Goitre iodide

Iodides should not be used alone since the normal gland will escape from iodide blockade in 2-8 weeks. Chronic use in pregnancy is not recommended because it crosses placenta and cause fetal goitre. Iodide treatment results in high intrathyroidal iodide content that can delay the onset of thioamide therapy or delay the use for radioactive iodine therapy for weeks if not months. Adverse effects include Hodism which is rare and reversible. The clinical symptoms are acneiform rash, sialadenitis, mucous membrane ulceration, conjuctivitis, rhinor-rhoea, metallic taste and rarely anaphylactoid reaction. 

Iodine occurs to a minute extent (less than 0.001 %) in sea water, but is found in greater concentration, combined in organic form, in certain seaweeds, in oysters and in cod livers. Crude Chile saltpetre, or caliche contains small amounts of sodium iodate, NalOj. from which iodine can be obtained (see below). Some insoluble iodides, for example liiose of silver and mercury(II), occur in Mexico. Iodine is found in the human body in the compound thyroxin in the thyroid gland deficiency of iodine in diet causes enlargement of this gland (goitre). 

Potassium iodide introduced as a remedy for goitre by J.-F. Coindet (Switzerland), the efficacy of extracts... 

Sodium and potassium iodides find limited use as expectorants but a much more important use is as additives, at levels around 5—100 fig/g to table salt in many countries as a prophylactic against goitre. This is a condition arising from iodine deficiency with the result that there is insufficient synthesis of the iodine-containing amino acids, thyroxine and 3,3, 5-triiodothyronine, that are essential components of the... 

Some degree of iodine dietary deficiency was estimated to affect 750 million people in the developing world in 1990 with around 10 million were suffering from stunted growth and mental retardation. In 1993 the WHO published a database of iodine deficiency based on the number of goitre victims in 121 countries where the element was in short supply. This shortage was most prevalent where soils have suffered repeated glaciations or heavy rainfall which had removed most of the iodide that may once have been present, because this is a particularly soluble material and so easily washed away. Those most at risk lived in India and China. 

Iodine radioiodine which destroys the cells making thyroid hormone iodide, an excess of which reduces the production of thyroid hormone temporarily by an unknown mechanism (it is also necessary for the formation of hormone, and both excess and deficiency can cause goitre). 

Iodide is well absorbed from the intestine, is distributed like chloride in the body and is rapidly excreted by the kidney. It is selectively taken up and concentrated (about x 25) by the thyroid gland, but more in hyperthyroidism and less in hypothyroidism. A deficiency of iodide reduces the amount of th)T oid hormone produced, which stimulates the pituitary to secrete TSH. The result is hyperplasia and increased vascularity of the gland, with eventual goitre formation. 

In euthyroid subjects with normal glands an excess of iodide from any source can cause goitre (with or without hyperthyroidism), e.g. use of iodide-containing cough medicines, iodine-containing radio-contrast media, amiodarone, seaweed eaters. 

Iodine therapy maximises iodide stores in the thjToid, which delays response to thionamides. Prophylactic iodide (1 part in 100 000 parts) may be added to the salt, water or bread where goitre is endemic. 

Goitre can occur (see above) with prolonged use of iodide-containing expectorant by bronchitics and asthmatics. Such therapy should therefore be intermittent, if it is used at all. 

A deficiency of iodine is one of the possible causes of the enlargement of the thyroid gland (goitre). Dietary sources of iodine are often supplemented by iodinated table salt, for which potassium iodide and sodium iodide are used. 

Kahaly GJ, Dienes HP, Beyer J, Hommel G (1998) Iodide induces thyroid autoimmunity in patients with endemic goitre a randomised, double-blind, placebo-controlled trial. Eur J Endocrinol, 139(3) 290-297. 

Iodine in minute quantity is a normal constituent of the human body and the average person requires a daily dose of 0 000,017 gm. Absence of the requisite amount leads to general debility and in more severe cases to goitre or big-neck . In very severe cases mental weakness develops known as cretinism, from Latin creta, chalk, because of its prevalence in Alpine districts. In Switzerland sodium iodide is added to table salt by legal regulation to ensure that everybody receives his necessary ration of iodine. In Britain there are several areas of iodine deficiency in the soil and addition of iodides to the feeding-stuffs of cattle, etc, effects an enormous improvement in the herds. 

Severe iodine deficiency was produced in sheep (4) with a low-iodine diet of crushed maize and pelleted pea pollard (8-15 ]ig iodine/Kg) which provided 5-8 yg iodine per day. After a period of 5 months, although body weights were maintained, iodine deficiency was evident with the appearance of goitre, low plasma T/ and T3 values, elevated TSH levels and low daily urinary excretion of iodine. Control animals received the same diet but were supplemented with 2 mg sodium iodide administered by subcutaneous injections each week or by a single iodized oil injection (1 ml = 480 mg iodine). The ewes were mated with normal fertile rams, the dates of conception established, and fetuses delivered at 56, 70, 98 and 140 days gestation by hysterotomy. (The normal gestation period for the sheep is 150 days). 

In areas where goitre is endemic, precautions are generally taken by supplementing the diet with the element, usually in the form of iodised salt. This contains the element either as sodium or potassium iodide or as sodium iodate. 

Essential trace elements with their functions in enzymes and hormones are distributed in different parts of the body. Iodine is special. Some 75% of the total iodine content in the human body (about 14 mg) is found in the thyroid gland, a small organ in the neck. There, it participates in the formation of the important thyroid hormone, thyroxine. This is vital for normal mental and physical development and for regulating the body s metabolism. A recommended daily intake is 100-200 pg. Deficiency of iodine will cause goitre. This has to be treated by additional potassium iodide or iodine casein. In developed countries, iodine deficiencies are now rare because iodine is added to table salt. 

Hall R., Turner-Warwick M., Doniach D. 1966. Autoantibodies in iodide goitre and asthma. Clin.exp.Immunol. 1 285-296. 

In the United Kingdom current average dietary iodine intake is approximately 255ng/day, higher than the recommended daily allowance of ISOjig per day. There are wide variations due to contamination of milk and dairy produce due to addition of iodide to cattle feeds and the use of iodophor disinfectants in dairying. Areas of borderline iodine deficiency still exist but goitre prevalence is low. 

These results suggest that in the Netherlands the presence of nitrate can be seen as a factor in the high goitre frequency. It suggests that nitrate itself or nitrate as an indicator of environmental pollution interacts with the availability of iodide to the thyroid. Its influence expresses itself especially in the situation where the iodine supplementation is already marginal. 

In conclusion, the study indicates that the three types of therapy for endemic goitre are equally effective, provided the patients receive a sufficient quantity of iodine. The form of iodine administration, whether as iodide or as L-Thyroxine, is not important except for compliance, which is best when the patient takes only one tablet per day. 

It has long been assumed that in relatively iodine deficient areas, IHT occurred in nodular goitres as a consequence of an underlying thjnroid dysfunction. Our data suggest that there exists 2 types of toxic nodules one, relat to autoimmune phenomena, that has lost the capability to store iodine, the other, true autonomous , that has kept this capability. The latter type seems to be at the origin of IHT in iodine deficient areas. They also support the notion that iodide excess results in the preferential secretion of T4 and show unexpect y that an increased IU does not exclude the diagnosis of IHT. 

Iodides should never be used as expectorants in patients with goitre. 

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