scholarly journals Impact of Thyroid Hormone Therapy on Atherosclerosis in the Elderly With Subclinical Hypothyroidism: A Randomized Trial

2018 ◽  
Vol 103 (8) ◽  
pp. 2988-2997 ◽  
Author(s):  
Manuel R Blum ◽  
Baris Gencer ◽  
Luise Adam ◽  
Martin Feller ◽  
Tinh-Hai Collet ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Subclinical Hypothyroidism ◽  
Carotid Plaque ◽  
Carotid Atherosclerosis ◽  
Controlled Trial ◽  
Hormone Replacement ◽  
Intima Media Thickness ◽  
Thyroid Stimulating Hormone ◽  
Double Blind ◽  
The Impact

Abstract Context Subclinical hypothyroidism (SHypo) has been associated with atherosclerosis, but no conclusive clinical trials assessing the levothyroxine impact on carotid atherosclerosis exist. Objective To assess the impact of treatment of SHypo with levothyroxine on carotid atherosclerosis. Design and Setting Randomized, double-blind, placebo-controlled trial nested within the Thyroid Hormone Replacement for Subclinical Hypothyroidism trial. Participants Participants aged ≥65 years with SHypo [thyroid-stimulating hormone (TSH), 4.60 to 19.99 mIU/L; free thyroxine level within reference range]. Intervention Levothyroxine dose-titrated to achieve TSH normalization or placebo, including mock titrations. Main Outcome Measures Carotid intima media thickness (CIMT), maximum plaque thickness measured with ultrasound. Results One hundred eighty-five participants (mean age 74.1 years, 47% women, 96 randomized to levothyroxine) underwent carotid ultrasound. Overall mean TSH ± SD was 6.35 ± 1.95 mIU/L at baseline and decreased to 3.55 ± 2.14 mIU/L with levothyroxine compared with 5.29 ± 2.21 mIU/L with placebo (P < 0.001). After a median treatment of 18.4 months (interquartile range 12.2 to 30.0 months), mean CIMT was 0.85 ± 0.14 mm under levothyroxine and 0.82 ± 0.13 mm under placebo [between-group difference = 0.02 mm; 95% CI, −0.01 to 0.06; P = 0.30]. The proportion of carotid plaque was similar (n = 135; 70.8% under levothyroxine and 75.3% under placebo; P = 0.46). Maximum carotid plaque thickness was 2.38 ± 0.92 mm under levothyroxine and 2.37 ± 0.91 mm under placebo (between-group difference −0.03; 95% CI, −0.34 to 0.29; P = 0.86). There were no significant interactions between levothyroxine treatment and mean CIMT, according to sex, baseline TSH (categories 4.6 to 6.9, 7.0 to 9.9, and ≥10 mIU/L), or established cardiovascular disease (all P for interaction ≥ 0.14). Conclusion Normalization of TSH with levothyroxine was associated with no difference in CIMT and carotid atherosclerosis in older persons with SHypo.

scholarly journals Patterns of Thyroid Hormone Prescription in Patients with Bipolar or Schizoaffective Disorder: Findings from the LiSIE Retrospective Cohort Study

2021 ◽  
Vol 10 (21) ◽  
pp. 5062
Author(s):  
Ingrid Lieber ◽  
Michael Ott ◽  
Louise Öhlund ◽  
Robert Lundqvist ◽  
Mats Eliasson ◽  
...  
Keyword(s):  
Cohort Study ◽  
Thyroid Hormone ◽  
Schizoaffective Disorder ◽  
Subclinical Hypothyroidism ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Hormone Replacement ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Thyroid Hormone Replacement Therapy

The prescription of thyroid hormone replacement therapy (THRT) has increased in the general population; the thyroid stimulating hormone (TSH) threshold to initiate THRT has decreased. It remains unclear whether a similar trend has occurred in patients with bipolar disorder (BD). In this work we explore patterns and trends of prescribing THRT in patients with BD or schizoaffective disorder (SZD) with an observational study and time-trend analysis in the framework of the LiSIE (Lithium—Study into Effects and Side Effects) retrospective cohort study. In most patients, THRT was initiated for subclinical hypothyroidism. The median TSH at which THRT was started was 6.0 (IQR 4.0) mIU/L and the median free serum thyroxine (fT4) at which THRT was started was 11.8 (IQR 3.9) pmol/L. The median TSH concentration at the start of THRT decreased annually with 0.10 mIU/L (p = 0.047) and was higher in patients treated with lithium than in patients treated with other mood stabilisers (p = 0.02). In conclusion, THRT was typically initiated in the context of mild or absent alterations of thyroid function tests with a decreasing TSH threshold. As THRT is rarely reversed once initiated, clinicians need to weigh up potential benefits and risks when prescribing THRT for subclinical hypothyroidism in patients with BD or SZD.

scholarly journals Combined Treatment with Myo-Inositol and Selenium Ensures Euthyroidism in Subclinical Hypothyroidism Patients with Autoimmune Thyroiditis

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Maurizio Nordio ◽  
Raffaella Pajalich
Keyword(s):  
Autoimmune Thyroiditis ◽  
Subclinical Hypothyroidism ◽  
Controlled Trial ◽  
Combined Treatment ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Chronic Lymphocytic Thyroiditis ◽  
Double Blind ◽  
Chronic Autoimmune Thyroiditis ◽  
Tsh Levels

Background. Hashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis or chronic autoimmune thyroiditis, is the most common form of thyroiditis affecting more than 10% of females and 2% of males. The present study aims to evaluate the beneficial effect of a combined treatment, Myo-Inositol plus selenomethionine, on subclinical hypothyroidism.Methods. The study was designed as a double-blind randomized controlled trial. Eligible patients were women diagnosed with subclinical hypothyroidism having Tg antibodies (TgAb) titer higher than 350 IU/mL. Outcome measures were Thyroid Stimulating Hormone (TSH) levels, thyroid peroxidase antibodies (TPOAb) and TgAb titer, selenium, and Myo-Inositol plasma concentration.Results. In the present paper, we demonstrated that the beneficial effects obtained by selenomethionine treatment on patients affected by subclinical hypothyroidism, likely due to the presence of autoantibody (TPOAb and TgAb), are further improved by cotreatment with Myo-Inositol.Conclusions. Indeed, due to its action as TSH second messenger, Myo-Inositol treatment reduces TSH levels closer to physiological concentrations.

scholarly journals Growth hormone in heart failure revisited: An old story retold

2018 ◽  
Vol 88 (3) ◽  
Author(s):  
Antonio Cittadini ◽  
Roberta D'Assante
Keyword(s):  
Heart Failure ◽  
Growth Hormone ◽  
Clinical Performance ◽  
Controlled Trial ◽  
Hormone Replacement ◽  
Indirect Costs ◽  
Deficiency Syndrome ◽  
Hormone Deficiency ◽  
Double Blind ◽  
The Impact

Heart failure (HF) is a disease characterized by increasing prevalence, huge direct and indirect costs, and an ominous prognosis, worse than many cancers. At the beginning of the 90s, growth hormone (GH) was proposed as potential adjunctive therapy in HF mostly due to its growth-promoting, vasodilating, and anti-apoptotic actions. However, although several uncontrolled clinical studies showed that GH therapy improved several cardiovascular parameters, two robust trials failed to confirm these findings. Dwelling upon potential explanations for such apparent discrepancy led to the hypothesis that HF patients exhibit an inhomogeneous basal activity of the GH/insulin-like growth factor 1 (IGF-1) axis, ranging from GH/IGF-1 deficiency to GH resistance. This complex phenomenon was then reconsidered in the context of the so-called multiple hormone deficiency syndrome (MHD), that is the recognition that HF is characterized not only by the hyperactivation of several signaling pathways including the adrenergic, the renin-angiotensin-aldosterone and cytokine systems, but also by a reduced anabolic drive leading to a state of anabolic/catabolic imbalance. Mounting evidence support the concept that such imbalance is not a mere epiphenomen, since it exerts a significant impact on clinical performance and more importantly, on survival. Therefore, the paradigm shift to reconsider HF as MHD represented the underpinning to implement clinical trials focused on hormone replacement therapies in congestive heart failure (CHF). With regard to GH replacement therapy, one controlled single-blind study yielded promising results, and we are currently conducting a double-blind controlled trial, as well a large Registry study to evaluate the impact of MHD on HF progression.

scholarly journals A REVIEW: MECHANISTIC INSIGHTS INTO THE EFFECT OF THYROID DISORDERS ON ESTROGEN LEVEL AND BONE MINERAL DENSITY

2019 ◽  
pp. 9-17
Author(s):  
MINAKSHI JOSHI ◽  
SHRADHA BISHT ◽  
MAMTA F. SINGH
Keyword(s):  
Bone Mineral Density ◽  
Thyroid Hormone ◽  
Bone Turnover ◽  
Bone Mineral ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Disorders ◽  
Hypothyroid Patient ◽  
Mineral Density ◽  
Estrogen Level ◽  
The Impact

Thyroid hormone serves as an indispensable component for the optimum functioning of various biological systems. They curb body’s metabolism, regulates the estrogen level, regulates bone turnover, essential for skeletal development and mineralization. Within the scope of knowledge, it is intimately familiar that thyroid disorders have widespread systemic manifestations, among which in hypothyroidism, even though elevated TSH (thyroid-stimulating hormone) may reduce estrogen level which in turn stimulates osteoclasts and thus cause osteoporosis, while hyperthyroidism accelerates bone turnover. Hypothyroidism does not directly interfere with the skeletal integrity, but treatment with levothyroxine for the suppression of TSH to bring the hypothyroid patient to euthyroid state for a long haul; lead to simultaneous reduction in bone mass and in (bone mineral density) BMD. After the initial relevation of the correlation between thyroid disorders and osteoporosis in numerous studies have emphasized that both hypo and hyperthyroidism either directly or indirectly affects the bone mineral density or leads to the progression of osteoporosis. Therefore the present study is aimed and so designed to review all the possible associations between them and the impact of thyroid disorders on estrogen level and bone mineral density. The main findings of this review indicate that both excesses as well as deficiency of thyroid hormone can be potentially deleterious for bone tissue.

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