Thyroid Hormone Imbalance Research Articles

Thyroid hormone imbalance and the mechanism by which it causes memory loss

Thyroid hormone imbalance is the cause of many cognitive dysfunctions such as memory loss, anxiety and depression. A study conducted by Yu et al suggests that hypothyroidism as well as hyperthyroidism causes depression, anxiety and hippocampal dysfunction in rats. The mechanism of these dysfunctions is not yet completely understood.

Thyroid Dysfunction Secondary to Endocrine Disruptive Chemicals – A Systematic Review

Objectives: To assess the epidemiological data and potential connection between different endocrine chemical disruptors and thyroid hormone abnormalities. Study Design: The 2020 PRISMA standards were followed when conducting the systematic review. Ten research studies were found and examined after an in-depth review of the scientific literature. Methodology: The systematic review was aimed to gather all pertinent information, including observational studies (prospective or retrospective cohorts) that address the relationship between exposure to endocrine disruptors and thyroid hormone imbalance. Results: Ten studies were found, and they demonstrated that these substances, especially in adulthood, impact the level of thyroid hormone and the incidence of thyroid nodules. Conclusions: Endocrine disruptive chemicals can compromise thyroid function by affecting hormone transporters, gene expression, and the hypothalamic-pituitary-thyroid axis.

Combined transcriptome and microbiome analysis reveals the thyrotoxic effects of PM2.5 in female rats

Pervasive environmental pollutants, specifically particulate matter (PM2.5), possess the potential to disrupt homeostasis of female thyroid hormone (TH). However, the precise mechanism underlying this effect remains unclear. In this study, we established a model of PM2.5-induced thyroid damage in female rats through intratracheal instillation and employed histopathological and molecular biological methods to observe the toxic effects of PM2.5 on the thyroid gland. Transcriptome gene analysis and 16S rRNA sequencing were utilized to investigate the impact of PM2.5 exposure on the female rat thyroid gland. Furthermore, based on the PM2.5-induced toxic model in female rats, we evaluated its effects on intestinal microbiota, TH levels, and indicators of thyroid function. The findings revealed that PM2.5 exposure induced histopathological damage to thyroid tissue by disrupting thyroid hormone levels (total T3 [TT3], (P < 0.05); total T4 [TT4], (P < 0.05); and thyrotropin hormone [TSH], (P < 0.05)) and functional indices (urine iodine [UI], P > 0.05), thus further inducing histopathological injuries. Transcriptome analysis identified differentially expressed genes (DEGs), primarily concentrated in interleukin 17 (IL-17), forkhead box O (FOXO), and other signaling pathways. Furthermore, exposure to PM2.5 altered the composition and abundance of intestinal microbes. Transcriptome and microbiome analyses demonstrated a correlation between the DEGs within these pathways and the flora present in the intestines. Moreover, 16 S rRNA gene sequencing analysis or DEGs combined with thyroid function analysis revealed that exposure to PM2.5 significantly induced thyroid hormone imbalance. We further identified key DEGs involved in thyroid function-relevant pathways, which were validated using molecular biology methods for clinical applications. In conclusion, the homeostasis of the "gut-thyroid" axis may serve as the underlying mechanism for PM2.5-induced thyrotoxicity in female rats.

Effects of selenium and iodine on Kashin-Beck disease: an updated review.

Kashin-Beck disease (KBD) is an endochondral osteogenesis disorder characterised by epiphysis damage and secondary deformable arthropathy induced by multiple external factors, among which selenium (Se) and iodine deficiency are important influencing factors. Iodine deficiency is usually accompanied by a low Se content in the soil in the KBD areas of China. Se can reverse oxidative damage to chondrocytes. In addition, Se is related to the bone conversion rate and bone mineral density. Low Se will hinder growth and change bone metabolism, resulting in a decrease in the bone conversion rate and bone mineral density. Thyroid hormone imbalance caused by thyroid dysfunction caused by iodine deficiency can damage bone homeostasis. Compared with Se deficiency alone, Se combined with iodine deficiency can reduce the activity of glutathione peroxidase more effectively, which increases the vulnerability of chondrocytes and other target cells to oxidative stress, resulting in chondrocyte death. Clinical studies have shown that supplementation with Se and iodine is helpful for the prevention and treatment of KBD.

Thyroid diseases and female sexual dysfunctions.

Female sexual dysfunctions (FSDs) have received little attention in the context of thyroid diseases, despite the high prevalence of both conditions. This review aims to update and summarize the state of knowledge on the association between thyroid diseases and FSDs and to investigate the complex mechanisms through which thyroid hormone imbalance can impact female sexual health in the context of the biopsychosocial model. A comprehensive literature search was performed through the PubMed, MEDLINE, and Scopus databases, using the following keywords: "female sexual function," "sexual dysfunction," "hypoactive sexual desire disorder," "thyroid disease," "thyroiditis," "hypothyroidism," and "hyperthyroidism." To date, well-designed studies that describe the relationship between FSDs and thyroid disorders are lacking. However, despite the limitations on available studies, current data indicate that sexual alterations are frequently associated with thyroid diseases in women. A complex interplay of direct and indirect hormonal and nonhormonal mechanisms has been hypothesized, including hormonal changes, neurotransmitter imbalance, reduced nitric oxide release, mood disorders, and other systemic consequences of both hypothyroidism and hyperthyroidism. Thyroid hormone receptors have also been identified in the genitourinary system. In a clinical setting, physicians should investigate the sexuality of patients consulting for thyroid disease. At the same time, an evaluation of thyroid function should be performed in patients presenting with FSD, especially after menopause, when the risk of thyroid diseases and FSDs increases strongly.

Relationship of Endometriosis with Cortisol and Thyroid Function in Young Working Females

Objective: The study was focused to evaluate the role of endometriosis in development of hypothyroidism in working females subjected to chronic stress. Study Design: cross sectional study. Settings: This research was conducted at department of Gynecology &amp; Obstetrics, The University of Lahore Teaching Hospital, Lahore. Duration: The research was completed in from February 2023 to February 2024. Methods: Serum samples of fifty-five endometriosis patients and fifteen controls were analyzed for T3, T4, TSH, cortisol and estrogen levels by using ELISA kits. Results: The levels of TSH in patient’s serum is (1.02±0.168mIU/L) as related to control (3.08±1.090 mIU/L) were lower in females with endometriosis. Serum estrogen levels in endometriosis patients (67.07±5.54 pg/ml) were higher than normal controls (21.07±3.66pg/ml). Elevated levels of serum cortisol (27.25±3.27) than normal values (11.19±4.18) in endometriosis patients were observed. Thyroid problems may result from this imbalance. Furthermore, there is a change in the quantity of thyroid hormones (T3 and T4) in endometriotic cells. Production of T4 rose whereas that of T3 fell. Thus, our research shows that endometriosis increases the risk of thyroid malfunction and hormone imbalance in women. Conclusion: We came to the conclusion that thyroid hormone contributes to endometriosis because endometrial cells are sensitive to changes in TSH. The thyroid gland and its related hormone concentrations described a varied picture between healthy subjects and patients of endometriosis. Moreover, thyroid hormones and estrogen are found to play their significant roles in the disease.

Study of Oxidative Stress and Inflammatory Status in Thyroid Dysfunction: A Systematic Review

Background: The frequency of thyroid disorders is rising quickly, making them a major socioeconomic issue. Oxidative stress is also connected to thyroid disorders with increasing frequency. Moreover, an association between underlying inflammatory processes and oxidative damage must be considered because most thyroid ailments are seen to have an underlying inflammatory basis. Aim &amp; objectives: This systematic review assesses the oxidative stress in thyroid dysfunctions and their association with inflammatory processes. Methodology: A systematic review of the literature was done using databases that included- PubMed, Scopus, Science Direct, Research Gate and Google Scholar using the keywords “oxidative stress”, “inflammatory markers,” and “thyroid disorders” from 2000-2022. After separately evaluating citations and abstracts, two reviewers examined full-text publications and came to an agreement on the research that should be included. We conducted this research using the preferred reporting items for systematic research and meta-analysis (PRISMA). Results: A total of 531 articles were found, out of which only 51 met the criteria of inclusion. A significant heterogeneity across the studies was found. In these studies, various oxidant/antioxidant and inflammatory markers were used to determine oxidative stress and its association with inflammatory processes. Most studies found a high level of reactive oxygen species (ROS) induced by an imbalance of thyroid hormones that can cause oxidative stress with a consequent lipid peroxidation response and accelerated inflammatory response. Conclusion: Data from the literature demonstrated a significant correlation between oxidative damage results and elevated ROS production. Thyroid issues can potentially trigger or exacerbate oxidative stress and ROS generation, which can worsen oxidative damage. Additionally, recent research indicates that OS and inflammation may be related in some way since mitochondrial reactive species are signalling molecules that cause the release of proinflammatory cytokines

Brain hypothyroidism silences the immune response of microglia in Alzheimer's disease animal model.

Thyroid hormone (TH) imbalance is linked to the pathophysiology of reversible dementia and Alzheimer's disease (AD). It is unclear whether tissue hypothyroidism occurs in the AD brain and how it affects on AD pathology. We find that decreased iodothyronine deiodinase 2 is correlated with hippocampal hypothyroidism in early AD model mice before TH alterations in the blood. TH deficiency leads to spontaneous activation of microglia in wild-type mice under nonstimulated conditions, resulting in lowered innate immune responses of microglia in response to inflammatory stimuli or amyloid-β. In AD model mice, TH deficiency aggravates AD pathology by reducing the disease-associated microglia population and microglial phagocytosis. We find that TH deficiency reduces microglial ecto-5'-nucleotidase (CD73) and inhibition of CD73 leads to impaired innate immune responses in microglia. Our findings reveal that TH shapes microglial responses to inflammatory stimuli including amyloid-β, and brain hypothyroidism in early AD model mice aggravates AD pathology by microglial dysfunction.

Cutaneous manifestations of endocrine diseases and their assessment in reconstructive surgery

The skin is the largest organ of the human body, and its main function is protection from external injuries and infectious influences. It is a metabolically active organ that works mainly by self-renewal of the squamous epithelium through continuous differentiation. The surface layer of the skin “epidermis” is updated every four weeks. It is also the body’s largest sensory organ, which can respond to external stimuli such as heat, cold, touch and pressure, which is necessary to maintain the body’s thermostat. Being the largest organ of the body, the skin is an active immune organ and an important peripheral neuro-endocrine organ. It is closely related to the endocrine system and, therefore, contributes to the homeostasis of peripheral hormones. A complex pathophysiology occurs when thyroid hormones are exposed to the skin, especially in the case of a continuing apparent violation of the regulation of thyroid hormones. Thyroid hormone is considered one of the key hormones regulating skin homeostasis. The release of peripheral thyroid hormones (T4 and T3) affects many organs, additionally regulating various functions at the cellular level. In particular, the skin is considered an important target organ, on which the thyroid hormone has a significant effect. Numerous skin diseases are associated with a violation of the regulation of thyroid hormones. Rough skin manifestations are usually the first sign of an imbalance of thyroid hormones, in which they play an integral role in maintaining natural function. This article reviews the pathology of thyroid hormones, as well as skin diseases associated with diseases of the pancreas. The interaction of thyroid gland diseases with the skin, manifested in the form of various skin pathologies, will be considered. It is known that endocrine disorders affect all organ systems of the body, including the skin.

Why More Prevalence of Thyroid Disorders in Women in Present Scenario

It is no surprise that women nowadays face a slew of health challenges. Thyroid dysfunctions, which are primarily caused by an imbalance of thyroid hormones are growing more frequent, with the American Thyroid Association estimating that one out of every eight women may experience thyroid challenges over her lifetime. Furthermore, it is expected that women are 5 to 8 times more prone than males to acquire thyroid issues. Because of modernity and increased stress in everyday life, Vega dharana, hormonal changes, iodine insufficiency, auto-immune disorders resulting in numerous endocrinal disorders in females. Hypothyroidism and hyperthyroidism is a prevalent endocrine illness that affects people all over the world. These figures point to an increase in the number of women experiencing health issues such as menstrual cycle imbalance, polycystic ovarian syndrome, sudden weight gain or loss, hypertension, lethargy, dry skin and hair, constipation and so on, all of which have their own effects on the body and are directly or indirectly related. The review will be useful in understanding the pathophysiology of Thyroid disorders and changing the disease's treatment regimen.

Sesamin alleviated fluoride – induced thyroid endocrine disruption in zebrafish (Danio rerio)

Previous studies have indicated that fluoride could induce the damage of thyroid. However, the effects of sesamin on thyroid endocrine function in zebrafish exposed to fluoride have not been clarified. This study was designed to investigate the alleviating effects of sesamin on thyroid endocrine disruption in zebrafish induced by fluoride. The results showed that sesamin significantly improved growth performance in adults exposed to fluoride; decreased significantly the mortality rate, increased remarkably the hatching rate and body length, and alleviated the phenomenon of spinal curvature, yolk cyst and pericardial cyst to varying degrees in fluoride-exposed embryos and larvae. Sesamin alleviated remarkably the damage of thyroid tissues in fluoride-exposed adults. Moreover, sesamin obviously reduced oxidative stress and improved the imbalance of thyroid hormones in fluoride-exposed adults or larvae. In addition, sesamin reversed the expression of endocrine-related genes of thyroid in fluoride-exposed adults or larvae. This indicates that sesamin can affects the thyroid tissue structure, hormone levels, and the expression of endocrine-related genes of thyroid, thus alleviating the thyroid endocrine disorder induced by fluoride and improving the growth and development. This study also demonstrates that sesamin can be a promising novel treatment for thyroid endocrine disorder caused by fluoride.

НИКОТИНОВАЯ ЗАВИСИМОСТЬ И ГОРМОНАЛЬНЫЙ ДИСБАЛАНС У БЕРЕМЕННЫХ КУРИЛЬЩИЦ С РАЗНОЙ СТЕПЕНЬЮ ТЯЖЕСТИ ХОБЛ

Introduction. The relationship between the degree of nicotine addiction and the functional state of the thyroid gland, the adrenocorticotropic hormone-cortisol system and hormone imbalance in pregnant women smokers with chronic obstructive pulmonary disease was studied. Aim. The aim of the study was to identify and evaluate the relationship between the degree of nicotine dependence and hormonal imbalance of the thyroid gland, cortisol and progesterone in pregnant smokers with varying degrees of chronic obstructive pulmonary disease severity. Material and methods. The study is based on the results of studying changes in blood hormone indicators in 107 smoking women with chronic obstructive pulmonary disease and 136 non-smoking women in different trimesters of pregnancy observed in the antenatal clinic. The control group consisted of healthy non-smoking patients. The diagnosis of chronic obstructive pulmonary disease was made based on the clinical recommendations of the Russian Respiratory Society (2021). The reliability of the results was evaluated using parametric statistics methods. The data obtained were processed using the Statistica 10 program, Microsoft Excel 2010. Results and discussion. The presented data revealed the presence in smokers of a statistically significant and very close relationship between the degree of nicotine dependence and the indicators of the imbalance of the hormones studied in all trimesters of pregnancy, with maximum values in the third trimester.This is due to the fact that it is in the third trimester of pregnancy that the maximum increase in the indicators of all studied hormones occurs, even if at the initial stage of pregnancy the indicator could be less than the lower limit of the reference interval, as in the case of thyroid-stimulating hormone.Conclusion. Nicotine addiction creates environment for the development of endocrine imbalance of thyroid hormones, adrenocorticotropic hormone, cortisol and progesterone.

Exploring the underlying molecular mechanism of tri(1,3-dichloropropyl) phosphate-induced neurodevelopmental toxicity via thyroid hormone disruption in zebrafish by multi-omics analysis

Tri(1,3-dichloropropyl) phosphate (TDCPP) is widespread in the environment as a typical thyroid hormone-disrupting chemical. Here, we aimed to explore the toxicological mechanisms of the thyroid hormone-disrupting effects induced by TDCPP in zebrafish embryos/larvae using multi-omics analysis. The results showed that TDCPP (400 and 600 µg/L) induced phenotypic alteration and thyroid hormone imbalance in zebrafish larvae. It resulted in behavioral abnormalities during zebrafish embryonic development, suggesting that this chemical might exhibit neurodevelopmental toxicity. Transcriptomic and proteomic analysis provided consistent evidence at the gene and protein levels that neurodevelopmental disorders were significantly enhanced by TDCPP exposure (p < 0.05). Additionally, multi-omics data indicated that membrane thyroid hormone receptor (mTR)-mediated non-genomic pathways, including cell communication (ECM–receptor interactions, focal adhesion, etc.) and signal transduction pathways (MAPK signaling pathway, calcium signaling pathway, neuroactive ligand–receptor interaction pathway, etc.), were significantly disturbed (p < 0.05) and might contribute to the neurodevelopmental toxicity induced by TDCPP. Therefore, behavioral abnormalities and neurodevelopmental disorders might be important phenotypic characteristics of TDCPP-induced thyroid hormone disruption, and mTR-mediated non-genomic networks might participate in the disruptive effects of this chemical. This study provides new insights into the toxicological mechanisms of TDCPP-induced thyroid hormone disruption and proposes a theoretical basis for risk management of this chemical.

Evaluating the Incidence of Audiological Derangement in Cases of Thyroid Hormone Imbalance.

Thyroid hormone disorders are both congenital as well as acquired. According to a projection from several studies on thyroid diseases, it has been estimated that about 42 million people in India suffer from various kind of thyroid diseases (1) Thyroid hormone is closely associated with the development of the cognitive functions, thus deficiency of this hormone is said to have effect an overall impact on proper functioning of the body. The normal functioning of the thyroid gland and adequate levels in the blood are Needed for the formation and functioning of the middle ear, inner ear and the central auditory pathway. Thus, congenital hypothyroidism (CH) can be a potential risk factor for hearing impairment (2) if the hormones decrease or are absent during the development of the peripheral and central auditory system structures. This study was undertaken with the objective of studying the pattern of hearing loss in patients who have a deranged thyroid profile. The study was conducted among 50 patients who were known cases of thyroid disorder in the Otorhinolaryngology Department of our institute. The study was hospital based observational clinical study. The patients were subjected to thyroid profile test After this, those who satisfied the inclusion and exclusion criteria and were included, after detailed history and examination, patients were subjected to PTA, hearing loss was classified according to WHO guidelines. The age group of the patients was from 30-55 yrs. with the mean age being 42. On the basis of the t3, t4 and tsh levels, in the current study out of 50 patients,40 were hypothyroid (80%),with male to female ratio of 6:4. On pure tone audiometry, 15 patients had decreased hearing. The other 25 had normal hearing. The incidence of hearing loss in hypothyoroid patients in our study is 37.5%. On analaysis the PTA reports of these patients,9 patients (22.5%) had conductive hearing loss of mild variety, the mean value of hearing loss being 26.2 decibels. 2 (5%) patients had mixed variety of hearing loss, with sensorineural hearing loss at higher frequencies. All the remaining patients had sensorineural type of hearing loss, i.e., 10%. Of the 10 patients, that have hyperthyroidism 8 were female and 2 were male. 3 patients (30%) had hearing loss, all these 3 patients reported hearing losses at high frequencies and had moderate type of sensorineural hearing loss. Conclusion- From our current study, we could see that hearing loss is present in both extremes of thyroid hormone imbalance The dominant variety of hearing loss in thyroid disorder is sensorineural type, because thyroid hormone imbalance affects the inner ear function.

THYROID-ASSOCIATED OPHTHALMOPATHY WITH SUSPECTED SECONDARY GLAUCOMA

Thyroid-associated ophthalmopathy (TAO) is a thyroid hormone imbalance thatmanifests in the eye. The most common TAO is in Grave’s Disease. TAO could increase theintraocular pressure and could cause a glaucoma optic neuropathy and therefore secondaryglaucoma could happen.

Comparative Evaluation of the Effects of Legacy and New Generation Perfluoralkyl Substances (PFAS) on Thyroid Cells In Vitro.

BackgroundPer- and poly-fluorinated alkyl substances (PFAS) are environment-persitent emerging endocrine disrupting chemicals raising health concerns worldwide. Exposure to PFAS has been associated with the imbalance of thyroid hormones. However, available studies addressing the cell mechanism underlying thyroid disrupting feature of legacy PFAS, such as perfluoro-octanoic acid (PFOA), perfluoro-octane-sulfonic acid (PFOS), and the new generation substitutes, such as C6O4, are still lacking. In this study the potential disrupting effect of PFOA, PFOS, and C6O4 on a murine thyroid cell model was assessed.MethodsA rat FRTL-5 cell line was used as the normal thyroid follicular cell model. Cell iodide-uptake, induced by thyroid stimulating hormone (TSH), was used to assess the functional impact of PFAS exposure on cell function. Tetrazolium salt-based cell viability assay and merocyanine 540-based cell staining were used to address the possible involvement of cell toxicity and membrane biophysical properties on altered cell function. The possible direct interaction of PFAS with TSH-receptor (TSH-R) was investigated by computer-based molecular docking and analysis of molecular dynamics. Evaluation of intracellular cAMP levels and gene expression analysis were used to validate the direct impairment of TSH-R-mediated downstream events upon PFAS exposure.ResultsDifferent from PFOS or C6O4, exposure to PFOA at a concentration ≥ 10 ng/mL was associated with significant impairment of the iodide uptake upon TSH stimulation (respectively: basal 100.0 ± 19.0%, CTRL + TSH 188.9 ± 7.8%, PFOA 10 ng/mL + TSH 120.4 ± 20.9%, p= 0.030 vs CTRL + TSH; PFOA 100 ng/mL + TSH 115,6 ± 12,3% p= 0.017 vs CTRL + TSH). No impairment of cell viability or membrane stability was observed. Computational analysis showed a possible direct differential interaction of C6O4, PFOA, and PFOS on a same binding site of the extracellular domain of TSH-R. Finally, exposure to PFOA was associated with a significant reduction of downstream intracellular cAMP levels and both sodium-iodide transporter and thyroperoxidase gene expression upon TSH-R stimulation.ConclusionsOur data suggest that legacy and new generation PFAS can differentially influence TSH dependent signaling pathways through the direct interaction with TSH-R.

Protective effects of curcumin against thyroid hormone imbalance after gas explosion-induced traumatic brain injury via activation of the hypothalamic-pituitary-thyroid axis in male rats.

Gas explosion (GE)-induced traumatic brain injury (TBI) can affect thyroid hormone (TH) homeostasis in miners. This study evaluated the effects of hepatic transthyretin and hypothalamic-pituitary-thyroid (HPT) axis on thyroids and explored the protective effect and mechanism of curcumin on GE-induced TBI. Thirty rats were randomly divided into three groups (10 per group): first group (control group)-rats received GE treatment once; second group (GE group)-rats received GE treatment (200m from the source of the explosion once); third group (GE + Cur group)-rats received curcumin (Cur) by lavage at a dose of 100mg/kg/day once every other day for 7days after receiving GE. After GE, the pathological changes were analyzed by hemotoxylin and eosin staining, and the levels of serum reactive oxygen species (ROS), urine iodine (UI), THs, nuclear factor-kappa B (NF-κB), superoxide dismutase (SOD), glutathione peroxidase (Gpx), and malondialdehyde (MDA) were analyzed using ELISA. Expression of proteins in the HPT axis of rats was examined by immunohistochemistry and Western blotting. We found that GE could induce pathologic changes in rat thyroid and liver. Serum levels of THs, NF-κB and serum redox state became unbalanced in rats after GE. GE could inhibit the biosynthesis and biotransformation of THs by affecting key HPT axis proteins. Additionally, GE reduced the level of hepatic transthyretin. Serum THs levels and thyroid sections were almost recovered to normal after curcumin treatment. The aforementioned key HPT axis proteins in the curcumin group showed opposite expression trends. In summary, GE affected THs balance while curcumin can protect against these injury effects by affecting TH biosynthesis, biotransformation, and transport, and inducing oxidative stress and inflammatory responses.

Endocrine Regulation on Bone by Thyroid.

BackgroundAs an endocrine organ, the thyroid acts on the entire body by secreting a series of hormones, and bone is one of the main target organs of the thyroid.SummaryThis review highlights the roles of thyroid hormones and thyroid diseases in bone homeostasis.ConclusionThyroid hormones play significant roles in the growth and development of bone, and imbalance of thyroid hormones can impair bone homeostasis.

Features of ultrasound and dopplerometric endometry examination in autoimmune thyroiditis patients with abnormal uterine bleeding

Abnormal uterine bleeding occurs in 10–30% of reproductive age women. Ultrasound examination is one of the most effective methods of diagnosing lesions of the pelvic organs while it has high sensitivity (96%), but low specificity (13.8%) in relation to endometrial lesions, the informativeness of ultrasound in the diagnosis of abnormal uterine bleeding ranges from 60 to 93.3%. It had been revealed revealed that the imbalance of thyroid hormones can have a direct effect on the endometrium. Thus, the analysis of ultrasound examinations data together with dopplerometric assessment of the blood flow of the internal genital organs in autoimmune thyroiditis patients with abnormal uterine bleeding is an urgent task of modern gynecology. The purpose is to determine the features of ultrasound exanimation with Doppler assessment of the endometrium in autoimmune thyroiditis patients with abnormal uterine bleeding. Materials and methods. The patients’ examinations were carried out from 2019 to 2022 We examined 120 patients, of whom 90 (75%) suffered from abnormal uterine bleeding and 30 (25%) did not have signs of gynecological and somatic pathology (control group). Abnormal bleeding patients average age was 36.3±3.2 years. The average age of bleeding and thyroid pathology women was 34.8±2.6 years, the control group average age was 30.7±2.9 years. Results. Echographic signs of endometrium structural changes were detected in 83 (92.2%) of abnormal nautoimmune bleeding women and in 7 (7.8%) women ultrasound signs of pathology were not detected. Significant differences were found when analyzing the results of ultrasonographic examination of patients with bleeding and bleeding + thyroid pathology. Conclusion. Ultrasound is an important method that contributes to a significant improvement in the diagnosis of isolated or combined benign uterine diseases in women with abnormal autoimmune bleeding at the background of thyroid pathology, and in most cases corresponds to the histological diagnosis.

Prevalence of Risk Factors for Thyroid Hormone Imbalance

This study was aimed to assess the frequency of thyroid hormone imbalance risk factors. A cross-sectional survey was conducted using the convenience sampling technique, from July-2018 to September-2018 in different cities of Punjab, Pakistan. A total of 150 patients, having thyroid hormone imbalance with or without any comorbidity were included and the subjects having normal thyroid levels were excluded. Thyroid hormone imbalance was more frequent in females having 40-60 years of age. Gender was significantly associated with 'pregnancy or delivery in last six months' (p=0.029) and iodine deficiency (p=0.036). Marital status was significantly associated with 'symptoms observed' (p=0.009), 'radioactive iodine exposure' (p=0.001), 'autoimmune disease' (p=0.050), 'smoking' (p=0.014) and 'stress' (p=0.040). Family income was significantly associated with 'family history of disease' (p=0.039) and 'iodine deficiency' (p=0.049). Residential area was significantly associated with 'autoimmune disease' (p=0.050), 'smoking' (p=0.036) and 'stress' (p=0.029). Use of iodized salt and stress were prevalent risk factors and disease was common among females, especially age group 40-60 years.