کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2564647 1561023 2016 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Elevated levels of circulating thyroid hormone do not cause the medical sequelae of hyperthyroidism
ترجمه فارسی عنوان
سطح بالای هورمون تیروئید در حال گردش باعث عوارض پزشکی هیپرتیروئیدیسم نمی شود
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی روانپزشکی بیولوژیکی
چکیده انگلیسی

BackgroundClinicians have been reluctant to use high dose thyroid (HDT) to treat affective disorders because high circulating levels of thyroid hormone have traditionally been equated with hyperthyroidism, and understood as the cause of the medical sequelae of hyperthyroidism, such as osteoporosis and cardiac abnormalities. This conclusion is not supported by (HDT) research.MethodsA literature review of research related to the morbidity and mortality of HDT treatment was performed.ResultsThere exists a large body of research involving the use of HDT treatment to prevent the recurrence of differentiated thyroid cancer and to treat affective disorders. A review of this literature finds a lack of support for HDT as a cause of osteoporosis, nor is there support for an increase in morbidity or mortality associated with HDT. This finding contrasts with the well-established morbidity and mortality associated with Graves' disease, thyroiditis, and other endogenous forms of hyperthyroidism.DiscussionThe lack of evidence that exogenous HDT causes osteoporosis, cardiac abnormalities or increases mortality compared with the significant morbidity and mortality of hyperthyroidism requires an alternative cause for the medical sequelae of hyperthyroidism. One possibility is an autoimmune mechanism.ConclusionHigh circulating levels of thyroid hormone is not the cause of the sequela of hyperthyroidism. The reluctance to using high dose thyroid is unwarranted.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 71, 3 November 2016, Pages 1–6
نویسندگان
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