Decreased Thyroid Hormone Research Articles

Sex Differences in the Association Between Thyroid Hormone Sensitivity and Cardiovascular-Kidney-Metabolic Syndrome.

The relationship between thyroid hormone sensitivity and cardiovascular-kidney-metabolic (CKM) syndrome remains unclear. This study aims to investigate the association between thyroid hormone sensitivity and the early-stage of CKM syndrome, with a specific focus on the moderating effects of sex and age. A total of 8,391 euthyroid participants were enrolled in this cross-sectional study. Data on metabolic parameters and thyroid hormone levels were collected. Thyroid hormone sensitivity indices-thyroid feedback quantile index (TFQI), thyroid-stimulating hormone index (TSHI), TT4 resistance index (TT4RI), and free thyroxine to free triiodothyronine ratio were calculated. Logistic regression models and restricted cubic spline regression (RCS) were used to analyze the association between thyroid hormone sensitivity and stage 2 of CKM syndrome stratified by sex and age. In men, the higher TFQI, TSHI, and TT4RI values were significantly associated with increased risks of stage 2 of CKM. In women, these associations were weaker but still present, particularly for TSHI. RCS analysis also showed that the risk of CKM tended to increase with decreasing thyroid hormone sensitivity in men. However, these associations in women were not as significant as in men. Age-stratified analysis revealed that older men (>50 years) showed a stronger correlation between thyroid hormone sensitivity and CKM syndrome compared to women. This study demonstrated that impaired thyroid hormone sensitivity is significantly associated with the early-stage of CKM syndrome, particularly in older men. These findings provide the evidence of the importance of thyroid hormone sensitivity in CKM syndrome, especially in men over the age of 50.

Thyroid Endocrine Disrupting Potential of Fluoxetine in Zebrafish Larvae.

Fluoxetine (FLX), a typical selective serotonin reuptake inhibitors, has been frequently detected in aquatic environment and wild fish. However, little is known about its effect on thyroid endocrine system. In the present study, zebrafish (Danio rerio) embryos were exposed to 1, 3, 10, and 30 μg/L of FLX for 6 days. Chemical analysis demonstrated that FLX and its metabolic product (nonfluoxetine, NFLX) were accumulated in zebrafish larvae. The exposure resulted in decreased thyroid hormones (THs) levels, indicating thyroid endocrine disruption. Moreover, thyroid-stimulating hormone (TSH) content was significantly inhibited in a concentration-dependent manner after exposure to FLX. Gene transcription in the hypothalamic-pituitary-thyroid (HPT) axis was further examined, and the results showed that the genes encoding corticotrophin-releasing hormone (crh) and thyrotropin-releasing hormone (trh) were significantly up-regulated as a compensatory mechanism for the decreased TH contents accompanied with decreased tshβ mRNA expression. In addition, genes involved in thyroid hormone synthesis (sodium/iodide symporter, nis, thyroglobulin, tg) and transport (transthyretin, ttr) were down-regulated after exposure to FLX in a concentration-dependent manner. The increased gene transcription of deiodinases (dio2) and uridinediphosphate-glucuronosyltransferase (ugt1ab) might be responsible for the decrease of TH contents. In addition, a significant inhibition in thyroid hormone receptors (trα and trβ) gene expression was observed upon treatment with FLX. All these results demonstrated that FLX could alter THs and TSH content as well as gene transcription in the HPT axis, exerting an endocrine disruption of the thyroid system in zebrafish larvae.

Evaluation of zinc oxide nanocomposites and L-ascorbic acid on meat quality during transport induced stress in birds of Sonali breed

The study assessed the efficacy of phytofabricated zinc oxide nanoparticles (CF-ZnONPs) and L-ascorbic acid in alleviating pre-slaughter transport induced stress in birds of Sonali breed (Cross bred of Rhode Island Red cocks and Fayoumi hens). A total of 120 birds were divided into four groups: negative control (T1) which were loaded in vehicle but not transported, Positive control (T2) birds were transported without any prior supplementation, T3 and T4 birds were transported with prior supplementation (a day before transportation) of CF-ZnONPs @100 µg/ml and L-ascorbic acid @82 µg/ml in drinking water. Results obtained observed significant reduction in live weight, meat colour and pH but increased drip loss percentage in T2 group. Significantly elevated H/L ratio was recorded in all transported groups. Increased cortisol and TSH levels and decreased thyroid hormones, Triiodothyronine and thyroxin (T3 and T4) levels were recorded in T2 group. However, supplementation with CF-ZnONPs and L-ascorbic acid notably reversed these adverse effects, restoring meat quality and other metabolic profiles. Notably, ascorbic acid exhibited greater efficacy, suggesting its superior role in mitigating transportation-induced stress. Overall, these findings highlight the importance of antioxidant supplementation in alleviating transport induced stress in birds.

6770 Graves’ disease induced by COVID-19 infection in a 49 year old male

Abstract Disclosure: N. Al-hosainat: None. A. Al Najada: None. T. Salar: None. S. Iqbal: None. K. Abdel Gadir: None. Introduction: Graves’ disease is an autoimmune disease causing hyperthyroidism, characterized by elevated thyrotropin-receptor antibodies. COVID-19 infection has been increasingly reported as a trigger of thyroid illness including Graves’ disease. We present a unique case of 49-year-old patient who was diagnosed with Graves’ disease after COVID-19 infection. Case description: A 49-year-old male patient with history of prediabetes presented with complaints of tremor, fatigue, generalized itching, and unintentional weight loss (30 Ibs in 6 months). He had COVID-19 infection 3 months prior. The remainder of review of systems was negative. No family history of thyroid disease. On exam, the patient had sinus tachycardia with otherwise normal vital signs. Diffuse thyromegaly was noted along with an intermittent fine tremor of the extremities. Blood work was notable for low TSH <0.01 uIU/mL, elevated free T4 (3.4 ng/dL), free T3 (17.6ng/dL), and TSH receptor antibody (12 IU/L). Thyroid ultrasound showed mild goiter with 2 nodules, one of which was TIRADS 4 and 1.5cm. This nodule was biopsied and found to be benign. Radioactive iodine uptake scan revealed homogeneous diffuse increased thyroid uptake. The diagnosis of Graves’ disease was made, and the patient was started on propranolol and methimazole with significant improvement of his symptoms and his laboratory tests normalizing. Discussion: Graves' disease is an autoimmune disease, characterized by hyperthyroidism, goiter, occasional orbitopathy and dermopathy. Caused by antibodies against thyroid-stimulating hormone receptors which stimulate thyroid hormone secretion and thyroid growth. Treatment is aimed to decrease thyroid hormone synthesis by either a Thionamide, radioiodine ablation, or surgery. Remission rates with antithyroid drugs average under 40 percent after one to two years of treatment and could exceed 80 percent after 5 to 10 years of treatment. COVID-19 is a multi-system disease, caused by SARS-CoV-2 virus, transmitted by large droplets and small particle aerosols, was declared a pandemic in 2020 and affected millions of people worldwide. There is emerging data showing the association of COVID-19 with various thyroid diseases including thyroiditis and relapse of known Graves' disease after the infection. We present a case of newly diagnosed Graves’ disease after COVID-19 infection in a patient with no personal or family history of such disease which raises the concern of autoimmune pathway activation induced by the infection. The onset of Graves’ disease after COVID-19 infection does not depend on the presence of pre-existing thyroid pathology and in this case responded well to antithyroid medication. Conclusion: COVID-19 can lead to the development of a range of medical illnesses. In patients who develop symptoms of thyrotoxicosis, Graves’ disease should be suspected, investigated, and treated appropriately Presentation: 6/3/2024

7099 Severe Hypothyroidism from Potassium Iodide Supplements: A Case of Failure to Escape from Wolf- Chaikoff Effect

Abstract Disclosure: M.G. Hamilton: None. A. Kulkarni: None. P. Lekprasert: None. Introduction: The Wolf-Chaikoff effect (WCE) is a physiological response of the thyroid gland to supraphysiologic iodide levels. Failure to escape the WCE can lead to thyroid dysfunction, and we present such a case in a patient with Hashimoto’s thyroiditis taking high-dose potassium iodide (KI). Case Description: A 44-year-old female with hypothyroidism secondary to Hashimoto’s thyroiditis presented with 10-pound weight gain, extremity swelling, fatigue, and abnormal menstruation. She was prescribed Levothyroxine several years ago but stopped taking it shortly after as she felt no improvement. On physical exam, she was bradycardic with heart rate of 58 bpm. There is no goiter but dry skin and edematous lower extremities. Labs revealed TSH of 127 pg/mL (0.35-4.94), free T4 0.1ng/dL (0.8-1.8), TPO Ab 645 (<9) IU/mL in comparison to her labs 2 months ago of TSH 11 pg/mL and free T4 0.9 ng/dL. Suspicion for worsening hypothyroidism from Hashimoto’s was low given this dramatic change on labwork and clinically. On further questioning, she had been taking KI 130 mg/day (Iodine 100 mg, daily requirement 150 mcg/day) as advised by her homeopathic doctor. The supplements were stopped, and she was re-started on Levothyroxine. After 8 weeks, she reported improvement of symptoms and weight loss. TSH is normal at 3.54pg/ml and free T4 1.2 ng/dL. Discussion:The WCE serves as a protective mechanism to decrease thyroid hormone production in the setting of high iodide levels to prevent development of hyperthyroidism. WCE is explained by the formation of Iodopeptides inhibits thyroid peroxidase (TPO) mRNA and protein synthesis resulting in an inhibition of thyroglobulin iodination. WCE is temporary and expected to wane over a few days to weeks and is known as the Wolf-Chaikoff escape due to down regulation of the sodium iodine symporter (NIS) thereby decreasing the intrathyroidal inorganic iodine concentration and permitting normal TPO activity. Rarely, failure to escape WCE can lead to hypothyroidism due to continued suppression of thyroid hormone synthesis. Risk factors include underlying thyroid diseases i.e. Hashimoto’s or other causes of thyroiditis, use of Amiodarone, Lithium or Iodine-containing radiocontrast media and KI supplements. In our case, Hashimotos’ thyroiditis predisposed her to thyroid dysfunction and failure to escape from WCE after taking high-dose KI supplements causing severe hypothyroidism. Thus, this report highlights that in clinical practice, especially in patients with pre-existing thyroid dysfunction, a significant TSH increase, a high suspicion index is needed to investigate for other causes like concurrent use of iodine-containing food/drug leading to the failed escape from WCE apart from verifying compliance to thyroid replacement therapy. Presentation: 6/3/2024

5150 When Few Options Exist: Graves’ Disease Treated with Potassium Iodide and Levothyroxine Block-and-Replace Therapy

Abstract Disclosure: O. Magvanjav: None. S.K. Majumdar: None. Background: In the US, methimazole and propylthiouracil are effective first-line agents for the treatment of Graves’ disease. However, side effects including liver dysfunction may limit their use. In such instances, alternative non-conventional agents such as potassium iodide (KI) may be considered. Here, we present a case of a patient with Graves’ disease successfully treated with KI, drawing on the example of similar treatment experiences in Japan. Clinical case: Our patient is a 29-year-old woman who presented with a 3-week history of palpitations accompanied by fatigue, heat intolerance, itchiness, insomnia, and unintentional weight loss. Exam was notable for tachycardia (135 bmp), elevated blood pressure (BP) (150/81 mmHg), normal temperature, slight thyromegaly, brisk reflexes, mild anxiousness, and tremulousness. She was found to have a TSH of 0.007 mIU/ml (normal: 0.270-4.200 mIU/ml), elevated free T4 of 5.19 ng/dl (normal: 0.80-1.70 ng/dL), total T3 of 330 ng/dl (normal: 72.0-153.0 ng/dl), total T4 of 12.1 ug/dl (normal: 4.5-11.7 ug/dl), and positive antibodies (TSI 443%; TRAB 5.42 IU/L). A thyroid ultrasound showed diffuse hyperemia and a 1.4 cm right lobe TR3 nodule. She had a normal baseline neutrophil count with mild eosinophilia; a baseline hepatic function panel was not obtained. She was started on methimazole 20 mg daily and metoprolol XL 50 mg daily for symptom control. One week into treatment, a hepatic function panel showed elevated liver enzyme levels: AST 70 U/L (normal: 10-35 U/L) and ALT 223 U/L (normal: 10-35 U/L); previous values from 2 years prior were normal. Repeat levels a few days later showed increasing liver enzyme levels (AST 83 U/L; ALT 268 U/L) despite decreasing thyroid hormone levels. Methimazole was stopped, and she was then seen by a gastroenterologist, who concurred with the possibility of an adverse drug reaction to methimazole. She declined definitive therapy with surgery or radioactive iodine therapy and wanted to pursue alternative and less invasive options. Drawing on a previous successful experience from Japan, we initiated her on KI (50 mg twice daily), which resulted in normalization of her thyroid hormones within two weeks of initiation. She subsequently developed hypothyroidism 2 months later, at which point we initiated block-and-replace therapy with the addition of 50 mcg of levothyroxine. Her liver enzymes normalized with normalization of thyroid hormones. Conclusions: We present a patient with symptomatic Graves’ disease who was successfully treated with KI in the setting of limited treatment options, specifically an adverse reaction to methimazole (transaminitis), and who declined both surgery and radioactive iodine. This case demonstrates that KI may be useful in Graves’ disease as either a bridge to more definitive therapy when thioamides are not tolerated, or perhaps as a treatment option for those most likely to go into remission. Presentation: 6/1/2024

Thyroid, neurodevelopmental, and kidney toxicities of common organic UV filters in embryo-larval zebrafish (Danio rerio), and their potential links

Organic UV filters (OUVFs) have been commonly used in sunscreen and many consumer products. Following dermal application, these compounds can enter circulation and may cause systemic effects in humans. In the present study, we chose four OUVFs frequently detected in the environment, i.e., avobenzone (AVB), benzophenone-3 (BP-3), octocrylene (OC), and octyl methoxycinnamate (OMC), and evaluated their thyroid, neurodevelopmental, and kidney toxicities. For this purpose, zebrafish embryos (<4 h post fertilization, hpf) were exposed to sublethal concentrations of AVB, BP-3, OC, or OMC until 120 hpf. Exposure to all OUVFs decreased thyroid hormone (TH) levels, probably by enhanced metabolism and excretion of THs (ugt1ab and/or sult1 st5) in the larval fish. Exposure to the OUVFs also induced hypoactivities and/or anxiety-like behaviors: Regulatory changes of mbp, gfap, c-fos, syn2a, sty1a, and stxbp1b genes, support the changes in normal neurobehavior of the larval fish. Moreover, the OUVFs exposure caused increased proteinuria in the fish, along with transcriptional changes of wt1, nephrin, podocin, and cdh17 genes, which could explain the observed reduction in kidney functions. Principal component analysis (PCA) implied the potential interplay of THs with neurogenesis, or podocyte differentiation of the larval fish. Toxicological consequences of altered TH homeostasis, neurobehavior, and kidney function at the early life stage warrant further investigations not only in humans but also in aquatic ecosystems.

Customized Management of Hypothyroidism Through Ayurvedic Intervention

Hypothyroidism is a condition characterized by decreased thyroid hormone production, resulting in diminished metabolic rate, manifesting as a spectrum of symptoms from subclinical hypothyroidism (SCH) to overt hypothyroidism, with associated physiological derangements. In this study Anu taila Nasya was used. A female patient age 22 years weight 58kg was diagnosed with Hypothyroidism from a clinical point of view. There was a dyspnoea, loss of appetite, weakness, weight gain in the last 2 months with irregular menstruation in the past 4 months. Blood report of TSH value shows 6.35µIU/ml. She was treated with Panchakarma Anu taila Nasya followed by Shamana Chikitsa for 6 months follow up. The result of patient was assessed on the basis of subjective and objective criteria. The TSH value after the treatment shows significant result of 4.65µIU/ml. Significant changes were also observed in the clinical features before and after the treatment. So, this study concludes, Anu taila Nasya has Ushna Tikshna dravyas and Vata Kaphahara properties which causes Shodhana and Lekhana of Kapha doshas, along with palliative treatment has shown good and significant result by its Guna-dharma and Shodhana action in hypothyroidism. Hence it can be used as a preferred treatment for hypothyroidism.

Indications for Intravenous T3 and T4.

Therapy with thyroid hormones normally is restricted to substitution therapy of patients with primary or secondary hypothyroidism. Typically, thyroid hormones are given orally. There are few indications for intravenous use of thyroid hormones. Indications for parenteral application are insufficient resorption of oral medications due to alterations of the gastrointestinal tract, partial or total loss of consciousness, sedation in the intensive care unit or shock. In almost all cases, levothyroxine is the therapy of choice including congenital hypothyroidism. In preterm infants with an altered thyroid hormone status, studies with thyroid hormones including intravenous liothyronine showed a normalisation of T3 levels and in some cases an amelioration of parameters of ventilation. A benefit for mortality or later morbidity could not be seen. Effects on neurological improvements later in life are under discussion. Decreased thyroid hormone levels are often found after cardiac surgery in infants and adults. Intravenous therapy with thyroid hormones improves the cardiac index, but in all other parameters investigated, no substantial effect on morbidity and mortality could be demonstrated. Oral liothyronine therapy in these situations was equivalent to an intravenous route of application. In myxoedema coma, intravenous levothyroxine is given for 3 to 10 days until the patient can take oral medication and normal resorption in the gastrointestinal tract is achieved by restoring at least peripheral euthyroidism. Intravenous levothyroxine is the standard in treating patients with myxoedema coma. A protective effect on the heart of i.v. levothyroxine in brain-dead organ donors may be possible.

Subclinical central hypothyroidism in patients with hypothalamic-pituitary disease: does it exist?

Central hypothyroidism (CH) is characterized by decreased thyroid hormone production due to insufficient stimulation of an otherwise normal thyroid gland by TSH. In patients with established hypothalamic-pituitary disease, a low FT4 concentration is considered highly specific, although poorly sensitive, for the diagnosis of CH. That would be comparable to diagnosing primary hypothyroidism in patients at risk only when serum FT4 concentrations are below the reference range, missing all patients with subclinical primary hypothyroidism and preventing proper therapy in patients in which thyroxine replacement is clearly beneficial. Cardiac time intervals, especially the isovolumic contraction time (ICT), have been considered the gold standard of peripheral thyroid hormone action. Using Doppler echocardiography, we have previously shown a very high proportion of prolonged ICT in patients with hypothalamic-pituitary disease and serum FT4 levels indistinguishable from controls. As ICT decreased/normalized after thyroxine-induced increases in FT4 concentrations within the normal reference range, prolonged ICT was considered a bona fide diagnostic biomarker of subclinical CH. Those findings challenge the usual interpretation that FT4 concentrations in the mid-reference range exclude hypothyroidism in patients with hypothalamic-pituitary disease. Rather, subclinical central hypothyroidism, a state analogous to subclinical primary hypothyroidism, seems to be frequent in patients with hypothalamic-pituitary disease and normal FT4 levels. They also challenge the notion that thyroid function is usually the least or the last affected in acquired hypopituitarism. The relevance of Doppler echocardiography to correctly diagnose and monitor replacement therapy in both clinical and subclinical forms of CH should improve quality of life and decrease cardiovascular risk, as already demonstrated in patients with clinical and subclinical primary hypothyroidism.

Exploring Thermoregulatory Responses and Hormonal Changes in Heat Stressed Assam Hill Goats

Background: Livestock productivity and health are adversely affected by heat stress (HS). The aim of this study was to determine the effects of HS on the thermoregulation and hormonal profile in Assam Hill Goats reared in the subtropical hilly regions of Meghalaya so as to arrive at a conclusion on its heat adaptation abilities. Methods: An experiment was conducted during the year 2022 for 120 days with twelve (12) Assam Hill Goats, aged between 3-5 months, randomly divided into 2 groups (n=6 per group). The goats in group I were exposed to HS through natural exposure to sunlight during the extreme summer months (May to August) for 07 hours (8 AM to 3 PM) during grazing. The control animals (CON, group II) were maintained under shade with no exposure to sunlight. Thermoregulatory responses viz., rectal temperature, respiratory rate and pulse rate and body weight data were recorded every 15 days interval of the sampling period. The hormonal profile viz., serum T3 (nmol/L), T4 (nmol/L) and Cortisol (ng/mL) were also determined. Result: Results revealed a significant (p less than 0.05) increase in rectal temperature, pulse rate (day 45 onwards to day 120) and respiratory rate in HS group in comparison to CON. A significantly (p less than 0.05) lower average daily gain was recorded in HS group. Serum T3 and T4 concentrations were significantly (p less than 0.05) reduced and cortisol concentration was significantly (p less than 0.05) elevated in HS group in comparison to CON. In conclusion, Assam Hill Goats exposed to environmental HS shows elevated thermoregulatory responses, decreased thyroid hormone activity and increased cortisol activity to reduce production to support life sustaining activities in the hilly regions.

Arsenic-Induced Thyroid Hormonal Alterations and Their Putative Influence on Ovarian Follicles in Balb/c Mice.

Thyroid issues are common among women in their reproductive years, and women with thyroid dysfunction often encounter challenges with fertility. Arsenic is known for its toxic effects on the thyroid and ovaries, investigated independently. However, there is no known study directly or indirectly addressing the association between arsenic, thyroid function, and ovarian reserve. This study aims to investigate the effect of arsenic on thyroid function and its possible implications on ovarian follicular reserve. Female Balb/c mice were given sodium arsenite (0.2ppm, 2ppm, and 20ppm) via drinking water for 30days. Findings showed that arsenic decreased thyroid hormone levels (fT3 and fT4) while increasing TSH levels, which might have led to elevated levels of FSH and LH. Furthermore, arsenic treatment not only decreased thyroid follicle sizes but also altered the ovarian follicular count. The finding demonstrates that arsenic significantly reduced the expression of LAMP1, a lysosomal marker protein. This reduction leads to increased lysosomal permeability in the thyroid, resulting in a significant release of cathepsin B. These changes led to hypothyroidism, which might indirectly affect the ovaries. Also, the elevated levels of growth differentiation factor-8 in arsenic-treated ovaries indicate impaired folliculogenesis and ovulation. Furthermore, arsenic significantly increased the expressions of pAkt and pFoxo3a, implying that arsenic accelerated the activation of the primordial follicular pools. In conclusion, arsenic disrupts lysosomal stabilization, potentially leading to a decline in circulating fT3 and fT4 levels. This disturbance could, in turn, affect the estrous cycle and may alter the pattern of follicular development.

Impaired thyroid hormone sensitivity increases the risk of papillary thyroid cancer and cervical lymph node metastasis.

The association of thyroid hormone sensitivity with papillary thyroid carcinoma (PTC) is unclear. This study investigated the relationship between the thyroid hormone sensitivity indices and the risk of PTC and the influence of thyroid hormone sensitivity on the aggressive clinicopathologic features of PTC. This retrospective study recruited 1225 PTC patients and 369 patients with benign nodules undergoing surgery in Zhongshan Hospital in 2020. The thyroid hormone sensitivity indices were thyroid feedback quantile-based index (TFQI), TSH index (TSHI) and thyrotropin thyroxine resistance index (TT4RI). We employed logistic regression models to explore the correlation between the thyroid hormone sensitivity indices and the risk of PTC and its cervical lymph node metastasis (LNM). PTC patients had significantly higher levels of TSH, TFQI, TSHI and TT4RI compared to the patients with benign nodules, but thyroid hormone levels did not differ significantly between the two groups. Logistic regression analysis revealed that the higher levels of TFQI, TSHI, and TT4RI were associated with an increased risk of PTC after adjustment for multiple risk factors (TFQI: OR = 1.92, 95% CI: 1.39-2.65, P < 0.001; TSHI: OR = 2.33, 95% CI:1.67-3.26, P < 0.001; TT4RI: OR = 2.41, 95% CI:1.73-3.36, P < 0.001). In addition, patients with decreased thyroid hormone sensitivity had a higher risk of cervical LNM in multiple logistic regression analysis (TFQI: OR = 1.38, 95% CI:1.03-1.86, P = 0.03; TSHI: OR = 1.37, 95% CI:1.02-1.84, P = 0.04; TT4RI: OR = 1.41, 95% CI:1.05-1.89, P = 0.02). Impaired sensitivity to thyroid hormone was associated with an increased risk of PTC, and it is also associated with a higher risk of cervical LNM in PTC patients.

SERUM VITAMIN D LEVELS IN EUTHYROID AND HYPOTHYROID FEMALES VISITING A TERTIARY CARE CENTER OF WESTERN NEPAL

Background: Thyroid function and vitamin D levels may be intricately related. The purpose of the current study was to investigate the relationship between thyroid hormones and vitamin D levels in females attending a tertiary care center in western Nepal. Methods: This hospital-based cross-sectional study enrolled 300 women advised to get a thyroid function test (TFT) were included in the study population. They were grouped as euthyroid and hypothyroid based on the TFT status and their serum vitamin D concentrations were measured. Vitamin D levels were classified as normal, deficient, and insufficient using the standard criteria. Statistical tests like Chi-square analysis, Mann-Whitney U test, Kruskal Wallis test, and Spearman’s correlation analysis were performed. Finally, a multiple linear regression analysis was done to adjust for the effects of confounding variables. Results: Majority of the study population (n=214, 71%) had insufficient serum vitamin D levels. The median Vitamin D levels were significantly lower in hypothyroid group as compared to the euthyroid group (16.88 vs. 25.01 ng/ml, p &lt;0.001). Similarly, serum Vitamin D levels were negatively associated with obesity, winter and spring seasons, and vegetarian diet. After adjustment for the confounders, the Vitamin D levels were significantly lower in hypothyroid population than the euthyroid group (P&lt;0.001). Conclusions: In conclusion, majority of our study participants had insufficient vitamin D, whose concentration further dropped with decreasing thyroid hormone levels. This could have potentially adverse clinical implications.

284-LB: From Metabolically Healthy Obesity (MHO) to Metabolically Unhealthy Obesity (MUHO)—Decreased Thyroid Hormone Sensitivity

Background: To explore the difference of thyroid hormone sensitivity between metabolically healthy and metabolically unhealthy obesity patients and its influence on obesity phenotype. Methods: 10927 euthyroid adults were enrolled, 4 groups based on the presence/absence of metabolic disorders (MD) and BMI were divided: 1) NC (n=1441): no MD and 22≤BMI &amp;lt; 25Kg/m2. 2) NMu (n=3765): MD and 22≤BMI &amp;lt; 25Kg/m2. 3) MHO (n=148): obese with no MD (BMI≥28Kg/m2). 4) MuHO (n=1981): obese with MD (BMI≥28Kg/m2). MD was defined as meeting none of the following criteria: fasted blood glucose ≤6.1 mmol/L; triglycerides ≥1.7 mmol/L; high density lipoprotein (HDL) &amp;lt;1.0 mmol/L (male) and &amp;lt;1.3 mmol/L (female); elevated SBP (≥130 mmHg) or/and DBP (≥85 mmHg). Thyroid hormone central sensitivity indices were calculated by thyroid feedback quantile-based index (TFQI), TSH index (TSHI), Chinese-referenced parametric TFQI (PTFQI) and thyrotropin thyroxine resistance index (TT4RI). Peripheral thyroid hormone sensitivity was evaluated by FT3/FT4 ratio. Results: Compared with MHO group, TFQI, PTFQI and TT4RI elevated in MuHO group, and the trend still existed after adjusting for confounding factors. High FT3/FT4 ratio was an independent risk factor for MuHO (OR = 1.22, 95%CI: 1.13, 1.37, P&amp;lt;0.001). In euthyroid obese patients, decreased TFQI was a protective factor for MHO (OR=0.71, 95%CI 0.51, 0.83, P=0.036), while TSHI (OR= 1.27, 95%CI: 1.11, 1.38, P =0.027) and TT4RI (OR= 1.08, 95%CI: 1.03, 1.16, P =0.022) were significantly correlated with the occurrence of MuHO. Conclusions: Thyroid hormone sensitivity is impaired with elevated BMI. Impaired thyroid hormone sensitivity associated with the development of metabolically unhealthy obesity in patients with similar BMI. Keywords Metabolically Healthy Obesity, Thyroid Hormone Sensitivity Disclosure N. Zhang: None. G. Wang: None. Funding National Natural Science Foundation of China (81770792)

Abstract #1407449: Successful Plasma Exchange and Thyroidectomy in Thyroid Storm

Thyroid storm is a severe manifestation of thyrotoxicosis that is defined by hyperthyroidism with multi-organ failure. Typical treatment revolves around decreasing thyroid hormone production and peripheral conversion of T4 to T3. TPE (Therapeutic Plasma Exchange) removes cytokines, antibodies, and thyroid hormones with their bound proteins, but this is mostly a transient option until medications take effect. TPE +/- thyroidectomy is not an ATA (American Thyroid Association) recommended practice but can be considered in individuals. Multiple case reports have been published showing successful resolution of storm with plasmapheresis and surgery if medical management failed or in cases of severe iodine-induced storms. Here, we present a patient in thyroid storm with history of untreated Graves complicated with iodine-induced disease. A 49-year-old male with untreated Graves disease was brought to the hospital after a motor vehicle accident. He underwent multiple contrasted CT studies and found to have several traumatic fractures requiring urgent surgical fixation. In the ER, he was in clinical heart failure with Atrial fibrillation with rapid response, which was treated with an amiodarone drip. He was later found to have suppressed TSH and elevated free thyroid hormones. Full medical treatment for thyroid storm including cholestyramine and steroids was started with initial biochemical improvement for 7 days; however, his thyroid function and clinical status began to deteriorate. During his ICU course, he had worsening Atrial Fibrillation, life-threatening Upper GI bleed with altered mental status which led to his intubation and eventual tracheostomy. We then decided to proceed with TPE and plans for urgent thyroidectomy. He underwent 5 sessions of TPE with nearly a 50% drop in hormones allowing him to be stable enough to undergo a successful total thyroidectomy without surgical complications. Although he did develop presumed catheter associated blood stream infection, it did resolve after antibiotics and central line removal. Soon after, he was discharged to inpatient rehab for ongoing physical therapy. There are currently no ATA guideline recommendations for TPE and thyroidectomy for thyroid storm. In our case, this approach appeared effective in relieving the life-threatening storm our patient presented in. Perhaps, the addition of TPE +/- thyroidectomy after medical treatment failure should be considered earlier for patients with life-threatening thyroid storm and at higher risks for decompensation.

Obesity and Impact On Thyroid Hormone and Subclinical Hypothyroidism

Background: Obesity is a metabolic disorder due to physical inactivity associated with increased consumption of calories. The excess calorie is stored as fat in adipose tissue, the fat loaded adipose tissue stimulates inflammatory pathway. The secreted inflammatory cytokines influence the sodium iodide transporter on the surface of thyroid gland. It causes decreased Thyroid hormone (TH) secretion &amp; elevated Thyroid Stimulation Hormone (TSH). the energy metabolism of the body is regulated by TH, decreased TH secretion in obesity disturbs energy metabolism. Material &amp; Methods: The study population are the patients attending OPD of medicine a tertiary hospital in Bhopal, Madhya Pradesh (Central India). Total 25 patients are selected for the study based on their anthropometric measurements (Weight, Height, BMI) confirmed them as obese. Of them 16 are males and 9 are females aged &gt;35 years and are compared with equal number of age matched control population. Results: The values obtained after investigation of various parameters of study as well as control is analysed using SPSS software. The obtained mean, SD values of these parameters are as follows. Conclusion: The obesity due to excessive calorie intake with low physical activity deposits more fat into adipose tissue. The fat loaded adipocytes not only increases blood lipids but also aggravates inflammatory pathways. The secreted inflammatory cytokines (IL-1, 12,18, TNF- α , IFN influences thyroid function by a change in lodide transport across the thyroid gland.

Thyroid hormone decreasing after mechanical thrombectomy for cerebral infarction (P3-5.018)

<h3>Objective:</h3> The aim of this study wasto clarify the changes in thyroid hormone levels in the acute phase and the effects of the iodine contrast agent on thesehormones. <h3>Background:</h3> Mechanical thrombectomy (MT) is an established treatment for large vessel occlusion in patients with cerebral infarction. The use of iodine contrast agent decreases thyroid hormone levels via the so-called Wolff-Chaikoff effect. Low triiodothyronine (T3) syndrome caused by a severe illness status can contribute to decreased thyroid hormones. Reportedly, a low T3 level is associated with poor prognosis in patients with cerebral infarction. <h3>Design/Methods:</h3> This was a single-center, prospective, and single-arm trial. Thyroid stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) were tested on admission and 24 h postoperatively in patients who were approved for MT. <h3>Results:</h3> A total of 37 patients were screened during the study period and 31 patients were enrolled. Significant decreases were observed in TSH (<i>P</i> &lt; 0.001) and FT3 (<i>P</i> &lt; 0.001) levels 24 h after MT. Moreover, there was a correlation between the decrease ratio of change in FT3 levels and the amount of iodine contrast agent used per body surface area (<i>r</i> = 0.43, <i>P</i> = 0.019), while no such correlations were detected for TSH and FT4. <h3>Conclusions:</h3> We demonstrated that decrease in TSH and FT3 levels in the acute phase after MT and that FT3 levels were associated with the amount of iodine contrast agent used. <b>Disclosure:</b> Dr. Kobayashi has nothing to disclose.

Comparison of the Effect of a Protein-Free and Restricted High Protein—Low Carbohydrate Diet on Ventricular Myosin ATPase Activity and Isomyosin Profile in Young Rats: Evidence That Protein-Depleted Animals Are Euthyroid

Young rats fed a protein-deficient diet have elevated total triiodothyronine (T3) levels in spite of decreased skeletal muscle protein turnover. Interpretation of the thyroid status of these animals is complicated by increased T3 binding by serum proteins. Free T3 levels ranging from normal to low and decreased resting oxygen consumption have been reported. To investigate the thyroid status of animals fed a protein-free diet, ventricular myosin ATPase activity and isomyosin profile have been used as an index of thyroid hormone activity. The effect of the protein-free diet has been compared to a restricted high protein-low carbohydrate diet, which causes clear evidence of decreased thyroid hormone effect. After 28 d, calcium-activated myosin ATPase activity was 1.50 ± 0.05 µmol P1/(mg protein · min) in animals fed the basal diet, 1.16 ± 0.03 µmol P1/ (mg protein · min) in animals fed the restricted high protein-low carbohydrate diet and 1.48 ± 0.04 µmol P1/(mg protein · min) in animals fed the protein-free diet. In addition, a shift in isomyosin content with the appearance of V2 and V3 isomyosins occurred with the restricted high protein-low carbohydrate diet but not the protein-free diet. The failure of the protein-depleted rats to decrease myosin ATPase activity and alter isomyosin content suggests that they are euthyroid.

Investigating the Effect of Thyroid Hormones on Diabetic Nephropathy in Type 2 Diabetic Patients Referred to Ahvaz Hospitals in 2017

Background: Nephropathy is one of the most common microvascular complications of diabetes. Type 2 diabetic patients with subclinical hypothyroidism are associated with a high prevalence of diabetic nephropathy. Objectives: This study aims to investigate the effect of thyroid hormones on diabetic nephropathy in type 2 diabetic patients referred to Ahvaz hospitals in 2017. Methods: In this case-control study, 200 diabetic patients (100 with nephropathy and 100 without nephropathy) referred to Ahvaz hospitals were randomly selected. After sampling, biochemical parameters such as fasting blood sugar, BUN, creatinine, uric acid, calcium, and phosphorus were measured. Then, thyroid hormones and thyroid-stimulating hormone (TSH) hormones were measured by the quantitative luminescence method. Results: Thyroid hormones in the patient group were lower than in the control group (P &lt; 0.001). The concentration of TSH in the patient group was higher than in the control group (P &lt; 0.001). Thyroid hormones were negatively and significantly related, and TSH hormone was positively and significantly related to kidney assessment markers. Other results showed that increased TSH and decreased thyroid hormones could increase the risk of developing diabetic nephropathy. So that the T3 hormone was associated with diabetic nephropathy with a greater effect (0.000002 - 0.001057) (CI) = 0.000048 = Odds ratio T3 hormone at 0.73 ng/mL levels has a diagnostic value with a sensitivity of 83% and the specificity was 84% for the differentiation of nephropathy in diabetic patients. Conclusions: The results of this study showed that an increase in TSH hormone and a decrease in thyroid hormones could increase the chance of developing diabetic nephropathy. The T3 hormone is more effective with diabetic nephropathy, and with high diagnostic value, it can be suggested as a biomarker for predicting nephropathy in diabetic patients.