scholarly journals Thyroid stimulating hormone resistance syndrome – a case report

2015 ◽  
Vol 8 (1) ◽  
pp. 32-33
Author(s):  
SM Ashrafuzzaman ◽  
Zafar A Latif
Keyword(s):  
Case Report ◽  
Normal Limit ◽  
Thyroid Stimulating Hormone ◽  
Young Girl ◽  
Ectopic Thyroid ◽  
Overt Hypothyroidism ◽  
Hormone Resistance ◽  
Free T4 ◽  
Euthyroid State ◽  
Stimulating Hormone

Resistance to thyrotropin or thyroid stimulating hormone (RTSH) can be defined as decreased responsiveness to thyroid stimulating hormone (TSH) characterized by high TSH with normal but occasionally low T4 and T3 usually in absence of goiter or ectopic thyroid. It can be diagnosed when TSH is >30 mIU/L but free T4 (FT4) is within normal limit. Patient usually presents in euthyroid state with abnormally high TSH but may also present with mild to overt hypothyroidism. The precise prevalence is not known, but 20-30% infants may show transient mild RTSH. In adults it is rare.Here we report a case of RTSH in which a 19 years old young girl presented in euthyroid state with mild goiter.Ibrahim Med. Coll. J. 2014; 8(1): 32-33

scholarly journals Thyroid dysfunction in patients of metabolic syndrome: A study from a tertiary care center in India

2021 ◽  
Vol 12 (10) ◽  
pp. 47-50
Author(s):  
Ritu Gupta ◽  
Akhil K Vijayan ◽  
Sushma Choudhary
Keyword(s):  
Metabolic Syndrome ◽  
Thyroid Dysfunction ◽  
Care Center ◽  
Tertiary Care ◽  
Cross Sectional Study ◽  
Thyroid Stimulating Hormone ◽  
P Value ◽  
Overt Hypothyroidism ◽  
Free T4 ◽  
Cross Sectional

Background: Metabolic syndrome is characterized by hypertension, dyslipidemia, central obesity, glucose intolerance, insulin resistance. Thyroid hormone acts as general pacemaker, accelerating metabolic process and may be associated with metabolic syndrome. There is no information available in literature regarding the prevalence and association of thyroid dysfunction in metabolic syndrome in this central region of the country. Aims and Objective: To estimate the prevalence of thyroid dysfunction in patients of metabolic syndrome. Materials and Methods: It is a duration based prospective cross sectional study including 200 patients of metabolic syndrome. A detailed history, clinical examination and relevant investigations including serum Free T4 (FT4), Free T3 (FT3), Thyroid Stimulating Hormone (TSH) were done. Range, frequencies, percentage, mean, standard deviation and P value were calculated. P value of < 0.05 was taken as significant. Results: Prevalence of thyroid dysfunction in metabolic syndrome patients was 28.5%. Prevalence of subclinical and overt hypothyroidism was 18.5% and 8.5% respectively. In patients with both metabolic syndrome and thyroid dysfunction, most common components associated are diabetes mellitus and hypertriglyceridemia. Conclusion: Thyroid dysfunction is significantly common in metabolic syndrome patients. It should be aggressively detected and treated in these patients for better outcome.

Genetic thyroid stimulating hormone regulation of atrial fibrillation risk is mediated through an effect on height

2021 ◽  
Author(s):  
Mingjian Shi ◽  
Ali M Manouchehri ◽  
Christian M Shaffer ◽  
Nataraja Sarma Vaitinadin ◽  
Jacklyn N Hellwege ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Genetic Association ◽  
Multiple Testing ◽  
Mendelian Randomization ◽  
Later Life ◽  
Thyroid Stimulating Hormone ◽  
Hormone Regulation ◽  
Nucleotide Polymorphisms ◽  
Free T4 ◽  
Stimulating Hormone

Abstract Background A genetic predisposition to lower thyroid stimulating hormone (TSH) levels associates with increased atrial fibrillation (AF) risk through undefined mechanisms. Defining the genetic mediating mechanisms could lead to improved targeted therapies to mitigate AF risk. Methods We used two-sample Mendelian randomization (MR) to test associations between TSH-associated single nucleotide polymorphisms (SNPs) and 16 candidate mediators. We then performed multivariable Mendelian randomization (MVMR) to test for a significant attenuation of the genetic association between TSH and AF, after adjusting for each mediator significantly associated with TSH. Results Four candidate mediators (free T4, systolic blood pressure, heart rate, and height) were significantly inversely associated with genetically predicted TSH after adjusting for multiple testing. In MVMR analyses, adjusting for height significantly decreased the magnitude of the association between TSH and AF from -0.12 (s.e. 0.02) occurrences of AF per standard deviation change in height to -0.06 (0.02) (p=0.005). Adjusting for the other candidate mediators did not significantly attenuate the association. Conclusions The genetic association between TSH and increased AF risk is mediated, in part, by taller stature. Thus, some genetic mechanisms underlying TSH variability may contribute to AF risk through mechanisms determining height occurring early in life that differ from those driven by thyroid hormone level elevations in later life.

scholarly journals Thyroid-stimulating Hormone and Insulin Resistance: Their Association with Polycystic Ovary Syndrome without Overt Hypothyroidism

2017 ◽  
Vol 39 (05) ◽  
pp. 224-228 ◽  
Author(s):  
Cristina Benetti-Pinto ◽  
Vanessa Piccolo ◽  
Daniela Yela ◽  
Heraldo Garmes
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Thyroid Stimulating Hormone ◽  
Metabolic Parameters ◽  
Overt Hypothyroidism ◽  
Model Assessment ◽  
Ovary Syndrome ◽  
Cross Sectional ◽  
Stimulating Hormone

Objective This study analyzed the effectiveness of the thyroid-stimulating hormone (TSH) as a predictor of insulin resistance (IR) and its association with the clinical and metabolic parameters of women with polycystic ovary syndrome (PCOS) without overt hypothyroidism. Study Design A cross-sectional study was performed. Women with PCOS and without overt hypothyroidism (n = 168) were included. Methods Receiver operating characteristic (ROC) curve was used to determine the cut-off point for TSH that would maximize sensitivity and specificity for a diagnosis of IR using homeostatic model assessment of insulin resistance (HOMA-IR) ≥ 2.71. Clinical and metabolic parameters were compared as a function of the TSH cut-off limit and the presence of IR. Results Thyroid-stimulating hormone ≥ 2.77 mIU/L was associated with a diagnosis of IR, with sensitivity of 47.9% and specificity of 65.3%. There were no differences in clinical, hormonal or metabolic parameters between TSH < 2.77 and TSH of 2.77 – 10 mIU/L. Conclusion In women with PCOS without overt hypothyroidism, TSH ≥ 2.77 mIU/L is associated with IR; however, with poor sensibility, showing TSH to be a poor predictor of IR in this population. No clinical or metabolic alterations were found that would justify a change in clinical management. Thus, the IR should be investigated in all women with PCOS irrespective of TSH level.

scholarly journals Decrease of Free Thyroxine Levels after Controlled Ovarian Hyperstimulation1

2000 ◽  
Vol 85 (2) ◽  
pp. 545-548 ◽  
Author(s):  
A. F. Muller ◽  
A. Verhoeff ◽  
M. J. Mantel ◽  
F. H. de Jong ◽  
A. Berghout
Keyword(s):  
Controlled Ovarian Hyperstimulation ◽  
Thyroid Stimulating Hormone ◽  
Psychomotor Development ◽  
Ovarian Hyperstimulation ◽  
Free T4 ◽  
Before And After ◽  
Maternal Thyroid ◽  
A Prospective Study ◽  
Opposing Effects ◽  
Stimulating Hormone

Controlled ovarian hyperstimulation could lead to opposing effects on thyroid function. Therefore, in a prospective study of 65 women undergoing controlled ovarian hyperstimulation, thyroid hormones, T4-binding globulin, TPO antibodies, gonadotropins, estradiol, and PRL were measured before and after controlled ovarian hyperstimulation. After ovarian stimulation (mean ± se of mean): free T4 decreased, 14.4 ± 0.2 vs. 12.9 ± 0.2 pmol/L (P &lt; 0.0001); thyroid-stimulating hormone increased, 2.3 ± 0.3 vs. 3.0 ± 0.4 mU/L (P &lt; 0.0001); T4-binding globulin increased, 25.2 ± 0.7 vs. 33.9 ± 0.9 mg/L (P &lt; 0.0001); total T4 increased, 98.1 ± 2.3 vs. 114.6 ± 2.5 nmol/L (P &lt; 0.0001); total T3 increased, 2.0 ± 0.04 vs. 2.3 ± 0.07 nmol/L (P &lt; 0.0001); TPO antibodies decreased, 370 ± 233 U/mL vs. 355 ± 224 U/mL (P &lt; 0.0001); LH decreased, 8.1 ± 1.1 vs. 0.4 ± 0.1 U/L (P &lt; 0.0001); FSH did not change, 6.5± 0.6 vs. 7.9 ± 0.9 U/L (P = 0.08); human CG increased, &lt;2 ± 0.0 vs. 195 ± 16 U/L (P &lt; 0.0001); estradiol increased, 359.3 ± 25.9 pmol/L vs. 3491.8 ± 298.3 pmol/L (P &lt; 0.0001); and PRL increased, 0.23 ± 0.02 vs. 0.95 ± 0.06 U/L (P &lt; 0.0001). Because low maternal free T4 and elevated maternal thyroid-stimulating hormone levels during early gestation have been reported to be associated with impaired psychomotor development in the offspring, our findings indicate the need for additional studies in the children of women who where exposed to high levels of estrogens around the time of conception.

scholarly journals Obesity and hypothyroidism

2013 ◽  
Vol 10 (2) ◽  
pp. 54-58 ◽  
Author(s):  
S M Zakharova ◽  
L V Savelieva ◽  
M I Fadeeva
Keyword(s):  
Weight Loss ◽  
Energy Expenditure ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Thyroid Stimulating Hormone ◽  
Overt Hypothyroidism ◽  
Obese Patients ◽  
Common Diseases ◽  
The Relationship ◽  
Stimulating Hormone

Obesity and hypothyroidism are common diseases, and consequently clinicians should be particularly alert to the possibility of thyroid dysfunction in obese patients. The relationship between thyroid function and obesity is likely to be bidirectional, with hypothyroidism affecting weight, but obesity also influencing thyroid function. Both serum thyroid-stimulating hormone and fT3 are typically increased in obese individuals, an effect likely mediated by leptin. Following L-T4 treatment for overt hypothyroidism, weight loss appears to be modest and mediated primarily by loss of water weight rather than fat. Selected thyroid analogs might be a means by which to improve weight loss by increasing energy expenditure in obese patients during continued caloric deprivation

Sign in / Sign up

Export Citation Format

Share Document