.5 million children were anaemic. Through its effects on metabolic processes such as oxygen transport, oxidative metabolism and cell growth, iron deficiency also retards growth and development. It impairs the immune"
"iodate as dough conditioner in bread and baked goods was gradually replaced by the use of other conditioning agents such as bromide. Iodine deficiency resulting in goiter occurs in 187 million people globally (2.7% of the population). It resulted in 2700 deaths in 2013 up from 2100 deaths in 1990. A low amount of thyroxine (one of the two thyroid hormones) in the blood, due to lack of dietary iodine to make it, gives rise to high levels of thyroid stimulating hormone (TSH), which stimulates the thyroid gland to increase many biochemical processes; the cellular growth and proliferation can result"
"various presentations of one or more misplaced accessory thyroid glands. These can be asymptomatic. Iodine deficiency, most common in inland and mountainous areas, can predispose to goitre – if widespread, known as endemic goitre. Pregnant women deficient of iodine can give birth to infants with thyroid hormone deficiency. The use of iodised salt used to add iodine to the diet has eliminated endemic cretinism in most developed countries, and over 120 countries have made the iodination of salt mandatory. Because the thyroid concentrates iodine, it also concentrates the various radioactive isotopes of iodine produced by nuclear fission. In the event"
"damage). In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten, iodine deficiency also gives rise to hypothyroidism, the most serious symptoms of which are epidemic goitre (swelling of the thyroid gland), extreme fatigue, mental slowing, depression, weight gain, and low basal body temperatures. The addition of iodine to table salt (so-called iodized salt) has largely eliminated the most severe consequences of iodine deficiency in wealthier nations, but deficiency remains a serious public health problem in the developing world. Iodine deficiency is also a problem in"
"as a side effect of administration of iodine-containing contrast agents. In some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (Hashimoto's thyroiditis and Graves' disease). Iodine deficiency resulting in goiter occurs 187 million people globally (2.7% of the population). Certain areas of the world, due to natural deficiency and unavailability of iodine, are severely affected by iodine deficiency, which affects approximately two billion people worldwide. It is particularly common in the Western Pacific, South-East Asia and Africa. Among other nations affected by iodine deficiency, China and Kazakhstan have begun taking action, while Russia has not. Successful campaigns"
"hormone from the brain's hypothalamus (tertiary hypothyroidism). Primary hypothyroidism is about a thousandfold more common than central hypothyroidism. Iodine deficiency is the most common cause of primary hypothyroidism and endemic goiter worldwide. In areas of the world with sufficient dietary iodine, hypothyroidism is most commonly caused by the autoimmune disease Hashimoto's thyroiditis (chronic autoimmune thyroiditis). Hashimoto's may be associated with a goiter. It is characterized by infiltration of the thyroid gland with T lymphocytes and autoantibodies against specific thyroid antigens such as thyroid peroxidase, thyroglobulin and the TSH receptor. After women give birth, about 5% develop postpartum thyroiditis which can"
"in the characteristic swelling or hyperplasia of the thyroid gland, or goiter. In mild iodine deficiency, levels of triiodiothyronine (T) may be elevated in the presence of low levels of levothyroxine, as the body converts more of the levothyroxine to triiodothyronine as a compensation. Some such patients may have a goiter, without an elevated TSH. The introduction of iodized salt since the early 1900s has eliminated this condition in many affluent countries; however, in Australia, New Zealand, and several European countries, iodine deficiency is a significant public health problem. It is more common in developing countries. Public health initiatives to"
"thyroid disease while worldwide hypothyroidism and goiter due to dietary iodine deficiency is the most common. Hypothyroidism affects 3-10% percent of adults, with a higher incidence in women and the elderly. An estimated one-third of the world's population currently lives in areas of low dietary iodine levels. In regions of severe iodine deficiency, the prevalence of goiter is as high as 80%. In areas where iodine-deficiency is not found, the most common type of hypothyroidism is an autoimmune subtype called Hashimoto's thyroiditis, with a prevalence of 1-2%. As for hyperthyroidism, Graves' disease, another autoimmune condition, is the most common type"
"and jaundice. A goiter is rare, although it may develop later in children who have a thyroid gland that does not produce functioning thyroid hormone. A goiter may also develop in children growing up in areas with iodine deficiency. Normal growth and development may be delayed, and not treating infants may lead to an intellectual impairment (IQ 6–15 points lower in severe cases). Other problems include the following: large scale and fine motor skills and coordination, reduced muscle tone, squinting, decreased attention span, and delayed speaking. Tooth eruption may be delayed. In older children and adolescents, the symptoms of hypothyroidism"
"those areas without outside food sources are most at risk of iodine deficiency diseases. Iodine deficiency results in the impairments in varying degrees of physical and mental development. It also causes gradual enlargement of the thyroid gland, referred to as a goiter. It is being combated in many countries by public health campaigns of iodine administration. Congenital hypothyroidism can be endemic, genetic, or sporadic. If untreated, it results in mild to severe impairment of both physical and mental growth and development. Poor length growth is apparent as early as the first year of life. Adult stature without treatment ranges from"
"Goitrin Goitrin is a sulfur-containing oxazolidine, a cyclic thiocarbamate, that reduces the production of thyroid hormones such as thyroxine. It is found in cruciferous vegetables such as cabbage, brussels sprouts and rapeseed oil, and is formed by the hydrolysis of a glucosinolate: progoitrin or 2-hydroxy-3-butenyl glucosinolate. The unstable isothiocyanate (2-hydroxy-3-butenyl isothiocyanate) derived from the latter glucosinolate spontaneously cyclizes to goitrin, because the hydroxy group is situated in proximity to the isothiocyanate group (allowing a five-membered ring to be formed). Hence, the oxygen in the molecule stems from the hydroxy group of the original unstable isothiocyanate. Plants containing this specific glucosinolate"
"the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T), which has a longer half-life than T. In humans, the ratio of T to T released into the blood is between 14:1 and 20:1. T is converted to the active T (three to four times more potent than T) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (Ta) and thyronamine (Ta'). All three isoforms of the deiodinases are selenium-containing enzymes; thus dietary selenium is essential for T production. Iodine accounts for 65% of the"
"Glutaric aciduria type 1 Glutaric acidemia type 1 (or ""glutaric aciduria"", ""GA1"", or ""GAT1"") is an inherited disorder in which the body is unable to completely break down the amino acids lysine, hydroxylysine and tryptophan. Excessive levels of their intermediate breakdown products (glutaric acid, glutaryl-CoA, 3-hydroxyglutaric acid, glutaconic acid) can accumulate and cause damage to the brain (and also other organs), but particularly the basal ganglia, which are regions that help regulate movement. GA1 causes secondary carnitine deficiency, as glutaric acid, like other organic acids, is detoxified by carnitine. Mental retardation may also occur. The severity of glutaric acidemia type"
"Ornithine aminotransferase deficiency Ornithine aminotransferase deficiency (also known as gyrate atrophy of the choroid and retina) is an inborn error of ornithine metabolism, caused by decreased activity of the enzyme ornithine aminotransferase. Biochemically, it can be detected by elevated levels of ornithine in the blood. Clinically, it presents initially with poor night vision, which slowly progresses to total blindness. It is believed to be inherited in an autosomal recessive manner. Approximately 200 known cases have been reported in the literature. The incidence is highest in Finland, estimated at 1:50,000. Research suggests there can be some adverse effect on muscles and"
"the thyroid is permanently damaged. Cretinism is a condition associated with iodine deficiency and goiter, commonly characterised by mental deficiency, deafness, squint, disorders of stance and gait and stunted growth due to hypothyroidism. Paracelsus was the first to point out the relation between goitrous parents and their mentally disabled children. As a result of restricted diet, isolation, intermarriage, etc., as well as low iodine content in their food, children often had peculiar stunted bodies and retarded mental faculties, a condition later known to be associated with thyroid hormone deficiency. Diderot, in his 1754 ""Encyclopédie"", described these patients as ""crétins"". In"
"like goitre, brain damage and cretinism and is a problem in at least 130 different countries. Even though these deficiencies are invisible, they have great potential to impact human health on a global scale. It must also be noted that small increases in levels can cause a fertilization effect where the growth and reproduction abilities of C plants such as soybeans and rice are actually enhanced by 10-20% in laboratory experiments. This does not take into account, however, the additional burden of pests, pathogens, nutrients and water affecting the crop yield. While researchers acknowledge there are possible benefits of global"
"(lymphocytic infiltration) and destruction (fibrosis) of the gland. Goiter is the general enlargement of the thyroid that can be associated with many thyroid diseases. The main reason this happens is because of increased signaling to the thyroid by way of TSH receptors to try to make it produce more thyroid hormone. This causes increased vascularity and increase in size (hypertrophy) of the gland. In hypothyroid states or iodine deficiency, the body recognizes that it is not producing enough thyroid hormone and starts to produce more TSH to help stimulate the thyroid to produce more thyroid hormone. This stimulation causes the"
"retina and choroid, sometimes accompanying the metabolic condition hyperornithinemia. The presence of gyrate atrophy with iminoglycinuria stems from a deficiency of proline in chorioretinal tissues, while processes behind hyperornithinemia disrupt the metabolic pathway from ornithine to proline, which alters the catabolism of ornithine, and also results in reduced levels of proline. Thus, gyrate atrophy can be found with either disorder, with proline deficiency as an underlying feature. Hyperglycinuria is another disorder affecting reabsorption of glycine and imino acids, similar to iminoglycinuria and considered to be a heterozygous form. When accompanied by a specific type of kidney stone (nephrolithiasis), it is"
"and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida. Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue). Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitis around the eyes, nose and mouth. Vitamin B12 deficiency is sometimes responsible for AC, and"
"Gunther disease Gunther disease, also known as congenital erythropoietic porphyria (CEP), uroporphyrinogen III synthase deficiency and UROS deficiency, is a congenital form of erythropoietic porphyria. The word porphyria originated from the Greek word porphura. Porphura actually means ""purple pigment"", which, in suggestion, the color that the body fluid changes when a person has Gunther's disease. It is a rare, autosomal recessive metabolic disorder affecting heme, caused by deficiency of the enzyme uroporphyrinogen cosynthetase. It is extremely rare, with a prevalence estimated at 1 in 1,000,000 or less. There have been times that prior to birth of a fetus, Gunther's disease"
"Graves' disease Graves' disease, also known as toxic diffuse goiter, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea, and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy. About 25 to 80% of people with the condition develop eye problems. The exact"
"Some dietitians recommend that these be supplied from foods in which they occur naturally, or at least as complex compounds, or sometimes even from natural inorganic sources (such as calcium carbonate from ground oyster shells). Some are absorbed much more readily in the ionic forms found in such sources. On the other hand, minerals are often artificially added to the diet as supplements; the most well-known is likely iodine in iodized salt which prevents goiter. include the following: Many elements are required in smaller amounts (microgram quantities), usually because they play a catalytic role in enzymes. Some trace mineral elements"
"thyroid indices and may benefit aspects of cognitive function in school-age children, even in marginally iodine-deficient areas."" With iodine supplementation, goiters caused by iodine deficiency decrease in size in very young children and pregnant women. Generally, however, long-standing goiters caused by iodine deficiency respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism. Following the adoption of iodised salt in the United States in 1924, there was a gradual increase in average intelligence of 1 standard deviation, 15 points in iodine-deficient areas, 3.5 points nationally, but also an increase in deaths of"
"The ""proximal renal tubular dysfunction"" creates low phosphate levels in the blood (""hypophosphatemia""), causing muscle weakness and sometimes coma. The dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood (""hyperuricemia""). Another side effect is increased levels of chloride in the blood (""hyperchloremia""). The kidneys can also shrink up to 30%. Cadmium exposure is also associated with the development of kidney stones. Similar to zinc, long term exposure to cadmium fumes can cause life long anosmia. Inside cells, cadmium ions act as a catalytic"
"oil) to goiter patients, a treatment later advocated by the WHO. Through the thyroid clinic, Campos likewise pursued research on whether there was a genetic factor that contributed to endemic goiter. His findings, as contained in a paper that he published in 1961, proposed that the iodine intake deficiency thought to be the main cause of goiter was just one of the triggering factors of the disease, and that physiology and anatomy proved to be more important considerations as some people were born without the enzyme necessary to take in trace elements such as iodine even if it were present"
"as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy. The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About"
"Gaspard Adolphe Chatin Gaspard Adolphe Chatin (30 November 1813 – 13 January 1901) was a French physician, mycologist and botanist who was born in Isère, and died in Les Essarts-le-Roi. He was the first to prove that goiter was related of iodine deficiencies. He studied at the Faculté de Médecine in Paris and received his doctorate in May 1840. In 1841, he became Chief Pharmacist of the Beaujon Hospital in Paris. and in 1859, at the Hôtel-Dieu de Paris. He taught botany at the Ecole Superieure de Pharmacie, which he directed from 1874. In April 1886, there were student riots"
"may include fatigue, cold intolerance, sleepiness, muscle weakness, constipation, a delay in growth, overweight for height, pallor, coarse and thick skin, increased body hair, irregular menstrual cycles in girls, and delayed puberty. Signs may include delayed relaxation of the ankle reflex and a slow heart beat. A goiter may be present with a completely enlarged thyroid gland; sometimes only part of the thyroid is enlarged and it can be knobby in character. Hypothyroidism is caused by inadequate function of the gland itself (primary hypothyroidism), inadequate stimulation by thyroid-stimulating hormone from the pituitary gland (secondary hypothyroidism), or inadequate release of thyrotropin-releasing"
"clinical marker of either the direct or indirect insufficient intake of iodine in the human body. There is evidence of goiter, and its medical treatment with iodine-rich algae and burnt sponges, in Chinese, Egyptian, and Roman ancient medical texts. In 1848, King Carlo Alberto of Sardinia commissioned the first epidemiological study of congenital iodine deficiency syndrome, in northern Savoy where it was frequent. In past centuries, the well reported social diseases prevalent among the poorer social classes and farmers, caused by dietary and agricultural monocultures, were: pellagra, rickets, beriberi, scurvy in long-term sailors, and the endemic goiter caused by iodine"
"Lesch–Nyhan syndrome Lesch–Nyhan syndrome (LNS), also known as juvenile gout, is a rare inherited disorder caused by a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT), produced by mutations in the HPRT gene located on the X chromosome. LNS affects about one in 380,000 live births. The disorder was first recognized and clinically characterized by medical student Michael Lesch and his mentor, pediatrician William Nyhan, at Johns Hopkins. The HGPRT deficiency causes a build-up of uric acid in all body fluids. The combination of increased synthesis and decreased utilization of purines leads to high levels of uric acid production. This results"
"result of prolonged damage may result in post treatment deficiencies. Mineral deficiencies. GSE is associated with the following mineral deficiencies: Blood factors Megaloblastic anemia (MA) is associated with GSE and is believed to be the result of B and folate deficiency. In GSE, it appears to be associated with the IgA-less phenotype. Unlike other forms of megaloblastic anemia, GSEA MA is not a form of autoimmune gastritis. Pernicious anemia (PA). Pernicious anemia is associated with GSE and is believed to result primarily from malabsorption phenomena. Iron-deficiency anemia. Iron-deficiency anemia (IDA) may be the only symptom for CD, detected in subclinical"
"thyroxine (T4) into its more active counterpart, triiodothyronine, and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage. It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90). People dependent on food grown from selenium-deficient soil may be at risk for deficiency. Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as"