Author/Editor | Pirnat, Edvard | |
Title | Motnje zaradi pomanjkanja joda | |
Translated title | Iodine deficiency disorders | |
Type | članek | |
Source | Med Razgl | |
Vol. and No. | Letnik 41, št. Suppl 1 | |
Publication year | 2002 | |
Volume | str. 101-4 | |
Language | slo | |
Abstract | Iodine is essential for the synthesis of thyroid hormones. It is also important in the regulation of thyroid growth and function. Thyroid hormones stimulate metabolic processes in the organism and are necessary for the growth and development of most organs, especially the brain. Iodine actively enters thyroid cells in the form of iodide. The thyroid adapts to iodine deficiency by increasing iodide uptake in the thyroid cells, by producing more triiodothyronine (T3) than thyroxine (T4), by decreasing iodine storage in the colloid and increasing proteolysis of thyroglobulin as well as by effective recycling of iodide within the thyroid cell itself. Iodine deficiency ranges from mild to moderate to severe. It is evaluated according to the prevalence of goiter, urinary and maternal milk iodine levels as well as the percentage of neonatal hypothyroidism. Goiter is the major consequence of iodine deficiency; however, its most serious complication is mental retardation and endemic cretinism. An epidemiological study performed from 1991-94 demonstrated the presence of mild iodine deficiency in Slovenia. Consequently, the implementation of higher iodine content in salt was recommended (25 mg of KI or 32 mg of KI03 per kg of salt). In order to evaluate the iodine supply after the increase in salt iodination, a new epidemiological study is planned in a few years' time. | |
Summary | Jod je nujno potreben za tvorbo ščitničnih hormonov. Pomemben je tudi za uravnavanje rasti in delovanja ščitnice. Ščitnični hormoni v telesu spodbujajo presnovne procese. So nujno potrebni za rast in razvoj večine organov, še posebej možganov. Jod v obliki jodida aktivno vstopa v ščitnične celice. Na pomanjkanje joda v prehrani se ščitnica prilagodi s povečanim privzemom jodida v celice, nastaja več trijodtironina (T3) kot tiroksina (T4), zmanjšajo se zaloge jodida v koloidu, zveča se proteoliza tiroglobulina, jodid se v sami ščitnični celici učinkoviteje reciklira. Ločimo blago, zmerno in hudo pomanjkanje joda. Ocenjujemo ga s prevalenco golšavosti v populaciji, izločanjem joda v urinu, materinem mleku in z odstotkom neonatalne hipotiroze. Glavna posledica pomanjkanja joda je golša. Najresnejša posledica hudega pomanjkanja joda je mentalna zaostalost oziroma endemski kretenizem. Ker smo v Sloveniji z epidemiološko študijo 1991-1994 ugotovili blago endemsko golšavost, je bilo januarja 1999 izdano priporočilo o povečanju jodiranja soli (25 mg KI ali 32 mg KI03 na kilogram soli). Epidemiološko študijo, ki bo ocenila ustreznost preskrbe prebivalstva z jodom po zvečanju jodne profilakse, načrtujemo v prihodnjih letih. | |
Descriptors | IODINE GOITER, ENDEMIC THYROID HORMONES CRETINISM |