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RISS 인기검색어
- 검색키워드
- 저자 : Wilmar M. Wiersinga (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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T4+T3 Combination Therapy: An Unsolved Problem of Increasing Magnitude and Complexity
Wilmar M. Wiersinga 대한내분비학회 2021 Endocrinology and metabolism Vol.36 No.5
Thyroxine (T4)+triiodothyronine (T3) combination therapy can be considered in case of persistent symptoms despite normal serumthyroid stimulating hormone in levothyroxine (LT4)-treated hypothyroid patients. Combination therapy has gained popularity in thelast two decades, especially in countries with a relatively high gross domestic product. The prevalence of persistent symptoms hasalso increased; most frequent are complaints about energy levels and fatigue (80% to 90%), weight management (70% to 75%),memory (60% to 80%), and mood (40% to 50%). Pathophysiological explanations for persistent problems are unrealistic patient expectations, comorbidities, somatic symptoms, related disorders (Diagnostic and Statistical Manual of Mental Disorders [DSM-5]),autoimmune neuroinflammation, and low tissue T3. There is fair circumstantial evidence for the latter cause (tissue and specificallybrain T3 content is normalized by T4+T3, not by T4 alone), but the other causes are viewed as more relevant in current practice. Thismight be related to the ‘hype’ that has emerged surrounding T4+T3 therapy. Although more and better-designed trials are needed tovalidate the efficacy of T4+T3 combination, the management of persistent symptoms should also be directed towards alternativecauses. Improving the doctor-patient relationship and including more and better information is crucial. For example, dissatisfactionwith the outcomes of T4 treatment for subclinical hypothyroidism can be anticipated as recent trials have demonstrated that LT4 ishardly effective in improving symptoms associated with subclinical hypothyroidism.
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Clinical Relevance of Environmental Factors in the Pathogenesis of Autoimmune Thyroid Disease
Wilmar M. Wiersinga 대한내분비학회 2016 Endocrinology and metabolism Vol.31 No.2
Genetic factors contribute for about 70% to 80% and environmental factors for about 20% to 30% to the pathogenesis of autoimmunethyroid disease (AITD). Relatives of AITD patients carry a risk to contract AITD themselves. The 5-year risk can be quantifiedby the so-called Thyroid Events Amsterdam-score, based on serum thyroid-stimulating hormone, thyroid peroxidase(TPO)-antibodies and family history. Subjects at risk may ask what they can do to prevent development of AITD. This reviewsummarizes what is known about modulation of exposure to environmental factors in terms of AITD prevention. To stop smokingdecreases the risk on Graves disease but increases the risk on Hashimoto disease. Moderate alcohol intake provides someprotection against both Graves and Hashimoto disease. Low selenium intake is associated with a higher prevalence of thyroid autoimmunity,but evidence that selenium supplementation may lower TPO antibodies and prevent subclinical hypothyroidism remainsinconclusive. Low serum vitamin D levels are associated with a higher prevalence of TPO antibodies, but interventionstudies with extra vitamin D have not been done yet. Stress may provoke Graves hyperthyroidism but not Hashimoto thyroiditis. Estrogen use have been linked to a lower prevalence of Graves disease. The postpartum period is associated with an increasedrisk of AITD. Taking together, preventive interventions to diminish the risk of AITD are few, not always feasible, and probably oflimited efficacy.
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Graves’ Disease: Can It Be Cured?
Wilmar M. Wiersinga 대한내분비학회 2019 Endocrinology and metabolism Vol.34 No.1
Whether or not Graves’ hyperthyroidism can be really cured, depends on the definition of “cure.” If eradication of thyroid hormoneexcess suffices for the label “cure,” then all patients can be cured because total thyroidectomy or high doses of 131I will abolish hyperthyroidism albeit at the expense of creating another disease (hypothyroidism) requiring lifelong medication with levothyroxine. Iwould not call this a “cure,” which I would like to define as a state with stable thyroid stimulating hormone (TSH), free thyroxine,and triiodothyronine serum concentrations in the normal range in the absence of any thyroid medication. Surgery and radioiodine areunlikely to result in so-defined cures, as their preferable aim as stated in guidelines is to cause permanent hypothyroidism. Discontinuation of antithyroid drugs is followed by 50% recurrences within 4 years; before starting therapy the risk of recurrences can beestimated with the Graves’ Recurrent Events After Therapy (GREAT) score. At 20-year follow-up about 62% had developed recurrent hyperthyroidism, 8% had subclinical hypothyroidism, and 3% overt hypothyroidism related to TSH receptor blocking antibodies and thyroid peroxidase antibodies. Only 27% was in remission, and might be considered cured. If the definition of “cure” wouldalso include the disappearance of thyroid antibodies in serum, the proportion of cured patients would become even lower.
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