Elevated Thyroid-stimulating Hormone Research Articles

A study of association between serum thyroid stimulating hormone concentration and thyroid cancer and also to assess whether serum thyroid stimulating hormone levels are of value in predicting malignancy in patients with thyroid swelling

Background: Thyroid neoplasm includes both benign and malignant tumors arising in the thyroid gland. Although thyroid cancer accounts for less than 1% of all cancers, the challenge to clinicians is to identify the minority of thyroid nodules that harbor malignancy. There are a number of well-established predictors of malignancy in thyroid nodules. More recently a few studies have suggested that higher concentration of thyroid stimulating hormone (TSH), even within the normal range are associated with subsequent diagnosis of thyroid cancer in patients with thyroid nodules and even higher serum TSH levels have been found associated with advanced stages of thyroid cancer. Methods: A prospective study was conducted on 220 cases without overt thyroid dysfunction attending Department of general surgery, Pushpagiri institute of medical science, Thiruvalla. Results: In our study incidence of malignancy of thyroid carcinoma was highest in patients with serum TSH concentrations, in range of 3.5 mIU/l-5.25 mIU/l, 55 patients out of 220 patients. Individually, incidence of papillary carcinoma (PC) (36/55 patients), follicular carcinoma (FC) (17/55 patients) and Hurthle cell carcinoma (HCC) (2/55 patients) were more in patients with higher TSH. So, from the study it can be clearly state that elevated TSH can be used as an independent predictor of thyroid malignancy. Higher TSH values are associated with papillary thyroid carcinoma.Conclusions: An elevated TSH can be used as an independent predictor of thyroid malignancy, especially for anticipating a probability of papillary carcinoma of thyroid.

Thyroid-Related Hormone Levels in Clinical Patients With Moderately Severe-to-Profound Sudden Sensorineural Hearing Loss: A Prospective Study.

Objectives: Sudden sensorineural hearing loss (SSNHL) is a common otological emergency, causing a measure of hearing loss and affecting the quality of life. This study aims to investigate the association of thyroid-related hormone levels with moderately severe-to-profound SSNHL.Methods: The study included 70 patients with moderately severe-to-profound SSNHL and 100 age- and sex-matched healthy controls. Peripheral venous blood samples were taken from the participants, and their thyroid-related hormone levels were measured at admission and 1 week after treatment.Results: In moderately severe-to-profound SSNaHL patients, the concentrations of total triiodothyronine (TT3), total thyroxine (TT4), free triiodothyronine (FT3), and thyroid-stimulating hormone (TSH) (all P < 0.05) were significantly lower than in the control group. The TT3, TT4, FT3, and TSH levels were significantly higher in the effective group than in the ineffective group (all P < 0.05). Linear correlation analysis revealed that TSH level (R = 0.707, P < 0.05) elevation after treatment successfully predicted a favorable outcome of hearing recovery. Logistic regression analyses suggested low FT3 and TSH levels to be independent occurrence predictors, while the increase of TSH level may be an independent favorable outcome predictor.Conclusions: The results suggest that low FT3 and TSH levels are risk factors for moderately severe-to-profound SSNHL. By discovering the positive association between TSH elevation and hearing recovery, along with the potential novel predictors of FT3 and TSH, our study may contribute valuable insights to the research and treatment of moderately severe-to-profound SSNHL.

Cardiac Autonomic Modulation and Anti-Thyroid Peroxidase (TPO) Antibodies in Subclinical Hypothyroidism: Does a Correlation Exist?

Background: Heart rate variability (HRV) reflects the balance between the sympathetic and parasympathetic divisions of the autonomic nervous system. Anti-thyroid antibodies like anti-TPO and anti-Thyroglobulin have long been associated with thyroid dysfunction and abnormal thyroid profile testing. Subclinical hypothyroidism (SCHypo) is characterized by elevated thyroid-stimulating hormone (TSH) with normal thyroid hormones. We hypothesize that autonomic function may be deranged in anti-TPO positive sub-clinical hypothyroid cases, even before the onset of overt hypothyroidism.Objectives: To investigate the association between anti-Thyroid Peroxidase antibodies (anti-TPOAb) positive SCHypo and sympathovagal imbalance (SVI), if any.Methodology: The study was conducted on the age and body mass index (BMI) matched subclinical hypothyroid patients (n=52) and healthy controls (n=20). The cardiac autonomic activity was assessed by short-term HRV in the time (SDNN, RMSSD, pNN50) and frequency domains (LFms2, HFms2, LFnu, HFnu, TP, and LF/HF ratio). Nonlinear geometric measures (SD1, SD2, SD1/SD2, TINN, HRV triangular index) were also evaluated. Biochemical evaluation of serum thyroid profile and anti-TPOAb was done in all the subjects.Results: Decreased HRV was observed in the anti-TPOAb positive group when compared to the antibody-negative and control groups. Significant positive correlation of anti-TPOAb with TSH, LFnu, LF/HF and negative correlation with SDNN, RMSSD, pNN50, SD1, SD1/SD2, HFnu, and TP of HRV was observed.Conclusion: Anti-TPOAb positive SCHypo group exhibited modifications in HRV characterized by decreased parasympathetic modulation, as compared to controls. The findings were also suggestive of increased risk of autonomic dysfunction in TPOAb-positive patients, as compared to antibody negative. An increase in anti-TPO antibodies was significantly correlated with TSH and SVI in SCHypo patients.

TSH/miR-17-5p/ZNF367 axis is related to spontaneous abortion in patients with TSH above 2.5 mIU/L.

Elevated thyroid-stimulating hormone (TSH) is associated with an increased risk of spontaneous abortion (SA); however, the associated mechanism remains unclear. This study aimed to investigate the expression of miRNAs and pathogenesis in the chorionic villi of TSH > 2.5 mIU/L-related SA patients. The chorionic villi were collected from pregnant women in the first trimester with TSH > 2.5 mIU/L with or without SA, as well as TSH < 2.5 mIU/L with or without SA to determine the level of miRNA expression. Differentially expressed miRNAs were confirmed by qRT-PCR in a total of 92 subjects. Cell Counting Kit-8 (CCK8), wound healing, transwell assays, and Western blotting were used to measure cellular biological functions and related proteins in HTR-8/SVneo cells. The potential mechanisms were determined using a Luciferase reporter assay and rescue experiment. Compared with normal pregnant women, miR-17-5p was decreased and zinc finger protein 367 (ZNF367) was upregulated in the chorionic villi of TSH > 2.5 mIU/L-related SA patients. Using HTR-8/SVneo cells, we demonstrated that elevated TSH inhibited miR-17-5p expression, as well as trophoblast migration and invasion. The overexpression of miR-17-5p targeted and inhibited ZNF367 expression promoting the biological function of trophoblasts. Further studies confirmed that ZNF367 interference partially reversed the biological function of the miR-17-5p inhibitor on HTR-8/SVneo cells. Taken together, our results showed that miR-17-5p promoted the biological function of trophoblasts by suppressing ZNF367.

The Association between Thyroid-Stimulating Hormone and Long-Term Outcomes in Patients with ST Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention

ObjectiveThyroid hormones are closely related to the cardiovascular system. Our study aimed to explore the impact of admission thyroid-stimulating hormone (TSH) levels on long-term outcomes in patients with acute ST segment elevation myocardial infarction (STEMI) by detailed stratifications of TSH.MethodsConsecutive STEMI patients admitted to our hospital were divided into four groups: Group 1 (TSH <0.35 mIU/L), Group 2 (TSH 0.35–1.0 mIU/L), Group 3 (TSH 1.0–3.5 mIU/L), and Group 4 (TSH >3.5 mIU/L). The primary endpoint was all-cause mortality during follow-up, and the median follow-up was 2.5 years. Cox proportional hazard regression models were performed to identify the prognostic value of TSH.ResultsA total of 1186 patients were included. Group 4 was presented with higher systolic and diastolic blood pressure (all P < 0.001), and Group 1 had more patients complicated by heart failure (Killip class >I, P = 0.014). During follow-up, 138 deaths occurred. Patients in Group 4 had the worst long-term outcomes (P < 0.001). The cumulative survival in Group 4 was remarkably lower (Log rank P < 0.001), whereas the other three groups were comparable (Log rank P = 0.365). Through Cox regression analysis, only TSH >3.5 mIU/L was identified as an independent risk factor for long-term mortality after STEMI.ConclusionOnly TSH elevation beyond the normal range was associated with worse long-term prognosis in STEMI patients, while high-normal TSH or reduced TSH did not alter long-term prognosis of STEMI patients. TSH >3.5 mIU/L was an independent risk factor for long-term mortality in STEMI.

Transient high thyroid stimulating hormone and hypothyroidism incidence during follow up of subclinical hypothyroidism.

Objectives. Given the high prevalence of subclinical hypothyroidism (SCH), defined as high thyroid stimulating hormone (TSH) and normal free thyroxine (FT4), and uncertainty on treatment, one of the major challenges in clinical practice is whether to initiate the treatment for SCH or to keep the patients under surveillance. There is no published study that has identified predictors of short-term changes in thyroid status amongst patients with mild elevation of TSH (4.5-10 mIU/L). Subjects and Results. A cohort study was conducted on patients with SCH detected through a general population screening program, who were followed for six months. This project identified factors predicting progression to hypothyroid status, persistent SCH and transient cases. A total of 656 participants joined the study (431 controls and 225 were patients with SCH). A part of participants (12.2%) developed biochemical hypothyroidism during the follow-up, while 73.8% of the subjects became euthyroid and the remained ones (13.4%) stayed in the SCH status. The incidence of overt hypothyroidism for participants with TSH above 6.9 mIU/L was 36.7%, with incidence of 42.3% for females. Anti-thyroid peroxidase antibodies (TPO) positivity is an important predictor of development of hypothyroidism; however, it could be also positive due to transient thyroiditis. Conclusions. It can be concluded that females with TSH above 6.9 mIU/L, particularly those with free triiodothyronine (FT3) and FT4 in the lower half of the reference range, are more likely to develop biochemical hypothyroidism. Therefore, it is recommended to give them a trial of levothyroxine replacement. It is also recommended to repeat TSH after six months for male subjects and participants with baseline TSH equal or less than 6.9 mIU/L.

Evaluation of the Congenital Hypothyroidism Detection Strategy in Extremely Preterm Infants in Western Andalusia.

This study aimed to identify extremely premature infants (< 31 weeks of gestation and/or <1,500 g) affected by congenital hypothyroidism (CH) with delayed elevation of thyrotropin (TSH) and to evaluate the detection strategy for this pathology in our reference screening population. A descriptive and retrospective study was carried out with samples collected from western Andalusia and the autonomous city of Ceuta. This protocol allowed us to detect six neonates with delayed TSH elevation. One of them, due to serious heart problems, died without being able to confirm CH. In two neonates, however, it was possible to detect CH, another two presented a persistent TSH elevation but normal free T4, and another one presented a temporary TSH elevation. It is essential to repeat the CH screening in extremely premature infants, not only at the age of 15 days but also with a third sample at the moment of hospital discharge to detect cases with delayed TSH elevation. · The Newborn Screening Programs are an essential activity of preventive medicine.. · Extremely preterm infants have a very high risk of CH.. · Optimal management of thyroid dysfunction in this population remains to be established..

151 A RANDOMIZED,OPEN CLINICAL TRIAL TO COMPARE THE EFFICACY AND SAFETY OF ANLOTINIB PLUS IRINOTECAN VERSUS IRINOTECAN IN PATIENTS WITH ESCC

Abstract The benefit of systemic treatment in esophageal squamous cell carcinoma (ESCC) which has progressed after chemotherapy is still uncertain. Anlotinib (AL3818) is a novel multi-target TKI, inhibiting tumor angiogenesis and proliferation. A phase II trial (NCT02649361) has demonstrated that anlotinib has a durable antitumor activity with a manageable adverse event profile in refractory metastatic ESCC. This study (NCT03387904) aimed at comparing the effects and safety of Anlotinib Plus Irinotecan versus Irinotecan in patients with ESCC. Methods We conducted a prospective randomized, multicenter, phase II trial to compare the efficacy of Anlotinib Plus Irinotecan with Irinotecan in recurrent ESCC patients who had resistance to platinum or taxane-based chemotherapy. Eligible patients were adults with pathologically confirmed recurrent ESCC, and 82 patients were randomized 1:1 to Irinotecan (65 mg/m2/day 1 and day 8) with or without anlotinib (12 mg qd day 1 to 14) of a 21-day cycle till progression or intolerable. The primary endpoint is the disease control rate (DCR) and progression-free survival (PFS) and the secondary end points are objective response rate (ORR) and overall survival (OS). Results Between 13/1 2019 and 20/1 2020, a total of 43 patients were enrolled and randomly assigned to either the anlotinib plus irinotecan (n = 22) or the irinotecan group (n = 21).The mPFS was longer in trial group than in control group (89 days vs 66 days, HR = 0.447, P = 0.055). The Disease control rate (DCR) was 54.5% in trial group and 38.1% in the control group. The treatment-related adverse events (&amp;gt;10%) were fatigue (59.1%), nausea (50.0%), decreased appetite (36.4%), hoarseness (27.3%), thyroid-stimulating hormone elevation (22.7%), diarrhea (9.1%), and decreased lymphocytes count(9.1%) in trial group. Grade 3 AEs included fatigue (4.5% vs 4.8%), nausea (4.5% vs 0%) and diarrhea (4.5% vs 0%) in two groups. Conclusion Anlotinib plus irinotecan was similarly tolerable but prolonged PFS compared to irinotecan monotherapy as a second-line treatment in patients with recurrent ESCC.

Resistance to thyroid hormone syndrome due to p.Cys446Ser variant of THRbeta gene in a pedigree

To explore the genetic basis for a Chinese pedigree affected with resistance to thyroid hormone syndrome (RTH). Exons 7 to 10 of the THRbeta gene were sequenced for the proband and members of his pedigree. Three patients from the pedigree were identified. All have presented with palpitation, fatigue, goiter, elevated free thyroid hormone and free triiodothyronine, and normal or elevated thyrotropin. Genetic testing revealed that the proband, his mother, second sister and one of her daughters had carried a heterozygous c.1336T>A variant of the THRbeta gene, which resulted in substitution of Cysteine by Serine at position 446. The variant was unreported previously. Based on the American College of Medical Genetics and Genomics standards and guidelines, the c.1336T>A(p.Cys446Ser) variant of THRbeta gene was predicted to be lilely pathogenic(PM1+PM2+PM5+PP3). The c.1336T>A variant, identified in the exon 10 of the THRbeta gene, probably underlay the RTH in this pedigree. Genetic testing has validated the clinical diagnosis for this pedigree.

Does Subclinical Hypothyroidism Cause Symptoms

Many patients with subclinical hypothyroidism (i.e., elevated thyroid-stimulating hormone [TSH] but normal free thyroxine levels) have various symptoms

Impact of subclinical hypothyroidism on health-related quality of life: a narrative review.

A biochemical diagnosis of subclinical hypothyroidism (SCH) is defined by an elevated serum thyroid-stimulating hormone (TSH) with a normal serum free thyroxine (FT4). This paper discusses SCH in the Australian population, the impact of SCH on health-related quality of life (HRQoL), and the evidence for thyroid hormone therapy as well as exercise therapy to improve HRQoL in SCH. The prevalence of SCH in Australia is approximately 4-5% and is higher in females and the elderly. Current evidence suggests thyroid hormone therapy is not associated with an improvement in HRQoL. However, there does appear to be a subgroup of those with SCH that experience an impairment in HRQoL who may potentially benefit from treatment. Because the majority of research to date has been done in elderly, largely asymptomatic individuals, this may not be representative of the entire SCH population. In addition, alternative treatments, such as exercise therapy, have not been well explored in the literature, despite exercise therapy's effects on HRQoL in other populations. Further research is required to define clearly which individuals with SCH are likely to experience an impaired HRQoL, as well as explore the effects of thyroid hormone therapy and exercise therapy in these individuals.

Elevated thyroid-stimulating hormone levels are associated with poor sleep: a cross-sectional and longitudinal study.

Poor sleep accompanied by elevated TSH (thyroid stimulating hormone) levels is not uncommon since TSH secretion is controlled by the circadian rhythm. However, the relationship between poor sleep and TSH elevation is unclear; hence, we aimed to elucidate this relationship by conducting a cross-sectional and longitudinal study. Participants with isolated elevated (N = 168) and normal (N = 119) TSH concentrations were recruited, and the Pittsburgh Sleep Quality Index (PSQI) was used to assess the sleep status. Subjects with an isolated TSH elevation were followed up longitudinally. The serum TSH concentration was remeasured after sleep status improved. The proportions of poor sleep and occasional poor sleep in subjects with isolated TSH elevation were significantly higher than those with normal TSH levels (70.24% vs. 49.58%, p = 0.001; 9.52% vs. 1.68%, p = 0.006). Subjects with isolated TSH elevation had significantly higher PSQI scores in the subjective sleep quality, sleep latency, sleep duration, and habitual sleep efficiency dimensions than those with normal TSH levels (all p < 0.05). Poor sleep was significantly associated with isolated TSH elevation in the multiple logistic regression analysis [odds ratio (OR) = 2.396, p = 0.001]. Among subjects with an isolated TSH elevation at baseline, the percentage of TSH normalization was significantly higher in those who slept better than in those who still slept poorly (85.42% vs. 6.45%, p < 0.001). This study revealed that isolated elevated TSH concentrations normalize when the sleep status is improved; hence, we recommend that clinicians thoroughly assess the sleep status of patients and remeasure TSH concentrations after sleep status improves.

Is thyroid hormone supplementation avoidable for patients with low‐risk papillary thyroid cancer after thyroid lobectomy? A two‐center observational study

Changing insights regarding the extent of surgery for low-risk papillary thyroid cancer (PTC) stir up discussions on the benefits and harms of thyroid lobectomy versus total thyroidectomy. The chance of needing postoperative thyroid hormone supplementation after thyroid lobectomy is still unclear. The purpose of this retrospective two-center study was to identify the incidence and risk factors of postoperative thyroid-stimulating hormone (TSH) elevation (>2.0 μIU/ml) after thyroid lobectomy for low-risk PTC. Medical records of 201 consecutive patients with low-risk PTC from two tertiary centers who underwent thyroid lobectomy between 2015 and 2019 were retrospectively reviewed. Postoperative thyroid function tests were measured regularly and patients were prescribed levothyroxine if the TSH level was higher than 2.0 μIU/ml. Multivariable regression models were used to evaluate potential risk factors associated with postoperative TSH elevation after thyroid lobectomy. At 6 weeks postoperatively, 85% had TSH level of >2 μIU/ml; this increased to 88% by 3-6 months. Receiver operating characteristic analysis identified preoperative TSH cut-off (>1.7 μIU/ml) to predict postoperative TSH elevation. Multivariate analysis revealed that only a high preoperative TSH level (>1.7 μIU/ml) was an independent risk factor for a postoperative TSH level of >2 μIU/ml (odds ratio = 7.71; p < .001). Nearly 90% of the patients who underwent thyroid lobectomy for low-risk PTC had a postoperative TSH level of >2 μIU/ml, necessitating thyroid hormone supplementation in accordance with current guidelines. This finding highlights that preoperative patient counseling should also focus on raising awareness about postoperative thyroid hormone supplementation for low-risk PTC patients seeking thyroid lobectomy.

The Positive Association between Subclinical Hypothyroidism and Newly-Diagnosed Hypertension Is More Explicit in Female Individuals Younger than 65.

BackgroundSubclinical hypothyroidism (SCH) is the most common thyroid dysfunction, and its relationship with blood pressure (BP) has been controversial. The aim of the study was to analyze the association between SCH and newly-diagnosed hypertension.MethodsBased on data from the Thyroid disease, Iodine nutrition and Diabetes Epidemiology (TIDE) study, 49,433 euthyroid individuals and 7,719 SCH patients aged ≥18 years were enrolled. Patients with a history of hypertension or thyroid disease were excluded. SCH was determined by manufacturer reference range. Overall hypertension and stage 1 and 2 hypertension were diagnosed according to the guidelines issued by the American College of Cardiology/American Heart Association in 2017.ResultsThe prevalence of overall hypertension (48.7%), including stage 1 (28.9%) and 2 (19.8%) hypertension, increased significantly in SCH patients compared with euthyroid subjects. With elevated serum thyroid stimulating hormone (TSH) level, the hypertension prevalence also increased significantly from the euthyroid to different SCH subgroups, which was more profound in females or subjects aged <65 years. The age- and sex-specific regression analysis further demonstrated the same trends in the general population and in the 1:1 propensity matched population. Similarly, several BP components (i.e., systolic, diastolic, and mean arterial BP) were positively associated with TSH elevation, and regression analysis also confirmed that all BP components were closely related with SCH in female subjects aged <65 years.ConclusionThe prevalence of hypertension increases for patients with SCH. SCH tends to be associated with hypertension and BP components in females younger than 65 years.

Patterns of thyroid dysfunctions in adolescent patients suffering from severe acne during isotretinoin treatment.

Although oral isotretinoin has been widely used as a basic treatment of acne in adolescents, several studies have noted some alterations in thyroid functions during oral isotretinoin therapy. Therefore, the present study aims at evaluating the possible changes in thyroid-stimulating hormone (TSH), free thyroxin (fT4) and free triiodothyronine (fT3) levels during isotretinoin treatment and analyzing the possible factors which may contribute to such changes. In the present study, 47 patients received (0.5mg/kg oral isotretinoin) for treatment of severe acne. TSH, fT4 and fT3 were measured at baseline, after 3 and 6months. ANOVA tests were used for statistical analyses. The levels of fT4 and fT3 decreased significantly during isotretinoin treatment (from 0.85±0.04 and 3.1±0.26 at baseline to 0.81±0.023 and 2.76±0.2 after 6months, respectively). The decrease was accompanied by significant elevation of TSH (0.66±0.05 at baseline to 0.695±0.05 after 6months). The duration of therapy (but not the dose) has significantly affected all the hormonal changes. Previous incomplete or intermittent isotretinoin treatment had significantly influenced the changes in fT4 only, while gender affected the changes of TSH. Isotretinoin treatment can decrease fT4, fT3 and increase TSH. The pattern of these changes was affected by gender and previous isotretinoin therapy. Different doses of isotretinoin did not affect the hormonal changes, but the duration has been the major influencing factor.

Spontaneous ovarian hyperstimulation syndrome in a pregnant woman with hypothyroidism: a case report

ObjectiveTo study a rare case of spontaneous ovarian hyperstimulation syndrome in a naturally conceived pregnancy associated with overt hypothyroidism.DesignCase report.SettingEndocrinology private practice.Patient(s)A 32-year-old woman who was 13 weeks pregnant with bilaterally enlarged ovaries presumed to be secondary to hypothyroidism.Intervention(s)Administration of levothyroxine and titration of the dose.Main Outcome Measure(s)Regression of signs and symptoms of spontaneous ovarian hyperstimulation syndrome after 12 weeks of therapy.Result(s)The patient was diagnosed with severe hypothyroidism, as confirmed by her elevated thyroid-stimulating hormone level. Ultrasound evaluation revealed ovarian enlargement secondary to multiple contiguous cysts with anechoic content. The patient was administered levothyroxine 175 μg/day. Results of hormonal studies demonstrated thyroid function normality at week 12 after treatment. Incomplete regression of ovarian cysts was also noticed within this period. At week 37, the patient developed preeclampsia, and cesarean delivery was recommended. An 8-month postpartum ultrasound evaluation revealed complete regression of the cysts.Conclusion(s)Spontaneous ovarian hyperstimulation syndrome secondary to hypothyroidism may be the cause of ovarian enlargement, and levothyroxine replacement seems an appropriate primary therapeutic option. Proper endocrinological assessment of patients is recommended as it may avoid unfavorable outcomes.

Effects of iodine excess on serum thyrotropin-releasing hormone levels and type 2 deiodinase in the hypothalamus of Wistar rats.

Iodine is an important element in thyroid hormone biosynthesis. Thyroid function is regulated by the hypothalamic-pituitary-thyroid axis. Excessive iodine leads to elevated thyroid-stimulating hormone (TSH) levels, but the mechanism is not yet clear. Type 2 deiodinase (Dio2) is a Se-containing protease that plays a vital role in thyroid function. The purpose of this study was to explore the role of hypothalamus Dio2 in regulating TSH increase caused by excessive iodine and to determine the effects of iodine excess on thyrotropin-releasing hormone (TRH) levels. Male Wistar rats were randomised into five groups and administered different iodine dosages (folds of physiological dose): normal iodine, 3-fold iodine, 6-fold iodine, 10-fold iodine and 50-fold iodine. Rats were euthanised at 4, 8, 12 or 24 weeks after iodine administration. Serum TRH, TSH, total thyroxine (TT4) and total triiodothyronine (TT3) were determined. Hypothalamus tissues were frozen and sectioned to evaluate the expression of Dio2, Dio2 activity and monocarboxylate transporter 8 (MCT8). Prolonged high iodine intake significantly increased TSH expression (P < 0·05) but did not affect TT3 and TT4 levels. Prolonged high iodine intake decreased serum TRH levels in the hypothalamus (P < 0·05). Dio2 expression and activity in the hypothalamus exhibited an increasing trend compared at each time point with increasing iodine intake (P < 0·05). Hypothalamic MCT8 expression was increased in rats with prolonged high iodine intake (P < 0·05). These results indicate that iodine excess affects the levels of Dio2, TRH and MCT8 in the hypothalamus.

Mirtazapine use may increase the risk of hypothyroxinaemia in patients affected by major depressive disorder.

Hypothyroxinaemia could be easily neglected if attention is paid only to patients with elevated thyroid-stimulating hormone. We aimed to assess the association between mirtazapine use and hypothyroxinaemia in patients affected by major depressive disorder. We conducted a retrospective cohort study in the Second Affiliated Hospital of Xinxiang Medical University between January 2016 and December 2018. Patients affected by major depression disorder and admitted to the hospital for treatment during the study period and who had thyroid tests at admission and after treatment were included. Mirtazapine use during hospitalization was the exposure measure and newly developed hypothyroxinaemia was as the primary outcome and structure parameters of thyroid homeostasis were the secondary outcomes of this study. Log-binomial model was used to estimate the association between mirtazapine use and hypothyroxinaemia, after adjusting for potential confounding factors. A total of 220 eligible patients were included in the final analysis. The incidence of hypothyroxinaemia in patients who used mirtazapine was higher (37.5%) than those patients who did not use (19.7%). The relative risk of developing hypothyroxinaemia was 1.70 (95% confidence interval: 1.21-2.43) for mirtazapine use, after adjusting for confounding factors. The degree of reduction in thyroid feedback quantile-based index in mirtazapine group was significantly greater than that in nonmirtazapine group. Mirtazapine use was associated with the increased risk of developing hypothyroxinaemia. The underlying mechanism may be involved the changed central set point of thyroid homeostasis, in which pituitary was in a possibly impaired sensitivity to the lower level of thyroid hormones.

Exploration of the Underlying Nutritional, Inflammatory and Oxidative Stress Pathological Mechanisms in Preeclampsia using Principal Component Analysis

Normal pregnancy is characterized by a mild systemic inflammatory response and progressive increase in serum inflammatory cytokines that peak in the third trimester. During pregnancy pre-existing inflammatory conditions, acquired oxidative stress arising from the placenta malfunction and nutritional deficiencies can trigger intense systemic responses that lead to endothelial activation, dysfunction and preeclampsia. We investigated the principal nutritional, oxidative and inflammatory pathways that trigger the clinical manifestation of preeclampsia.&#x0D; This case-control study included 250 women with preeclampsia and 150 normotensive pregnant women. Urinary Iodine concentration (IUC) and serum levels of Ferritin, Thyroid-stimulating Hormone (TSH), selenium, Nitric Oxide (NO) gamma glutamyl transferase (GGT), Rheumatoid factor, and high sense C-reactive protein (hs-CRP) of cases and controls were compared using the student’s t and the Mann-Whitney U tests. Principal component analysis was carried out to delineate the patterns of association between nutritional, inflammatory and oxidative markers and preeclampsia.&#x0D; The main pathophysiological pathways identified were the interactions between selenium/iodine deficiency and elevated serum TSH (endothelial dysfunction); serum ferritin, GGT, CRP and low urinary iodine concentration (inflammatory oxidative stress); elevated serum hs-CRP and Rheumatoid factor subclinical inflammation and immune cell activation) and high T3/T4 ratio (acute TSH stimulation of thyroid with low thyroid iodine stores)&#x0D; Combined selenium and iodine deficiency resulting into elevated TSH, low NO and preferential T3 secretion; acute inflammatory conditions associated with elevated serum GGT, CRP, and Ferritin; and subclinical inflammatory conditions characterized by autoimmunity are some of the major oxidant and inflammatory pathways associated with increased risk of preeclampsia.

Recurrent Galactorrhoea: A consequence of unheeded primary hypothyroidism

Background: Primary hypothyroidism can lead to hyperprolactinemia through several mechanisms in both men and women, manifesting as galactorrhoea, loss of libido, and infertility in both sexes, as oligomenorrhea/amenorrhea in women, and as gynecomastia and erectile dysfunction in men. Case presentation: Here presented is a 28-year-old Nigerian woman with a history of recurrent bilateral painless galactorrhoea of 12 years’ duration and persistent low mood. Physical examination was unremarkable. The hormonal assay revealed elevated thyroid-stimulating hormone, elevated serum prolactin, low thyroxine, and low triiodothyronine levels. Magnetic resonance imaging of the brain revealed normal findings. A diagnosis of hyperprolactinemia secondary to primary hypothyroidism was made. Pharmacological therapy began with thyroid hormone replacement therapy and a dopamine agonist: 75 micrograms of levothyroxine daily and 0.5 micrograms of cabergoline twice weekly for 8 weeks. After 8 weeks of pharmacological therapy, hormonal assay revealed values within the reference range with significant symptomatic improvement evidenced by cessation of galactorrhoea and low mood. Conclusion: Primary hypothyroidism has been proven to be one of the numerous causes of hyperprolactinemia and it could be unheeded in a patient who does not present with the typical signs and symptoms of primary hypothyroidism.