Amiodaron i tiroidna disfunkcija
| العنوان: | Amiodaron i tiroidna disfunkcija |
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| المؤلفون: | Medić, Filip, Bakula, Miro, Alfirević, Maša, Bakula, Maja, Mucić, Katarina, Marić, Nikolina |
| المصدر: | Acta clinica Croatica Volume 61. Issue 2 |
| بيانات النشر: | Sestre Milosrdnice University hospital and Institute of Clinical Medical Research, 2022. |
| سنة النشر: | 2022 |
| مصطلحات موضوعية: | amiodarone, thyroid dysfunction, amiodarone-induced hypothyroidism, amiodarone-induced thyrotoxicosis, Amiodaron, Tireoidna disfunkcija, Amiodaronom izazvana hipotireoza, Amiodaronom izazvana tireotoksikoza, Amiodarone, Thyroid dysfunction, Amiodarone-induced hypothyroidism, Amiodarone-induced thyrotoxicosis |
| الوصف: | Thyroid gland has a key role in maintaining the body homeostasis. Thyroxine is the main hormone secreted from the thyroid gland, its effect being predominantly achieved after the intracellular conversion of thyroxine to triiodothyronine, 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 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 amiodarone-induced thyrotoxicosis (AIT). 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 patients with an underlying thyroid pathology, such as nodular goiter or Graves’ (Basedow’s) disease, while type 2 mostly develops in a previously healthy thyroid. AIH is more common in patients with previously diagnosed Hashimoto’s thyroiditis. Combined types of the 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 the thyroid gland. Supplementary levothyroxine therapy is the basis of AIH treatment. In such cases, amiodarone therapy quite often need not be discontinued. Type 1 AIT is treated with thyrostatic agents, like any other type of thyrotoxicosis. If possible, the underlying amiodarone therapy should be discontinued. In contrast to type 1 AIT, the basic pathophysiological substrate of which is the increased synthesis and release of thyroid hormones, the basis of type 2 AIT is destructive thyroiditis caused by amiodarone, desethylamiodarone as its main metabolite, and an increased iodine uptake. Glucocorticoid therapy is the basis of treatment for this type of disease. Štitna žlijezda zauzima ključno mjesto u održavanju homeostaze cijeloga organizma. Temeljni hormon koji luči je tiroksin, a učinak se dominantno ostvaruje nakon unutarnje konverzije tiroksina u aktivniji oblik, trijodotironin, koji pokazuje veći afinitet za receptorski kompleks te time modificira gensku ekspresiju ciljnih stanica. Amiodaron je jedan od najčešće upotrebljavanih antiaritmika i rabi se u liječenju širokog spektra aritmija, najčešće tahiaritmija. U svom sastavu sadrži velik udio joda, što je, uz intrinzični učinak lijeka, temelj utjecaja na tireoidnu funkciju. Smatra se kako 15%-20% bolesnika liječenih amiodaronom razvija neki oblik tireoidne disfunkcije. Amiodaron može biti uzrokom razvoja amiodaronom izazvane hipotireoze (amiodarone-induced hypothyroidism, AIH) ili amiodaronom izazvane tireotoksikoze (amiodarone-induced thyrotoxicosis, AIT). AIT se češće razvija u područjima sa smanjenim, dok se AIH razvija u područjima s dovoljnim unosom joda. Razlikujemo dva tipa AIT; tip 1 je češći u bolesnika s podležećom tireoidnom 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 tireoiditisom. Opisani su i miješani oblici bolesti. Bolesnike liječene amiodaronom potrebno je redovito pratiti, laboratorijski i klinički, kako bi se pravodobno otkrila bilo kakva odstupanja u tireoidnoj 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. Ako je moguće, preporuča se prekinuti podležeća amiodaronska terapija. Nasuprot AIT tipa 1, temeljni patofiziološki supstrat kojega je povećana sinteza i otpuštanje tireoidnih hormona, u AIT tipu 2 osnova je destruktivni tireoiditis uzrokovan amiodaronom, dezetilamiodaronom kao njegovim glavnim metabolitom i povećanim unosom joda. Osnova liječenja tog tipa bolesti je glukokortikoidna terapija. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 1333-9451 0353-9466 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::fbc45b471394d04ff0d0795b30171060Test https://hrcak.srce.hr/285013Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.dedup.wf.001..fbc45b471394d04ff0d0795b30171060 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13339451 03539466 |
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