Title Amiodaron i tiroidna disfunkcija Title (english) Amiodarone and thyroid dysfunction Author Filip Medić Mentor Miro Bakula (mentor)Committee member Edvard Galić (predsjednik povjerenstva)Committee member Jasenka Markeljević (član povjerenstva)Committee member Miro Bakula (član povjerenstva)Granter University of Zagreb Defense date and country 2018-07-13, Croatia Scientific / art field, BIOMEDICINE AND HEALTHCARE Scientific / art field, BIOMEDICINE AND HEALTHCARE Abstract Štitna žlijezda zauzima ključno mjesto u održavanju homeostaze cijeloga organizma. Temeljni hormon koji luči je tiroksin (T4), a učinak se dominantno ostvaruje nakon intracelularne konverzije T4 u aktivniji oblik, trijodtironin (T3), koji pokazuje veći afinitet za receptorski kompleks te time modificira gensku ekspresiju ciljnih stanica. Amiodaron je jedan od najčešće korištenih antiaritmika i upotrebljava se u liječenju širokog spektra aritmija, najčešće tahiaritmija. U svom sastavu sadrži veliki udio joda, što je, uz intrinzični učinak lijeka, temelj utjecaja na tiroidnu funkciju. Smatra se kako 15-20% bolesnika liječenih amiodaronom razvija neki oblik tiroidne disfunkcije. Amiodaron može biti uzrokom razvoja amiodaronom inducirane hipotireoze - AIH (eng.
amiodarone induced hypothyroidism) ili tireotoksikoze – AIT (eng. amiodarone induced thyrotoxicosis). AIT se češće razvija u područjima sa smanjenim, dok se AIH razvija u područjima s dovoljnim unosom joda. Tip 1 AIT češći je u bolesnika s podležećom tiroidnom patologijom, najčešće nodoznom strumom ili latentnom Gravesovom (Basedowljevom) bolešću, dok se tip 2 najčešće razvija u prethodno zdravoj štitnjači. AIH je znatno češća u bolesnika s otprije poznatim Hashimotovim tiroiditisom. Opisani su i miješani oblici bolesti. Bolesnike liječene amiodaronom potrebno je redovito pratiti, laboratorijski i klinički, kako bi se pravovremeno otkrila bilo kakva odstupanja u tiroidnoj funkciji. Temelj liječenja AIH-a je nadomjesna terapija levotiroksinom. Često u tim slučajevima nije potrebno izostavljati amiodaron iz terapije. AIT tipa 1 liječi se tireostaticima kao i ostale tireotoksikoze. Ukoliko je to moguće, preporuča se prekinuti podležeća amiodaronska terapija. Nasuprot AIT tipa 1, čiji je temeljni patofiziološki supstrat povećana sinteza i otpuštanje tiroidnih hormona, u AIT tipu 2 osnova je destruktivni tiroiditis uzrokovan amiodaronom, dezetilamiodaronom (DEA) kao njegovim glavnim metabolitom i povećanim unosom joda. Osnova liječenja tog tipa bolesti je glukokortikoidna terapija.
Abstract (english) The thyroid gland has a key role in maintaining the body's homeostasis. Thyroxine (T4) is the main hormone secreted from the thyroid gland, its effect being predominantly achieved after the intracellular conversion of thyroxine to triiodothyronine (T3), which exhibits a higher affinity for the receptor complex, thus modifying gene expression of the target cells. Amiodarone is one of the most commonly used antiarrhythmics and is used in the treatment of a broad spectrum of arrhythmias, usually tachyarrhythmias. Amiodarone contains a large proportion of iodine, which is, in addition to the intrinsic effect of the medication, the basis of the impact on thyroid function. It is believed that 15-20% of patients treated with amiodarone develop some form of thyroid dysfunction. Amiodarone may cause amiodarone-induced hypothyroidism (AIH) or thyrotoxicosis – AIT (amiodarone induced thyrotoxicosis). AIT is usually developed in the areas with too low uptake of iodine, while AIH is developed in the areas where there is a sufficient iodine uptake. Type 1 AIT is more common among the patients with an underlying thyroid pathology, such as nodular goiter or Graves (Basedow) disease, while Type 2 mostly develops in a previously healthy thyroid. AIH is more common in patients with the from before diagnosed Hashimoto's thyroiditis. Combined types of diseases have also been described. Patients treated with amiodarone should be monitored regularly, including laboratory testing and clinical examinations, to early detect any deviations in the functioning of a thyroid gland. Supplementary levothyroxine therapy is the basis for the AIH treatment. Often, in such cases it is not necessary to cease the amiodarone therapy. Type 1 AIT is treated as any other type of thyrotoxicosis, with thyreostatics. If possible, the underlying amiodarone therapy should be discontinued. In contrast to the Type 1 AIT, whose basic pathophysiological substrate is the increased synthesis and release of thyroid hormones, the basis of the Type 2 AIT is a destructive thyroiditis caused by amiodarone, desethylamiodarone (DEA) as its main metabolite and an increased iodine uptake. Glucocorticoid therapy represents the basis for treatment of this type of disease.
Keywords
amiodaron
tiroidna disfunkcija
amiodaronom inducirana hipotireoza
amiodaronom inducirana tireotoksikoza
Keywords (english)
amiodarone
thyroid dysfunction
amiodarone induced hypothyroidism
amiodarone induced thyrotoxicosis
Language croatian URN:NBN urn:nbn:hr:105:548091 Study programme Title: Medicine Type of resource Text File origin Born digital Access conditions Open access Terms of use Created on 2019-03-14 09:03:29
