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Physiologic Changes
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Hyperemesis gravidarum is associated with elevated levels of hCG, an increase in FT4, and a decrease in TSH (biochemical hyperthyroidism). However, this is largely transitory and rarely associated with clinical hyperthyroidism. Thus routine measuring of thyroid function in hyperemesis is not indicated in the absence of other signs of hyperthyroidism such as weight loss or persistent tachycardia [21]. Furthermore, treatment of transient hyperthyroidism associated with elevated hCG and hyperemesis should not be undertaken in the absence of evidence of intrinsic thyroid disease (see also Chap. 9 in Maternal-Fetal Evidence Based Guidelines) [21]. A large prospective observational study of 25,765 pregnant women who underwent thyroid screening in pregnancy showed no difference in pregnancy complications or in perinatal morbidity and mortality in women with subclinical hyperthyroidism [24].
Thyroid
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
TSH is the main regulator of thyroid function, differentiation, and proliferation. Binding of TSH to its receptor on thyroid cells primarily activates a cyclic adenosine monophosphate cascade, leading to thyroid hormone synthesis and release as well as to the expression of thyroid-specific genes, including those encoding Tg and thyroperoxidase. DTC retains some degree of thyroid-specific gene expression and function similar to normal thyroid cells; therefore, it is responsive to stimulation by TSH. In thyroid cancer cell lines, TSH has been shown to stimulate vascular endothelial growth factor (VEGF) secretion and angiogenesis. Thus, TSH may promote growth in some thyroid cancers.57
Differentiating Psychiatric and Medical Conditions
Published in Paul Ian Steinberg, Psychoanalysis in Medicine, 2020
In the second week in hospital, Mrs. Z experienced episodes of intense agitation of several minutes to an hour in duration. No psychological precipitant was discovered to account for them. They clearly were more severe than her baseline persecutory anxiety, which in itself was considerable. These episodes gradually became more severe and frequent, despite gradually increasing doses of trifluoperazine. They were accompanied by palpitations, hyperventilation, and dizziness. Mrs. Z denied feeling more afraid of being attacked during these episodes. They appeared to have a different quality than her presenting complaints, with more intense agitation, despite no increase in persecutory fears. Repeat physical examination revealed tachycardia of 120 beats/min, blood pressure of 150/195 mmHg, bilateral mild proptosis, and bilaterally moderately increased tendon reflexes. Thyroid function tests were consistent with a diagnosis of hyperthyroidism. Consultation with endocrinology confirmed the diagnosis of Graves’ disease and ruled out pheochromocytoma.
Real world clinical experience with a new formulation of levothyroxine engineered to meet new and stricter regulatory requirements
Published in Current Medical Research and Opinion, 2021
Ulrike Gottwald-Hostalek, Yorki Tayrouz
The current guideline-driven management of hypothyroidism is based on thyroid hormone replacement with levothyroxine (LT4), with the dosage titrated to maintain thyrotropin (TSH; thyroid stimulating hormone) within a defined euthyroid reference range1,2. The homeostatic regulation of thyroid function is such that small differences in the circulating level of thyroxine (T4) cause much larger (as much as ten-fold) and opposite changes in the level of TSH. Thus, small changes in the dose of LT4 may have a clinically significant effect on thyroid function causing a potential thyroid imbalance. Regulators around the world have defined LT4 as a “narrow therapeutic index drug”; as a result, they have adopted increasingly stringent requirements for the content of active ingredients, and bioequivalence between dosage strengths3,4.
Triiodothyronine alongside levothyroxine in the management of hypothyroidism?
Published in Current Medical Research and Opinion, 2021
Ulrike Gottwald-Hostalek, George J. Kahaly
Similar caveats are applied to data from randomized clinical trials, such as those summarized in Table 2, and improved trial designs are needed66–68. Briefly, new trials in this area should use validated, thyroid-specific instruments for measuring QoL, and should be adequately powered to detect clinically meaningful difference in their outcomes (as well as for biochemical outcomes related to thyroid function) that are determined a priori67,68. In addition, the level of residual thyroid function appears to be an important determinant of T3 homeostasis during LT4 replacement therapy69. Accordingly, the benefits of additional T3 are likely to vary according to patients’ residual thyroid function and their endogenous capacity for generating T3. Combining a heterogeneous collection of patients into a randomized trial is likely to lead to amalgamation bias, where important benefits in particular subgroups of patients are lost67. Future clinical trials must support the application of individualized thyroid care, including consideration of pre-treatment thyroid function and the presence of polymorphisms in DIO2, and be of sufficient duration (at least 1 year) to provide support for long-term routine management outside the clinical trial setting68. Achieving a physiological FT4:FT3 ratio should be a key objective68.
Thyroid Feedback Quantile-based Index correlates strongly to renal function in euthyroid individuals
Published in Annals of Medicine, 2021
Sijue Yang, Shuiqing Lai, Zixiao Wang, Aihua Liu, Wei Wang, Haixia Guan
The secretion of thyroid hormone is regulated by hypothalamic-pituitary-thyroid (HPT) axis. Thyrotropin-releasing hormone (TRH) from the hypothalamus promotes the synthesis and release of TSH from the anterior pituitary, which plays an important role in all stages related to the production and secretion of thyroid hormones from the thyroid gland. The levels of TRH and TSH are in turn modulated by the negative feedback of thyroid hormones. Thyroid hormones are mainly secreted in the form of T4, which is catalyzed by deiodinases to form the bioactive T3. Both will bind to carrier proteins in the circulation and enter cells via membrane transporters. T3 then further binds to the nuclear thyroid hormone receptors. Therefore, thyroid function is regulated by the HPT axis and other factors associated with thyroid hormone conversion and bioactivity [26].