Hypothyroidism has been found to have long-term effects on each of the senses, but with proper treatment, many of them can be significantly minimized. This paper analyzes the research on the impact of hypothyroidism on the senses of smell, taste, hearing, vision, and thermoregulation. Data were collected from the National Library of Medicine, PubMed, and Google Scholar databases using the keywords \"hypothyroidism,\" \"taste,\" \"smell,\" \"vision,\" \"hearing,\" and \"thermoregulation.\" Approximately 413 articles were found when searching with these parameters, and 30 were used in this paper. Studies were excluded if they were outside this paper\'s scope or older than 2012. Studies were included if they specifically focused on hypothyroidism and one of the five listed senses. Patients with hypothyroidism had a significantly increased risk of sensorineural hearing loss, decreased perception of the blue-yellow color axis, decreased sense of olfaction and number of olfactory bulbs, and decreased thermogenesis. Hypothyroidism was also found to show increased length of COVID-19-induced anosmia and decreased bitter taste perception. It can be concluded that hypothyroidism has many effects on the senses, particularly an increased risk of sensorineural hearing loss. More studies need to be done on these effects.

Primary congenital hypothyroidism is easily diagnosed on the basis of elevated plasma levels of thyroid-stimulating hormone (TSH). In contrast, in the rare disorders of thyroid hormone resistance, TSH and, in mild cases, also thyroid hormone levels are within the normal range. Thyroid hormone resistance is caused by defects in hormone metabolism, transport, or receptor activation and can have the same serious consequences for child development as congenital hypothyroidism. A total of n = 23,522 data points from a large cohort of children and young adults were used to generate normal values and sex-specific percentiles for the ratio of free triiodothyronine (T3) to free thyroxine (T4), the fT3/fT4 ratio. The aim was to determine whether individuals with developmental delay and genetically confirmed thyroid hormone resistance, carrying defects in Monocarboxylate Transporter 8 (MCT8), Thyroid Hormone Receptor alpha (THRα), and Selenocysteine Insertion Sequence-Binding Protein 2 (SECISBP2), had abnormal fT3/fT4 ratios. Indeed, we were able to demonstrate a clear separation of patient values for the fT3/fT4 ratio from normal and pathological controls (e.g., children with severe cerebral palsy). We therefore recommend using the fT3/fT4 ratio as a readily available screening parameter in children with developmental delay for the identification of thyroid hormone resistance syndromes. The fT3/fT4 ratio can be easily plotted on centile charts using our free online tool, which accepts various SI and non-SI units for fT3, fT4, and TSH.

BACKGROUND: Thyroid hormone is the key endocrine regulator of growth, development, metabolism, and other bodily functions. α-Klotho has been involved in the aging process and acts as an endocrine factor involved in the regulation of various metabolic processes in humans. However, the relationship between α-Klotho and thyroid profile has not been uniformly recognize.
OBJECTIVE: To determine the relationship between α-Klotho and thyroid profile in adult individuals.
METHODS: Population data of 4614 adult individuals were obtained from the NHANES database during the period of 2007-2012. Weighted multivariable regression analysis was performed using a general linear model with serum α-Klotho as the independent variable and thyroid profile as the dependent variables, respectively. The generalized additive model was used for smoothing curve fitting and threshold effect analysis.
RESULTS: α-Klotho was associated with a slightly higher FT3, TT3 and TT4 level in unadjusted and adjusted regression models. However, a higher α-Klotho level was associated with a lower TSH level. After α-Klotho was grouped as quantiles with reference (Q1), α-Klotho still showed a statistically significant positive correlation with FT3 and TT3 levels in Q2, Q3 and Q4. In addition, α-Klotho was positively corrected with TT4, but negatively associated with TSH in Q4.
CONCLUSIONS: Serum soluble α-Klotho was positively associated with FT3, TT3 and TT4, but negatively correlated with TSH. The significant effect of α-Klotho on thyroid profile suggests its potential as a predictive marker of thyroid functions, indicating its possible involvement in the regulation of thyroid hormone secretion.

UNASSIGNED: Thyroid-stimulating hormone (TSH) is a glycoprotein secreted by the anterior pituitary gland and is regulated by negative feedback from the serum free thyroid hormones. In this study we aimed to quantitate the relative bias caused by calibration drifting as seen in our TSH Levey-Jennings quality control (QC) charts and assess the magnitude of bias on patients\' samples.
UNASSIGNED: In the period from October 2021 to August 2022 we looked at the QC results of ten 28-days\' calibration time intervals and calculated relative bias compared to the mean. For each time interval the mean from three QC points before and after calibration was calculated. The average from 10 pre- and post-calibration means was calculated and the relative bias, pre- and post-calibration, was then calculated. We used 5 patient samples with low, normal and high TSH concentrations and calculated relative bias pre- and post-calibration. The allowed relative bias for TSH is ± 6.7%.
UNASSIGNED: At both QC levels, with the respective means of 5.14 mIU/L (coefficient of variation, CV% = 3.1%) and 27.80 mIU/L (CV% = 3.2%) had their respective relative bias - 8.2% and - 7.9%. The patient samples with low (0.586 mIU/L), normal (2.89 mIU/L and 5.19 mIU/L) and high (20.5 mIU/L and 39.8 mIU/L) TSH had - 4.1%, - 4.0%, - 3.5%, - 5.1% and - 4.1%, respectively.
UNASSIGNED: Even though the relative bias exceeded allowable criteria for the QC samples, this was not manifested on the patients\' samples.

Levothyroxine (LT4), being \"narrow therapeutic index\" drug, may lead to significant fluctuations in thyroid stimulating hormone (TSH) levels. Such fluctuations can result in clinically noteworthy disruptions in thyroid function and give rise to adverse clinical consequences. Consequently, regulatory standards for LT4 potency have been tightened, with the most stringent specifications requiring maintenance of potency within the range of 95-105% of the labeled dose throughout the entire shelf-life of the product. The LT4 new formulation with tightened specification adheres to these rigorous standards, demonstrating established bioequivalence to its older formulation while upholding an equivalent standard of safety and efficacy. Furthermore, the novel formulation exhibits enhanced stability and an extended shelf-life. Of paramount significance is its capacity to provide patients with accurate and consistent dosing, thereby effectively catering to their medical requirements. The primary objective of the Asia-Pacific advisory board meeting (held in June 2022 with endocrinologists, experts from India, Indonesia, Philippines, Thailand, Malaysia and Singapore) was to establish the importance of appropriate communication to HCPs, patients and other stakeholders regarding the LT4 new formulation. The aim of this brief review is to highlight the importance of communication with healthcare professionals that should focus on providing accurate information on the LT4 new formulation, emphasizing efficacy, safety, and bioequivalence with clear guidance and ensure that patients and clinicians are fully informed about any changes to medications such as LT4 to reduce the risk of unrelated adverse events being incorrectly attributed to the newer formulation.

Hypothyroidism is a prevalent thyroid condition in which the thyroid gland fails to secrete an adequate amount of thyroid hormone into the bloodstream. This condition may develop due to genetic or acquired factors. The most frequent cause of acquired hypothyroidism is chronic autoimmune thyroiditis, also known as Hashimoto\'s disease. Acquired hypothyroidism is diagnosed when patients present with overt hypothyroidism (also known as clinical hypothyroidism), as they exhibit increased TSH and decreased T3 and T4 serum levels. This article examines the prevalence of psychiatric disorders among patients diagnosed with acquired hypothyroidism with or without Levothyroxine treatment. We discuss the available evidence indicating that acquired hypothyroidism may be a risk factor for psychiatric disorders, and the effectiveness of thyroid treatment in relieving psychiatric symptoms. Additionally, we provide critical details on thyroid hormone cutoff values reported in the literature, their potential clinical importance, and their correlation with psychiatric symptoms. Finally, we examined the various mechanisms by which acquired hypothyroidism can lead to depression. The high rate of comorbidity between hypothyroidism and psychiatric disorders deserves special attention, indicating the importance of consistent monitoring and timely identification of psychiatric symptoms to prevent disease exacerbation and facilitate therapeutic management. On the other hand, several mechanisms underlie the strong association between depression and acquired hypothyroidism. Deeper research into these mechanisms will allow knowledge of the pathophysiology of depression in patients with acquired hypothyroidism and will provide clues to design more precise therapeutic strategies for these patients.

The past decade has witnessed significant advances in our understanding of skeletal homeostasis and the mechanisms that mediate the loss of bone in primary and secondary osteoporosis. Recent breakthroughs have primarily emerged from identifying disease-causing mutations and phenocopying human bone disease in rodents. Notably, using genetically-modified rodent models, disrupting the reciprocal relationship with tropic pituitary hormone and effector hormones, we have learned that pituitary hormones have independent roles in skeletal physiology, beyond their effects exerted through target endocrine glands. The rise of follicle-stimulating hormone (FSH) in the late perimenopause may account, at least in part, for the rapid bone loss when estrogen is normal, while low thyroid-stimulating hormone (TSH) levels may contribute to the bone loss in thyrotoxicosis. Admittedly speculative, suppressed levels of adrenocorticotropic hormone (ACTH) may directly exacerbate bone loss in the setting of glucocorticoid-induced osteoporosis. Furthermore, beyond their established roles in reproduction and lactation, oxytocin and prolactin may affect intergenerational calcium transfer and therefore fetal skeletal mineralization, whereas elevated vasopressin levels in chronic hyponatremic states may increase the risk of bone loss.. Here, we discuss the interaction of each pituitary hormone in relation to its role in bone physiology and pathophysiology.

BACKGROUND: Hypothyroidism is known to affect a wide range of physiological systems, including menstrual function, in women of reproductive age. This study aims to comprehensively analyze the association between hypothyroidism and menstrual irregularities in women attending a tertiary care center.
METHODS: The study included 120 women aged 18-45 who presented with menstrual abnormalities. Convenience sampling was used to select participants from the outpatient department of obstetrics and gynecology. Thyroid function tests were conducted in the hospital\'s biochemistry laboratory, including assessments of thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), and thyroid peroxidase antibodies (TPOAb). The study aimed to determine the prevalence of hypothyroidism and its association with various menstrual irregularities, such as oligomenorrhea, polymenorrhea, menorrhagia, and amenorrhea. Data analysis was performed using SPSS software, applying descriptive statistics, Pearson correlation for continuous variables, and Chi-square tests for categorical variables. A significance level of p<0.05 was set for the analyses.
RESULTS: The mean age of the participants was 33.1 years (SD ± 7.2). The distribution of menstrual irregularities was 60 (50%) oligomenorrhea, 24 (20%) polymenorrhea, 24 (20%) menorrhagia, and 12 (10%) amenorrhea. Elevated TSH levels (>4.0 mIU/L) were observed in 42 (35%) of the participants, low FT4 levels (<0.8 ng/dL) in 18 (15%), low FT3 levels (<2.5 pg/mL) in 12 (10%), and elevated TPOAb levels (>55 IU/mL) in 24 (20%). A significant association was found between elevated TSH levels and oligomenorrhea (66 (55%), p<0.05) and between reduced FT4 levels and menorrhagia (78 (65%), p<0.05). Additionally, elevated TPOAb levels were significantly associated with amenorrhea (60 (50%), p<0.05). The correlation analysis showed a moderately positive correlation between TSH levels and the severity of menstrual irregularities (r=0.35, p<0.01). Subclinical hypothyroidism was detected in 25% of the participants, while 15% had clinical hypothyroidism.
CONCLUSIONS: This study underscores a notable link between hypothyroidism and menstrual irregularities in women of reproductive age. The results highlight the necessity of routine thyroid function screenings for women experiencing menstrual abnormalities, facilitating precise diagnosis and suitable treatment.

OBJECTIVE: Hashimoto\'s thyroiditis (HT) is one of the most common causes of thyroid dysfunction in iodine sufficient worldwide areas, but its molecular mechanisms are not completely understood. To this regard, this study aimed to assess serum levels of miRNA-29a (miR-29a) and transforming growth factor beta 1 (TGFβ1) in HT patients with different patterns of thyroid function.
METHODS: A total of 29 HT patients, with a median age of 52 years (21-68) were included. Of these, 13 had normal thyroid function (Eu-HT); 8 had non-treated hypothyroidism (Hypo-HT); 8 had hypothyroidism on replacement therapy with LT4 (subst-HT). All patients had serum miR-29a assayed through qRT-PCR and serum TGFβ1 assayed by ELISA.
RESULTS: Serum miR-29a levels were significantly down-regulated in patients with Hypo-HT compared to Eu-HT patients (P < 0.01) and subst-HT patients (P < 0.05). A significant negative correlation was detected between serum miR-29a levels and TSH levels (r = -0.60, P < 0.01). Serum TGFβ1 levels were significantly higher in Hypo-HT than both Eu-HT (P < 0.01) and subst-HT patients (P < 0.05). A negative correlation was observed between serum miR-29a and TGFβ1 (r = -0.75, P < 0.01).
CONCLUSIONS: In conclusion, Hypo-HT patients had lower levels of serum miR-29a and higher levels of TGFβ1 in comparison with Eu-HT patients. Worthy of note, subst-HT patients showed restored serum miR-29a levels compared with Hypo-HT group, associated with lower serum TGFβ1. These novel findings may suggest a possible impact of replacement therapy with levothyroxine on serum miR-29a levels in HT.

OBJECTIVE: To evaluate the prevalence of thyroid dysfunction and its association with possible contributing factors related to diagnosis and treatment in children who received hematopoietic stem cell transplantation (HSCT) in the only national transplant unit in Greece.
METHODS: This is an observational, retrospective, single center cohort study that included 194 patients (58.6% boys) who survived for at least 1 year following allogeneic HSCT. Conditioning regimens depended upon diagnosis and protocols active at the time of transplantation. Some patients received irradiation, either central nervous system prophylaxis (n = 20), or total body irradiation (TBI) (n = 8). Thyroid gland evaluation included thyroid-stimulating hormone, free thyroxine, thyroid autoantibodies, and sonogram. Univariate and multivariate logistic models were used to examine the association of the above-mentioned factors with hypothyroidism.
RESULTS: The mean age at diagnosis and at bone marrow transplant (BMT) in years was 7.51 ± 0.46 and 7.58 ± 0.36, respectively. The median follow-up time was 4.83 years. Hypothyroidism was detected in 33 cases (17.7%), four of those patients having received TBI. Factors contributing to hypothyroidism as per the multivariate analysis were male sex, [OR: 3.005, 95% CI (1.145-7.890)], irradiation, [OR: 2.876, 95% CI (1.120-7.386)], and years after HSCT [OR: 1.148, 95% CI (1.042-1.266)], while malignancy was identified only in the univariate analysis. The multivariate model presents a good class separation capacity [AUC = 72%, 95% CI (61.4%-82.4%)], Two patients had papillary thyroid cancer, both among children who had received TBI.
CONCLUSIONS: These data highlight the fact that male sex and radiotherapy are two independent factors that lead to increased risk for hypothyroidism. Furthermore, the prevalence of hypothyroidism increases with time post HSCT.