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Abstract Background Systemic Lupus Erythematosus (SLE) patients are more likely than the general population to suffer from thyroid illness. The major goal was to assess the thyroid dysfunctions due to immunological factors in Egyptian SLE children and how they are related to the course and severity of the illness. Methods Fifty children and adolescents with SLE are included in this cross-sectional observational study. Every patient underwent a thorough physical examination and a comprehensive history taking. An enzyme-linked immunosorbent assay (ELISA) approach was used to evaluate the thyroid profile, anti-thyroglobulin (Anti-TG), and anti-thyroid peroxidase (anti-TPO) antibodies. Results Of the 50 patients, the female: male ratio (F: M = 7:1) was 44 females and 6 males (12%). They were between the ages of 5 and 17. Out of the patients, thirty-two (64%) had thyroid dysfunctions, 19 (38%) had euthyroid sick syndrome, ten (20%) had overt hypothyroidism, three (6%) had subclinical hypothyroidism, and none had hyperthyroidism. Of the 50 patients, one (2%) had increased anti-TPO, whereas all other patients had normal anti-TG levels. A statistically significant negative correlation (p-value 0.007) was seen between the disease duration and free thyroxine (FT4). Furthermore, a significant negative correlation (p-values 0.015 and 0.028) was found when comparing the disease duration with thyroid antibodies (anti-TG and anti-TPO). Conclusion In Juvenile Systemic Lupus Erythematosus (JSLE), thyroid dysfunctions can be identified. The disease duration but not its activity was significantly correlated with thyroid antibodies. For children with JSLE, thyroid function testing should be done on a regular basis. It is preferable to carry out additional thyroid antibody tests when necessary.

Background: Systemic Lupus Erythematosus (SLE) patients are more likely than the general population to suffer from thyroid illness. The major goal was to assess the thyroid dysfunctions due to immunological factors in Egyptian SLE children and how they are related to the course and severity of the illness. Methods: Fifty children and adolescents with SLE are included in this cross-sectional observational study. Every patient underwent a thorough physical examination and a comprehensive history taking. An enzyme-linked immunosorbent assay (ELISA) approach was used to evaluate the thyroid profile, anti-thyroglobulin (Anti-TG), and anti-thyroid peroxidase (anti-TPO) antibodies. Results: Of the 50 patients, the female: male ratio (F: M = 7:1) was 44 females and 6 males (12%). They were between the ages of 5 and 17. Out of the patients, thirty-two (64%) had thyroid dysfunctions, 19 (38%) had euthyroid sick syndrome, ten (20%) had overt hypothyroidism, three (6%) had subclinical hypothyroidism, and none had hyperthyroidism. Of the 50 patients, one (2%) had increased anti-TPO, whereas all other patients had normal anti-TG levels. A statistically significant negative correlation (p-value 0.007) was seen between the disease duration and free thyroxine (FT4). Furthermore, a significant negative correlation (p-values 0.015 and 0.028) was found when comparing the disease duration with thyroid antibodies (anti-TG and anti-TPO). Conclusion: In Juvenile Systemic Lupus Erythematosus (JSLE), thyroid dysfunctions can be identified. The disease duration but not its activity was significantly correlated with thyroid antibodies. For children with JSLE, thyroid function testing should be done on a regular basis. It is preferable to carry out additional thyroid antibody tests when necessary. [ABSTRACT FROM AUTHOR]

Background/Objective: To determine the prevalence of thyroid dysfunctions and thyroid autoantibodies in Thai systemic lupus erythematosus (SLE) patients, and compare them with age‐ and sex‐matched healthy controls (HCs). Associations between thyroid dysfunctions and SLE disease activity, and associated factors for thyroid dysfunctions in SLE also were determined. Method: One hundred SLE patients, without apparent clinical thyroid disease, attended the Rheumatology Clinic between November 2021 and October 2022, were enrolled into this study. HCs were matched to SLE cases by age and sex (ratio of 1:1). Clinical manifestations, SLE disease activity and medication received were collected in all SLE patients. Thyroid function tests and thyroid autoantibodies (anti‐thyroglobulin: anti‐TG and anti‐thyroid peroxidase: anti‐TPO) were collected from all participants. Results: When compared with HCs, SLE patients had higher prevalence of thyroid dysfunctions, hypothyroidism and euthyroid sick syndrome (28% vs. 7%, p <.001, and 12% vs. 2%, p =.010, and 6% vs. 0%, p =.013, respectively). Prevalence of isolated hypothyroxinemia was higher numerically in SLE patients (9% vs. 3%, p =.074). Prevalence of anti‐TG or anti‐TPO was no different between SLE patients and HCs (16% vs. 18%, p =.707). There was no association between SLE disease activity and abnormal thyroid functions or thyroid autoantibodies. Family history of thyroid disease and prednisolone use (>10 mg/day) were associated factors for thyroid abnormalities with adjusted OR (95% CI) of 6.13 (1.58–23.75), p =.009 and 4.00 (1.37–11.70), p =.011, respectively. Conclusion: Thyroid dysfunctions were more prevalent in SLE patients. Family history of thyroid disease and prednisolone use (>10 mg/day) were independent associated factors of thyroid abnormalities. [ABSTRACT FROM AUTHOR]

The relationship between serum iodine (SIC) and thyroid dysfunctions in adults is poorly understood, and this study aimed to explore their relationship. A total of 1320 participants were included in the final analysis. We collected basic demographic information, blood, and spot urine samples to determine serological indices and iodine nutritional status. The median (IQR) of urinary iodine (UIC)/urinary creatinine (UCr), UIC, SIC were 138.1 (91.1, 207.6) μg/g, 155.8 (94.5, 211.1) μg/L, and 70.6 (59.8, 83.9) μg/L, respectively. The 90% reference ranges for UIC/UCr and SIC were 66.5–349.8 mg/g and 49.3–97.1 μg/L. SIC was positively correlated with UIC and UIC/UCr. The prevalence of overt hypothyroidism and subclinical hypothyroidism in female was significantly higher than that in male (P = 0.02, P = 0.002). In male, subjects above the upper reference value of SIC (97.1 μg/L) had a higher risk of subclinical hyperthyroidism (OR = 4.46, 95% CI: 1.29, 12.8) and overt hypothyroidism (OR = 5.59, 95% CI: 1.88, 6.42). In female, subjects below the lower reference value of SIC (49.3 μg/L) had a higher risk of overt hypothyroidism (OR = 2.18, 95% CI: 1.10, 4.06), TgAb positive (OR = 1.97, 95% CI: 1.15, 3.32) and TPOAb positive (OR = 2.48, 95% CI: 1.41, 4.26). In conclusion, serum iodine can be used as an indicator to evaluate iodine nutritional status and thyroid dysfunctions. Higher serum iodine concentration was associated with an increased risk of subclinical hyperthyroidism and overt hypothyroidism in men; lower serum iodine concentration was associated with an increased risk of overt hypothyroidism and positive TgAb and TPOAb in women. [ABSTRACT FROM AUTHOR]

Objectives: To determine the frequency of endocrine disorders in Beta-Thalassemia Major (BTM) patients presenting for Endocrine Evaluation to the Department of Diabetes, Endocrinology and Metabolic Diseases, Hayatabad Medical Complex, Peshawar, Pakistan, a tertiary care hospital. Method: This descriptive study was conducted in the Department of Diabetes, Endocrinology and Metabolic Diseases, Hayatabad Medical Complex, Peshawar from October 2019 to August 2021. All patients with BTM presenting for endocrine evaluation were included in the study. Height and weight were assessed and plotted on the standard charts. For secondary sexual characteristics tanner staging was used. Blood samples for hormonal profile were taken according to standard protocol and sent for endocrine assessment. Results: A Total of 135 patients BTM were enrolled in the study comprising of 70 (51.9%) males and 65 (48.1%) females. Their mean age was 14.8±3.9 years, mean height 138.5±13.01 cm, mean weight 35.9±8.4 kg, mean BMI 18.6±2.8 kg/m2, mean age of transfusion started was 6.7±3.99 months, mean duration of transfusion 13.6±4.03 years and mean duration of chelation therapy received 6.1±4.5 years. Regarding endocrine complications, out of 135 patients assessed, one hundred (74.1%) had height less than 5th centile and fifteen (11.1%) had diabetes mellitus. For thyroid and parathyroid function, 58 and 13 were tested respectively, out of which 16 (27.6%) and 6 (46.2%) had thyroid dysfunction and hypoparathyroidism. Out of 91 patients assessed for pubertal delay, 61 (67.03%) had delayed puberty. Conclusions: High percentage of endocrine complications were found in patients with BTM. Severity and multiplicity of endocrine organs involvement was dependent on duration of the disease and lack of compliance with chelation therapy. [ABSTRACT FROM AUTHOR]

Introduction: Thyroid dysfunctions associated with SARS-CoV-2 acute infection have been extensively described since the beginning of COVID-19 pandemics. Conversely, few data are available on the occurrence of thyroid autoimmunity after COVID-19 resolution. We assessed the prevalence of autoimmune thyroid disease (ATD) and thyroid dysfunctions in COVID-19 survivors three months after hospital admission. Design and methods: Single-center, prospective, observational, cohort study performed at ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. 599 COVID-19 survivors were prospectively evaluated for thyroid function and autoimmunity thyroperoxidase antibodies (TPOAb), thyroglobulin antibodies (TgAb). When a positive antibody concentration was detected, thyroid ultrasound was performed. Multiple logistic regression model was used to estimate the association between autoimmunity and demographic characteristics, respiratory support, and comorbidities. Autoimmunity results were compared to a cohort of 498 controls referred to our Institution for non-thyroid diseases before the pandemic onset. A sensitivity analysis comparing 330 COVID-19 patients with 330 age and sex-matched controls was performed. Results: Univariate and multivariate analysis found that female sex was positively associated (OR 2.01, SE 0.48, p = 0.003), and type 2 diabetes (T2DM) was negatively associated (OR 0.36, SE 0.16, p = 0.025) with thyroid autoimmunity; hospitalization, ICU admission, respiratory support, or COVID-19 treatment were not associated with thyroid autoimmunity (p > 0.05). TPOAb prevalence was greater in COVID-19 survivors than in controls: 15.7% vs 7.7%, p = 0.002. Ultrasonographic features of thyroiditis were present in 94.9% of the evaluated patients with positive antibodies. TSH was within the normal range in 95% of patients. Conclusions: Autoimmune thyroid disease prevalence in COVID-19 survivors was doubled as compared to age and sex-matched controls, suggesting a role of SARS-CoV-2 in eliciting thyroid autoimmunity. [ABSTRACT FROM AUTHOR]

Thyroid dysfunctions are among the most common endocrine disorders and accurate biochemical testing is needed to confirm or rule out a diagnosis. Notably, true hyperthyroidism and hypothyroidism in the setting of a normal thyroid-stimulating hormone level are highly unlikely, making the assessment of free thyroxine (FT4) inappropriate in most new cases. However, FT4 measurement is integral in both the diagnosis and management of relevant central dysfunctions (central hypothyroidism and central hyperthyroidism) as well as for monitoring therapy in hyperthyroid patients treated with anti-thyroid drugs or radioiodine. In such settings, accurate FT4 quantification is required. Global standardization will improve the comparability of the results across laboratories and allow the development of common clinical decision limits in evidence-based guidelines. The International Federation of Clinical Chemistry and Laboratory Medicine Committee for Standardization of Thyroid Function Tests has undertaken FT4 immunoassay method comparison and recalibration studies and developed a reference measurement procedure that is currently being validated. However, technical and implementation challenges, including the establishment of different clinical decision limits for distinct patient groups, still remain. Accordingly, different assays and reference values cannot be interchanged. Two-way communication between the laboratory and clinical specialists is pivotal to properly select a reliable FT4 assay, establish reference intervals, investigate discordant results, and monitor the analytical and clinical performance of the method over time. [ABSTRACT FROM AUTHOR]

IntroductionThyroid dysfunctions associated with SARS-CoV-2 acute infection have been extensively described since the beginning of COVID-19 pandemics. Conversely, few data are available on the occurrence of thyroid autoimmunity after COVID-19 resolution. We assessed the prevalence of autoimmune thyroid disease (ATD) and thyroid dysfunctions in COVID-19 survivors three months after hospital admission.Design and methodsSingle-center, prospective, observational, cohort study performed at ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. 599 COVID-19 survivors were prospectively evaluated for thyroid function and autoimmunity thyroperoxidase antibodies (TPOAb), thyroglobulin antibodies (TgAb). When a positive antibody concentration was detected, thyroid ultrasound was performed. Multiple logistic regression model was used to estimate the association between autoimmunity and demographic characteristics, respiratory support, and comorbidities. Autoimmunity results were compared to a cohort of 498 controls referred to our Institution for non-thyroid diseases before the pandemic onset. A sensitivity analysis comparing 330 COVID-19 patients with 330 age and sex-matched controls was performed.ResultsUnivariate and multivariate analysis found that female sex was positively associated (OR 2.01, SE 0.48, p = 0.003), and type 2 diabetes (T2DM) was negatively associated (OR 0.36, SE 0.16, p = 0.025) with thyroid autoimmunity; hospitalization, ICU admission, respiratory support, or COVID-19 treatment were not associated with thyroid autoimmunity (p > 0.05). TPOAb prevalence was greater in COVID-19 survivors than in controls: 15.7% vs 7.7%, p = 0.002. Ultrasonographic features of thyroiditis were present in 94.9% of the evaluated patients with positive antibodies. TSH was within the normal range in 95% of patients.ConclusionsAutoimmune thyroid disease prevalence in COVID-19 survivors was doubled as compared to age and sex-matched controls, suggesting a role of SARS-CoV-2 in eliciting thyroid autoimmunity.

The alterations of circulating adipocytokines have been reported in thyroid diseases or type 2 diabetes mellitus (T2DM), but such data in T2DM coincident with clinical and subclinical thyroid-dysfunctions are limited, and remain to be investigated. We studied the changes in serum chemerin, resisitin and visfatin in T2DM patients with thyroid dysfunctions, and their association with inflammatory and insulin resistance-markers. A total of 272 female and male Iranian participants were selected and divided into six groups: the euthyroid group, T2DM, T2DM coincident with clinical and sub clinical hypothyroidism (SC-HO, and C-HO), and T2DM coincident with clinical and sub clinical hyperthyroidism (SC-HR, C-HR).Demographic characteristics, serum levels of adipocytokines, thyroid hormones, inflammatory factors (IL1-β, IL-6 and CRP) and insulin resistance-markers were determined in all participants. T2DM patients with clinical thyroid dysfunctions showed higher levels of circulating resistin, visfatin, chemerin and inflammatory factors, compared with the T2DM group and T2DM coexisted with subclinical thyroid diseases. No significant differences were observed in circulating adipocytokines and inflammatory markers between T2DM coexisting with subclinical thyroid diseases and those without thyroid dysfunctions. Our results revealed that clinical thyroid dysfunction in T2DM patients was associated with elevated levels of circulating resistin, chemerin, visfatin and inflammatory factors, while no such alteration was detected in T2DM coincident with subclinical thyroid dysfunction. [ABSTRACT FROM AUTHOR]

Objective: In this cross-sectional study we tried to evaluate the prevalence of thyroid dysfunctions and anemia in patients with type 2 diabetes mellitus in a cohort of diabetic patients from the southern region of Saudi Arabia. Method: This is a retrospective cross-sectional study. Archived clinical data from the different private labs, governmental labs and various specialized clinics following the diabetic patients, from three biggest cities located in the southern region of Saudi Arabia, i.e., Abha, Khamis Mushayt, and Najran. We screened the baseline demographic characteristics, glycosylated hemoglobin (HbA1c), thyroid profile, iron profile, and erythrocytes indices. Data were analyzed by SPSS statistics for the window. Results: There was a significant difference (p<0.05) in the mean value of FT4, TSH, Hbg, RBC, HCT, MCH, MCHC, serum ferritin and iron, respectively between female and male patients, while MCV and FBS showed no significant difference (p>0.05). Overall, 50.8% anemia was detected in the study population, among which there were 35.74% patients with a thyroid disorder (p=0.000). TSH shows a significantly negative correlation with Hbg, HCT, serum ferritin, iron, and a strong positive correlation with HbA1c. Conclusion: Our study demonstrated the high incidence of thyroid dysfunctions and anemia in type 2 diabetes mellitus patients and continuous positive correlation of TSH with HbA1c, and negative correlation between TSH and iron profile. Furthermore, HbA1c demonstrated the significantly negative correlation with iron profile. [ABSTRACT FROM AUTHOR]

Intrauterine growth restriction (IUGR) affects a large proportion of infants, particularly in underdeveloped countries. Among the main causes of IUGR, maternal endocrine-metabolic dysfunction is highlighted, either due to its high incidence or due to the severity of the immediate and mediated changes that these dysfunctions cause in the fetus and the mother. Although the effects of endocrine and metabolic disorders have been widely researched, there are still no reviews that bring together and summarize the effects of these conditions on bone development in cases of IUGR. Therefore, the present literature review was conducted with the aim of discussing bone changes observed in fetuses with IUGR caused by maternal endocrine-metabolic dysfunction. The main endocrine dysfunctions that occur with IUGR include maternal hyperthyroidism, hypothyroidism, and hypoparathyroidism. Diabetes mellitus , hypertensive disorders, and obesity are the most important maternal metabolic dysfunctions that compromise fetal growth. The bone changes reported in the fetus are, for the most part, due to damage to cell proliferation and differentiation, as well as failures in the synthesis and mineralization of the extracellular matrix, which results in shortening and fragility of the bones. Some maternal dysfunctions, such as hyperthyroidism, have been widely studied, whereas conditions such as hypoparathyroidism and gestational hypertensive disorders require further study regarding the mechanisms underlying the development of bone changes. Similarly, there is a gap in the literature regarding changes related to intramembranous ossification, as most published articles only describe changes in endochondral bone formation associated with IUGR. Furthermore, there is a need for more research aimed at elucidating the late postnatal changes that occur in the skeletons of individuals affected by IUGR and their possible relationships with adult diseases, such as osteoarthritis and osteoporosis. • Intrauterine growth restriction (IUGR) affects a large proportion of infants, particularly in underdeveloped countries. • Maternal endocrine-metabolic dysfunction has been highlighted as one of the main causes of IUGR. • Maternal endocrine-metabolic dysfunction can impair fetal bone development. • Reduced fetal bone growth occurs under conditions such as hyperthyroidism, hypertension, and obesity. [ABSTRACT FROM AUTHOR]

Objective of this research is to explore the complex correlations among FT3, FT4 and TSH in thyroid dysfunction states. A total of 3425 outpatients were included to analyze their thyroid function tests measured at the university teaching hospital. The subjects under study were categorized as euthyroid (70.45%), subclinical hypothyroid (18.95%), overt hypothyroid (3.30%), subclinical hyperthyroid (5.11%) and overt hyperthyroid (2.19%) patients. The linear and non-linear relations among FT3, FT4 and TSH were modeled statistically to understand their role in thyroid functions. The prevalence of hypothyroidism is higher than hyperthyroidism in which females are more vulnerable than males. The correlation between FT3 and FT4 increases from euthyroidism (r = 0.1, P < 0.001) to overt thyroid dysfunctions (r = 0.91, P < 0.001). The non-linear complex correlations between FT4 and TSH are significantly explained by well fitted sigmoid curves of four-parameter logistic (4PL) model (R2 = 0.97 and P < 0.001) in both hypothyroidism and hyperthyroidism interfaced with euthyroidism. The 4PL curves are response trajectories of pituitary TSH which exhibit the turning points of thyroid dysfunction states by the deviation in serum FT4. The negative slopes and correlations observed in the linear fits in TSH vs FT3 or FT4 are the indicators of negative feedback mechanism in the thyroid cycle. [ABSTRACT FROM AUTHOR]

The alterations of circulating adipocytokines have been reported in thyroid diseases or type 2 diabetes mellitus (T2DM), but such data in T2DM coincident with clinical and subclinical thyroid-dysfunctions are limited, and remain to be investigated. We studied the changes in serum chemerin, resisitin and visfatin in T2DM patients with thyroid dysfunctions, and their association with inflammatory and insulin resistance-markers. A total of 272 female and male Iranian participants were selected and divided into six groups: the euthyroid group, T2DM, T2DM coincident with clinical and sub clinical hypothyroidism (SC-HO, and C-HO), and T2DM coincident with clinical and sub clinical hyperthyroidism (SC-HR, C-HR).Demographic characteristics, serum levels of adipocytokines, thyroid hormones, inflammatory factors (IL1-β, IL-6 and CRP) and insulin resistance-markers were determined in all participants. T2DM patients with clinical thyroid dysfunctions showed higher levels of circulating resistin, visfatin, chemerin and inflammatory factors, compared with the T2DM group and T2DM coexisted with subclinical thyroid diseases. No significant differences were observed in circulating adipocytokines and inflammatory markers between T2DM coexisting with subclinical thyroid diseases and those without thyroid dysfunctions. Our results revealed that clinical thyroid dysfunction in T2DM patients was associated with elevated levels of circulating resistin, chemerin, visfatin and inflammatory factors, while no such alteration was detected in T2DM coincident with subclinical thyroid dysfunction.

Objective: To determine the prevalence of thyroid-stimulating hormone (TSH) alterations and different types of thyroid dysfunctions in both sexes with no age limitations from variety of sources in Duhok province. Patients and Methods: In this retrospective cross-sectional study, we screened 25040 suspicious cases of thyroid diseases in a year (2019), retrieving the data from the computer of three clinical laboratories in the Duhok City; following exclusion of 470 cases, 24568 cases were included to categorize the different types of thyroid dysfunctions. Results: The prevalence of TSH alteration was 25.03%, 20.55% of them had a high concentration being statistically higher in females, while only 4.48% was low TSH with equal prevalence among both sexes. Out of 24568 patients, the prevalence of subclinical hypothyroidism was 94.85%, followed by 2.20%, 1.20%, 0.78%, 0.67%, and 0.31% for each of subclinical hyperthyroidism, primary hypothyroidism, central hyperthyroidism, central hypothyroidism, and primary hyperthyroidism respectively. Conclusions: The studied population had high prevalence of high TSH level (20.55%), being more prevalent in female than in male. Our survey revealed that the distribution of thyroid disorders was vary among different age groups with highest prevalence of subclinical hypothyroidism in all age groups (94.85%); Also, we concluded that middle & advanced ages, and females were more susceptible to thyroid disorders.

The aim of this study was to evaluate whether there are thyroid diseases in which breast cancer will appear later as well as the role of autoimmunity. This was a retrospective observational study. A total of 410 females (thyroid surgery and later breast cancer) and 524 females (thyroid surgery only) were compared with regard to pathological thyroid findings, thyroid hormones, thyroid autoimmunity and type of breast cancer. Thyroid autoimmunity, especially antithyroid peroxidase antibodies, significantly increased the risk of breast cancer (p

This study aimed to determine the prevalence of Thyroid-Stimulating Hormone (TSH) alterations and different types of thyroid dysfunctions in both sexes with no age limitations from variety of sources in Duhok province. In this retrospective cross-sectional study, we screened 25040 suspicious cases of thyroid diseases in a year (2019), retrieving the data from the computers of three clinical laboratories of Duhok City. Following exclusion of 470 cases, 24568 cases were included to categorize the different types of thyroid dysfunctions. The prevalence of TSH alteration was 25.03%, 20.55% of them had a high concentration being statistically higher in females, while only 4.48% was low TSH with equal prevalence among both sexes. Out of 24568 patients, the prevalence of subclinical hypothyroidism was 94.85%, followed by 2.20%, 1.20%, 0.78%, 0.67%, and 0.31% for each of subclinical hyperthyroidism, primary hypothyroidism, central hyperthyroidism, central hypothyroidism, and primary hyperthyroidism respectively. In conclusion, the studied population had high prevalence of high TSH level (20.55%), being more prevalent in female than in male. Our survey revealed that the distribution of thyroid disorders varied among different age groups with highest prevalence of subclinical hypothyroidism in all age groups (94.85%). We also concluded that middle and advanced ages, and females were more susceptible to thyroid disorders. [ABSTRACT FROM AUTHOR]

Myo-Inositol (MYO) is the most abundant stereoisomer of inositols’ family, cyclic polyols with 6 hydroxyl groups. Myo-Inositol has a relevant role in thyroid function and autoimmune diseases, as a precursor of phosphoinositides that takes part in the phosphatidylinositol (PI) signal transduction pathway. Among phosphoinositides, phosphatidylinositol 4,5- bisphosphate (PIP2) is the precursor of inositol triphosphates (IP3), second messenger of several hormones including thyroid-stimulating hormone (TSH). As a second messenger in the phospholipase C (PLC)-dependent inositol phosphate Ca2+/DAG pathway, Myo-Inositol is essential to produce H2O2 required for the synthesis of thyroid hormones. Consequently, depletion of Myo-Inositol or impaired inositol dependent TSH signaling pathway may predispose to the development of some thyroid diseases, such as hypothyroidism. Many clinical studies have shown that after treatment with Myo-Inositol plus Selenium (MYO+Se), TSH levels significantly decreased in patients with subclinical hypothyroidism with or without autoimmune thyroiditis. The TSH reduction was accompanied by a decline of antithyroid autoantibodies. Moreover, Myo-Inositol supplementation seemed to be involved also in the management of thyroidal benign nodules, with a possible effect in the size reduction. This review proposes a summary of the role of inositol, especially of Myo-Inositol, in the thyroidal physiology and its contribution on the management of some thyroid diseases.

Myo-Inositol (MYO) is the most abundant stereoisomer of inositols' family, cyclic polyols with 6 hydroxyl groups. Myo-Inositol has a relevant role in thyroid function and autoimmune diseases, as a precursor of phosphoinositides that takes part in the phosphatidylinositol (PI) signal transduction pathway. Among phosphoinositides, phosphatidylinositol 4,5- bisphosphate (PIP2) is the precursor of inositol triphosphates (IP3), second messenger of several hormones including thyroid-stimulating hormone (TSH). As a second messenger in the phospholipase C (PLC)-dependent inositol phosphate Ca2+/DAG pathway, Myo-Inositol is essential to produce H2O2 required for the synthesis of thyroid hormones. Consequently, depletion of Myo-Inositol or impaired inositol dependent TSH signaling pathway may predispose to the development of some thyroid diseases, such as hypothyroidism. Many clinical studies have shown that after treatment with Myo-Inositol plus Selenium (MYO+Se), TSH levels significantly decreased in patients with subclinical hypothyroidism with or without autoimmune thyroiditis. The TSH reduction was accompanied by a decline of antithyroid autoantibodies. Moreover, Myo-Inositol supplementation seemed to be involved also in the management of thyroidal benign nodules, with a possible effect in the size reduction. This review proposes a summary of the role of inositol, especially of Myo-Inositol, in the thyroidal physiology and its contribution on the management of some thyroid diseases. [ABSTRACT FROM AUTHOR]

Abstract Background Immune checkpoint inhibitors including nivolumab, an anti-programmed cell death protein 1 antibody, are recently developed cancer immunotherapy agents. Immune checkpoint inhibitors are known to cause autoimmune-related side effects including endocrine dysfunctions. However, there are few reports on late-onset isolated adrenocorticotropic hormone (ACTH) deficiency caused by nivolumab. Case presentation The patient was a 72-year-old female. When she was 64 years old, she was diagnosed with malignant melanoma of the left thigh accompanied by left inguinal lymph node metastases, and she received several courses of chemotherapy for malignant melanoma followed by the resection of these lesions. At 71 years of age, multiple metastases were found and treatment with nivolumab 2 mg/kg every 3 weeks was initiated. Six months later, replacement with levothyroxine was started because of hypothyroidism following mild transient thyrotoxicosis. Eleven months after the beginning of nivolumab, the treatment was discontinued because of tumor expansion. Four months after the discontinuation of nivolumab, general malaise and appetite loss worsened, and 2 months later, hyponatremia (Na; 120–127 mEq/L) and hypoglycemia (fasting plasma glucose; 62 mg/dL) appeared. Her ACTH and cortisol levels were extremely low (ACTH; 9.6 pg/mL, cortisol; undetectable). Challenge tests for anterior pituitary hormones showed that responses of ACTH and cortisol secretion to corticotropin-releasing hormone were disappeared, although responses of other anterior pituitary hormones were preserved. Thus, she was diagnosed with isolated ACTH deficiency. Her symptoms were improved after treatment with hydrocortisone. Conclusions The present report showed a case of late-onset isolated ACTH deficiency accompanied by hyponatremia, which was diagnosed 6 months after the discontinuation of nivolumab. The effects of nivolumab last for a long time and the side effects of nivolumab can also appear several months after discontinuation of the drug. Repeated monitoring of serum sodium levels may be a beneficial strategy to find the unexpected development of adrenal insufficiency even after discontinuation of nivolumab.

Background: Type 2 diabetes mellitus is known to be associated with other endocrine dysfunctions and thyroid is one of them. In the current study we tried to evaluate the frequency of thyroid dysfunctions in patients with type 2 diabetes mellitus and compare them with a normal control population. Methods: This cross-sectional study was carried out in the Department of Physiology and Department of General Medicine, Kakatiya Medical College, and MGM Hospital, Warangal, India. A total of 50 consecutive patients with diabetes mellitus type 2 were selected as cases, and an equal number of age- and sex-matched individuals with normoglycemia as controls. Laboratory investigations included measurements of fasting blood sugar [FBS] and HbA1c values after overnight fasting for eight hours, serum triglycerides, along with serum TSH, FT3, and FT4, which were measured by chemiluminescence immunoassay. Results: Among all cases of type 2 diabetes mellitus, eight (16%) presented thyroid disorders, with 10% in male patients and 6% in female patients. The overall frequency of thyroid disorders was found in four (8%) cases, of which two (4%) in males and two in females. The values of TSH µIU/ml and FBS mg/dl in type 2 diabetes mellitus cases were plotted and a Pearson correlation coefficient of +0.70 was calculated, indicating a positive correlation between the TSH and FBS. Along with TSH levels, the values of HbA1c were plotted in patients with type 2 diabetes mellitus and a Pearson correlation coefficient of +0.76 was calculated. Conclusion: Within the limitations of the present study, it can be concluded that the prevalence of thyroid dysfunctions is more common in patients with type 2 diabetes mellitus. Also, a continuous positive correlation of TSH with FBS and HbA1c was found. Hence, a periodic screening for their coexistence in thyroid dysfunctions among diabetic patients is advisable. [ABSTRACT FROM AUTHOR]

Las enfermedades tiroideas son un importante problema de salud que afecta a un gran porcentaje de la población. Las pruebas bioquímicas constituyen el pilar fundamental para su diagnóstico y seguimiento. El desarrollo de ensayos de segunda y tercera generación ha supuesto un gran avance en el diagnóstico de estas enfermedades. El texto incluye los ensayos utilizados para diagnosticar y tratar las diferentes enfermedades tiroideas, provee información bioquímica y clínica actualizada contenida en secciones referidas a la utilidad clínica de las determinaciones de hormonas tiroideas totales y libres, anticuerpos antitiroideos, tirotropina humana y tiroglobulina, de manera que pueda ofrecer, tanto al laboratorio como al médico, un panorama general de la utilidad y la capacidad actual de estas pruebas.Thyroid diseases are a significant health problem affecting a high percentage of the population. The biochemical tests are the fundamental pillar for diagnosis and follow-up. The development of second and third-generation assays has represented a great advance in diagnosing these diseases. The text covers the tests to diagnose and treat a number of thyroid diseases, and provides the reader with updated biochemical and clinical information in sections about the clinical usefulness of total and free thyroid hormone determinations, antithyroid antibodies, human thyrotropin and thyroglobulin. In this way, it can offer both the lab and the physician a general overview of the usefulness and the current capability of these tests.

Abstract: The objective of this study was to verify the osteogenic potential of the bone marrow mesenchymal stem cells (MSCs) of ovariectomized and non-ovariectomized female rats with hypo- and hyperthyroidism. Sixty two-month-old female rats were assigned to the following groups: (1) control (sham-operated), (2) ovariectomized (OVX’d), (3) hypothyroid sham-operated (Hypo-), (4) hypothyroid OVX’d, (5) hyperthyroid sham-operated (Hyper-) and (6) hyperthyroid OVX’d. After 135 days of treatment, the female rats were euthanized. We collected plasma to measure the levels of free T4, and the femur for extraction of MSCs. At 7 and 21 days of osteogenic differentiation of MSCs, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) conversion, alkaline phosphatase activity, mineralized nodule number and gene expression for collagen I, osteocalcin, bone sialoprotein and osteopontin were analyzed. The hypothyroid group presented a significant reduction in the osteogenic differentiation of MSCs. The hyperthyroid group did not present changes in the synthesis of mineralized nodules for MSCs at day 21 of differentiation. However, in ovariectomized rats, hyperthyroidism increased the osteogenic differentiation of MSCs characterized by the increase of the alkaline phosphatase activity, the number of mineralized nodules and the expression of osteocalcin, sialoprotein and osteopontin. Our results demonstrated that the hypothyroidism reduces the osteogenic differentiation of MSCs only in non-ovariectomized rats and that the hyperthyroidism increases the osteogenic differentiation of MSCs only in ovariectomized rats. [Copyright &y& Elsevier]

Objective: The aim of this study was to determine the incidence of Post Partum Thyroiditis (PPT) at first month postpartum. Methodology: Fifty pregnant subjects were included. Control group was composed of 50 women who did not give birth in the recent year. Blood samples were obtained once in the control group and twice -at the third trimester and the first month postpartum-in the pregnant group. Results: PPT occurred at first month postpartum in 3 of 50 pregnant women. The incidence of PPT at first month postpartum was 6%. Among the pregnant group, there was a statistically significant increase in the Anti-TPO and Anti-Tg levels within the first month postpartum compared to the ones in the third trimester. Also, all patients who experienced PPT were positive for Anti-TPO and Anti-Tg. Conclusions: In our opinion, it will be useful to evaluate particularly the pregnants with positive thyroid auto-antibodies in early postpartum period. [ABSTRACT FROM AUTHOR]

Osteoblasts produce both osteoprotegerin (OPG) and Receptor Activator for Nuclear Factor B Ligand (RANKL), members of the tumor necrosis factor (TNF) super family that compete for the same receptor - RANK - expressed at the surface of osteoclasts, to play important roles in bone remodeling by controlling differentiation, activation and apoptosis of osteoclasts. Osteoprotegerin is secreted at different other sites such as endothelial and vascular smooth muscle cells, pulmonary or renal tissue, or the immune system. Hormones, cytokines and transcription factors, with osteotropic hormones playing a key role, control OPG synthesis. Thyroid hormones regulate bone turnover, as evidenced by important changes in bone turnover found in patients with thyroid dysfunction. In thyroid hormones excess, the increase in serum OPG is, probably, due to enhanced bone turnover, to compensate for excessive bone resorption. In hypothyroidism, the mechanisms are less clear, either cardiovascular changes or the low OPG kidney clearance or the increased TSH level being involved. In addition, OPG is held responsible for the development of endothelial dysfunction, an early stage of atherosclerosis progression, thyroid dysfunction being associated to increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

Thyroid hormones are essential for normal skeletal development and normal bone metabolism in adults but can have detrimental effects on bone structures in states of thyroid dysfunction. Untreated severe hyperthyroidism influences the degree of bone mass and increases the probability of high bone turnover osteoporosis. Subclinical hyperthyroidism, defined as low thyrotropin (TSH) and free hormones within the reference range, is a subtler disease, often asymptomatic, and the diagnosis is incidentally made during screening exams. However, more recent data suggest that this clinical condition may affect bone metabolism resulting in decreased bone mineral density (BMD) and increased risk of fracture, particularly in postmenopausal women. The main causes of exogenous subclinical hyperthyroidism are inappropriate replacement dose of thyroxin and TSH suppressive L-thyroxine doses in the therapy of benign thyroid nodules and thyroid carcinoma. Available data similarly suggest that a long-term TSH suppressive dose of thyroxin may decrease BMD and may induce an increased risk of fracture. These effects are particularly observed in postmenopausal women but are less evident in premenopausal women. Overt hypothyroidism is known to lower bone turnover by reducing both osteoclastic bone resorption and osteoblastic activity. These changes in bone metabolism would result in an increase in bone mineralization. At the moment, there are no clear data that demonstrate any relationship between BMD in adults and hypothyroidism. Despite these clinical evidences, the cellular and molecular actions of thyroid hormones on bone structures are not complete clear. [ABSTRACT FROM AUTHOR]

Background: Immune checkpoint inhibitors including nivolumab, an anti-programmed cell death protein 1 antibody, are recently developed cancer immunotherapy agents. Immune checkpoint inhibitors are known to cause autoimmune-related side effects including endocrine dysfunctions. However, there are few reports on late-onset isolated adrenocorticotropic hormone (ACTH) deficiency caused by nivolumab. Case presentation: The patient was a 72-year-old female. When she was 64 years old, she was diagnosed with malignant melanoma of the left thigh accompanied by left inguinal lymph node metastases, and she received several courses of chemotherapy for malignant melanoma followed by the resection of these lesions. At 71 years of age, multiple metastases were found and treatment with nivolumab 2 mg/kg every 3 weeks was initiated. Six months later, replacement with levothyroxine was started because of hypothyroidism following mild transient thyrotoxicosis. Eleven months after the beginning of nivolumab, the treatment was discontinued because of tumor expansion. Four months after the discontinuation of nivolumab, general malaise and appetite loss worsened, and 2 months later, hyponatremia (Na; 120–127 mEq/L) and hypoglycemia (fasting plasma glucose; 62 mg/dL) appeared. Her ACTH and cortisol levels were extremely low (ACTH; 9.6 pg/mL, cortisol; undetectable). Challenge tests for anterior pituitary hormones showed that responses of ACTH and cortisol secretion to corticotropin-releasing hormone were disappeared, although responses of other anterior pituitary hormones were preserved. Thus, she was diagnosed with isolated ACTH deficiency. Her symptoms were improved after treatment with hydrocortisone. Conclusions: The present report showed a case of late-onset isolated ACTH deficiency accompanied by hyponatremia, which was diagnosed 6 months after the discontinuation of nivolumab. The effects of nivolumab last for a long time and the side effects of nivolumab can also appear several months after discontinuation of the drug. Repeated monitoring of serum sodium levels may be a beneficial strategy to find the unexpected development of adrenal insufficiency even after discontinuation of nivolumab. [ABSTRACT FROM AUTHOR]

Background: Tendinopathies negatively affect life quality of affected individuals. A clear pathomechanism has not been established yet, however, metabolic disorders such as diabetes mellitus have long been reported to influence the occurrence of calcific tendinopathy, particularly of the shoulder joint. Recent studies highlight an association between thyroid hormones and tendon conditions, as thyroid hormone receptors (TR) have been reported in human tendons. It is believed that TR may have a role in tenocyte proliferation and apoptosis. Materials and Methods: 300 patients attending outpatient rheumatologic evaluations for an 11 month period, ages between 40 and 78 years old were consecutively screened for radiographic evidence of calcific tendinopathy in pelvis, ankle, knee, spine and shoulder regions. Each subject was investigated for the following metabolic conditions: hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia, and thyroid disorders. Results: Plain radiography was used for screening of calcific tendinopathy. Patients were classified as suffering from degenerative disease of the spine, hip or knee (63%), diffuse idiopathic skeletal hyperostosis-DISH (10%) and shoulder impingement syndrome (27%). Female patients were predominant gender in the study group. Thyroid disorders as well as diabetes mellitus were positively associated with shoulder impingement syndrome, and as expected, DISH was positively associated with diabetes mellitus. Conclusions: Plain radiography provides good imaging of calcific tendinopathy. Within a general rheumatic population, metabolic disorders represented by thyroid disease and diabetes mellitus have the highest risk for calcific tendinopathy development. [ABSTRACT FROM AUTHOR]

The Hippocratic tradition emphasized environmental causes of diseases and the need for harmony between the individual and the natural environment as the right philosophy to maintain a good health status. Public awareness and scientific attention concerning environmental pollution is usually focused on the consequent increased risk of developing cancer. Air pollution has been recognized by the World Health Organization (WHO) to cause cardiovascular and respiratroy diseases, as well as lung cancer, after acute/chronic exposure to fine particulates (PM2.5 and PM10) even at concentrations which are 50% lower than those accepted as legal limits in many developed countries. An increase of 10 µg/m³ of PM2.5 produces a +4%-6% of overall mortality, a +10% of cardiovascular disease prevalence (arithmyas, acute myocardial infarctions, and heart failure) and a +22% of lung cancer prevalence. In addition to these chronic effects, acute hospitalizations are also affected, especially among susceptible populations such as children and diabetic patients. Water and soil contamination also have an additional detrimental effect on people's health. Other issues concerning environment contamination and human health include male/female fertility, metabolic and thyroid conditions, but also professional exposures resulting in occupational diseases. Moreover, in the perspective of "gender medicine", different acute or chronic effects of environmental pollution should be specifically assessed both in men and in women. This special issue on "Environmental Diseases" is aimed at providing a global overview about different threats to human health possibily originating from environmental contamination.

Introduction: Recently, tyrosine kinase inhibitors (TKIs) have emerged as a new class of anticancer therapy. Although generally considered less toxic than cytotoxic chemotherapy, TKIs do cause significant side effects including fatigue and hypertension. In addition, thyroid dysfunction is a well-known adverse effect of TKI., Areas Covered: This review provides a comprehensive assessment of TKI-induced thyroid dysfunctions by sunitinib, sorafenib, pazopanib, imatinib, dasatinib, nilotinib, vandetanib, axitinib, motesanib and tivozanib. Furthermore, the potential mechanisms that result in this toxicity, the clinical impact of thyroid dysfunction in these patients and the controversies regarding treatment with thyroid hormone (TH) therapy are evaluated., Expert Opinion: Detection of TKI-induced thyroid dysfunction requires routine monitoring of thyroid function and may necessitate treatment. Potential benefits in developing thyroid dysfunction and potential harm in treating it necessitate controlled studies. Finally, if treatment is pursued, appropriate dosing and timing of TH replacement will require prospective clinical evaluation.