レボチロキシン療法中のアチレア症患者のトリヨドチロニン濃度
Jacqueline Jonklaas1, Bruce Davidson, Supna Bhagat
1Division of Endocrinology, Georgetown University Medical Center, Washington, DC, USA. jj@bc.georgetown.edu
JAMA
|February 21, 2008
まとめ
レボチロキシン (LT4) 単独の治療は,アチレア症患者の正常なトリヨドチロニン (T3) レベルを維持するのに十分です. この研究では,LT4治療による甲状腺切除術後のT3濃度の有意な低下は認められなかった.
科学分野:
- エンドクリノロジー エンドクリノロジー
- 甲状腺学 甲状腺学について
- 薬理学 薬理学とは
背景:
- 甲状腺のトリヨドチロニン (T3) 産生は,アチレア症の患者では存在しない.
- レボチロキシン (LT4) 治療は甲状腺機能低下症の標準治療ですが,T3欠乏症は避けられないと考えられていた.
- 以前のLT4とT3を併用した臨床試験では,一貫した利点が示されなかった.
研究 の 目的:
- LT4療法を受けた患者のT3レベルを,甲状腺切除術前の自身のベースラインレベルと比較するために.
- LT4治療中にT3欠乏症が本当に避けられないかどうかを判断する.
主な方法:
- トータル甲状腺切除術を受けた50人の甲状腺機能低下患者の前向きな研究.
- 患者は手術後にレボチロキシン (LT4) を投与された.
- タイロキシン (T4),T3,甲状腺刺激ホルモン (TSH) レベルは,手術前および手術後の測定を行いました.
主要な成果:
- 甲状腺切除術前のレベルと比較して,LT4治療を受けた患者でT3濃度の有意な低下は観察されなかった.
- 自由T4濃度は,LT4療法で有意に高かった.
- 94%の患者が目標のTSHレベルを達成し,目標のTSHに達していない患者ではT3が低下した.
結論:
- 伝統的なLT4療法だけで,甲状腺切除術後の患者の正常なT3レベルを達成することができます.
- 固有のT3レベルを維持するためにT3投与は必要ない場合があります.
- レボチロキシン単独治療は,T3レベルを正常化するのに有効です.
関連する概念動画
Synthesis and Regulation of Thyroid Hormones
Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Hyperthyroidism I: Introduction
Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hypothyroidism II: Pathophysiology
Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hyperthyroidism II: Pathophysiology
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Functions of Thyroid Hormones
The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Graves Disease II: Pathophysiology
Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
