Thyroid Hormone Secretion Research Articles

The role of laboratory medicine in the diagnosis of the hyperthyroidism.

Hyperthyroidism is a clinical condition characterized by inappropriately high synthesis and secretion of thyroid hormones by the thyroid gland. It has multiple aetiologies, manifestations and potential therapies. Graves' disease is the most common form of hyperthyroidism, due to the production of autoantibodies against thyrotropin receptor, capable of over-stimulating thyroid function. A reliable diagnosis of hyperthyroidism can be established on clinical grounds, followed by the evaluation of serum thyroid function tests (thyrotropin first and then free thyroxine, adding the measurement of free triiodothyronine in selected specific situations). The recent guidelines of both the American and European Thyroid Associations have strongly recommended the measurement of thyrotropin receptor autoantibodies for the accurate diagnosis and management of Graves' disease. If autoantibody test is negative, a radioiodine uptake should be performed. Considering the most recent laboratory improvements, binding assays can be considered the best first solution for the measurement of thyrotropin receptor autoantibodies in diagnosis and management of overt cases of Graves' disease. In fact, they have a satisfactory clinical sensitivity and specificity (97.4% and 99.2%, respectively) being performed in clinical laboratories on automated platforms together with the other thyroid function tests. In this setting, the bioassays should be reserved for fine and complex diagnoses and for particular clinical conditions where it is essential to document the transition from stimulating to blocking activity or vice versa (e.g. pregnancy and post-partum, related thyroid eye disease, Hashimoto's thyroiditis with extrathyroidal manifestations, unusual cases after LT4 therapy for hypothyroidism or after antithyroid drug treatment for Graves' disease). Undoubtedly, technological advances will help improve laboratory diagnostics of hyperthyroidism. Nevertheless, despite future progress, the dialogue between clinicians and laboratory will continue to be crucial for an adequate knowledge and interpretation of the laboratory tests and, therefore, for an accurate diagnosis and correct management of the patient.

The Spread of Thyroid Diseases and the Algorithm for Diagnosing Thyroid Dysfunction

Diseases of the thyroid gland are considered one of the most common endocrinopathies. This is due to the influence of ecologically unfavorable environmental factors, bad habits, malnutrition, comorbid conditions and genetic predisposition. Determining an algorithm for diagnosing thyroid dysfunction for the timely detection of diseases is expedient and relevant. The objective: to analyze the state of the spread of thyroid diseases among the population of the Kiev region and to determine the diagnostic algorithm based on the identification of the main clinical syndromes of thyroid dysfunction. Materials and methods. Among the adult population of the Kiev region, a high level of morbidity and spread of thyroid diseases is recorded. The increase in the number of cases occurred, first of all, due to the newly diagnosed patients with hypothyroidism, thyroiditis. The manifestation of most diseases is associated with the development of thyroid dysfunction. Under the hypothyroidism one can observe and diagnose the following: a syndrome of neuropsychiatric disorders with slowing down of motor activity, decrease in cognitive functions; syndrome of vegetative-trophic disorders with cutaneous mucinosis, polyneuropathy; syndrome of cardiovascular changes with decreased myocardial contractility, slow blood flow, progressive development of atherosclerosis; anemic syndrome; digestive tract syndrome with impaired motor and secretory functions of the gastrointestinal tract; syndrome of hormonal disorders with decreased secretion of thyroid hormones, especially T4, increased levels of TSH (in primary hypothyroidism) or decreased TSH (in secondary and tertiary). Results. Thyrotoxicosis in patients is determined by an enlarged thyroid gland with the development of: thyrotoxic cardiomyopathy and systolic arterial hypertension; thyrotoxic encephalopathy, syndrome of neuropsychiatric disorders with a predominance of excitation processes, vascular dysfunction; thyrotoxic ophthalmopathy, ectodermal disorders syndrome along with a decrease in TSH production and an increase in the level of free fractions T4, T3. Conclusions. The algorithm for diagnosing hypofunction and hyperfunction of the thyroid gland provides for: clarification of complaints and anamnesis data, examination of the patient, additional laboratory and instrumental examination, which includes the study of the thyroid status, possible autoaggression, analysis of metabolic processes, assessment of pathomorphological changes in the thyroid gland.

Вплив штучно подовженого світлового дня на концентрацію деяких гормонів, показники мінерального обміну та імунітету у студентів

In this work, we studied the influence of artificially prolonged daylight on the concentration of some hormones, the state of mineral metabolism, and immunity in students. Material and methods. The study involved 50 second-year students (44 girls and 6 boys) of Kharkiv National Medical University with different chronotypes. All students were on a proper diet, did not play sports, did not have any chronic diseases, and were healthy during the study period. Students were divided into 2 groups: 1) waking period from 5:00 to 23:00 (25 people), 2) waking period from 8:00 to 3:00 (25 people). Saliva was collected after careful oral hygiene at 8 a.m., 12 a.m., 4 p.m., and 12 p.m. Results and discussion. Our study showed that the artificial prolongation of daylight reduces the concentration of melatonin, especially at night (at the peak of secretion). It is established that at the artificial prolongation of the light day there is an inversion of a rhythm of thyroid's hormones secretion, decrease in their maximum concentration which probably is connected with the adaptation of an organism to an active mental activity at night. The obtained results showed that in students with the evening chronotype, the concentration of cortisol reduced both during the day and at 24 hours, which was probably associated with a decrease in melatonin secretion and its regulatory effect on the adrenal glands. Decreased concentrations of melatonin, cortisol, and thyroid hormones led to the impaired functional activity of the immune system, as evidenced by a decrease in secretory immunoglobulin and lysozyme in the saliva of students with evening chronotype, compared with students with morning chronotype of activity. Changing circadian rhythms of thyroid hormone secretion, reducing their concentration and cortisol content led to the development of metabolic disorders. We noted that dysfunction of mineral metabolism in students with evening chronotype caused a decrease in the concentration of calcium, magnesium, zinc in the saliva of students. The identified characteristics indicate that prolonged daylight reduced the ability to maintain the daily balance of the studied nutrients, which may be a manifestation of desynchrony. The concentration of immunoglobulin A in the saliva of students in the second group in the morning and the evening was significantly lower than in students of group 1, which indicated an absolute deficiency of immunoglobulin and, accordingly, a decrease in immunity with prolonged daylight. Students of group 2 also had a decrease in the content of lysozyme in saliva, which indicated a decrease in the degree of antibacterial protection. The peculiarities in the content of immunoglobulin A and lysozyme are most likely associated with a decrease in the concentration of melatonin. Conclusion. The artificial prolongation of daylight decreased the melatonin concentration in saliva and cortisol concentration. It also caused an inversion of secretion rhythm of thyroid hormones. The students with evening chronotype had a decrease in immunoglobulin A concentration, decrease in lysozyme in saliva and disturbance in a mineral metabolism

Щитовидная железа у женщин в пери- и постменопаузе: физиология и заболевания

The incidence of most thyroid diseases – hypothyroidism, nodular goiter, and cancer – is highest among peri- and postmenopausal women. Diagnosis of thyroid dysfunction in this group of patients is difficult, since the symptoms may be nonspecific, with complaints typical for the climacteric period. Interpreting thyroid function tests, physiological changes in the secretion and metabolism of thyrotropin and thyroid hormones, as well as the effect of concomitant diseases, must be considered. Unrecognized thyroid dysfunction leads to an increased risk of cardiovascular disease, bone fractures, cognitive impairment, depression, and mortality. Thyroid dysfunction therapy differs in peri- and postmenopausal women of reproductive age; hypothyroidism should be treated with caution because high doses of L-thyroxine can lead to cardiac arrhythmias and an increased risk of bone osteoporosis, and hyperthyroidism should preferably be treated with radioactive iodine. Thyroid cancer often affects women over the age of 50, the diagnostic and therapeutic approach is the same as in the general population, but the prognosis of cancer is worse than in younger patients. The article presents data concerning the differential diagnosis of menopausal symptoms and thyroid gland pathology in perimenopausal women, as well as the peculiarities of therapy for revealed thyroid disorders in this age group.

STUDY OF SERUM GHRELIN IN THYROID PATIENTS

Background: Hypothyroidism is a common endocrine disorder resulting from deciency of thyroid hormone. Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormone by the thyroid gland. Ghrelin is octanoylated peptide containing a 28 amino acid act as an energy balance regulator & play an important role in metabolic process .The aim of the study was to establish possible relationship between them. Materials and methods: The present study is a cross sectional study, was conducted in the Department of Biochemistry, J.L.N. Medical college and associated group of Hospitals, Ajmer (Raj.). 65 hypothyroid subjects (group-II) and 65 hyperthyroid subjects (group-III) attending Medical OPD of J.L.N. Hospitals were included and 130 age-sex matched euthyroid controls (group-I) were selected. Results: In hypothyroid subjects, mean serum Ghrelin levels were found to be signicantly higher in comparison to healthy subjects (p<0.0001). In hyperthyroid subjects, mean serum Ghrelin levels were found to be signicantly lower in comparison to healthy subjects (p<0.0001). Conclusion: The overall ndings of the present study thus conrm that serum Ghrelin level is signicantly higher in Hypothyroid subjects and the level is signicantly lower in the Hyperthyroid subjects, thus we have found positive association between serum TSH level and Ghrelin level. However, further experimental and observational studies are needed to illustrate the role of Ghrelin in Hypothyroidism and Hyperthyroidism.

Correlation of Dietary Zinc Intake and Serum Zinc with Thyroid Stimulating Hormone (TSH) and Free Thyroxine (FT4) Levels in Adult Hyperthyroid Patients

Background: Hyperthyroidism is a thyroid disorder caused by increased synthesis and secretion of thyroid hormone by the thyroid gland. Hyperthyroidism is characterized by low thyroid stimulating hormone (TSH) and high free thyroxine (FT4) levels. The prevalence of hyperthyroidism in Indonesia was 0.6% in female and 0.2% in male. Zinc acts as an enzyme cofactor that converts thyroxine into triiodothyronine and it affects TSH synthesis. Adequacy of dietary zinc intake and serum zinc levels in hyperthyroid patients indirectly affects TSH and FT4 hormones.Objective: to analyze the correlation of dietary zinc intake and serum zinc with TSH and FT4 levels in adult hyperthyroid patients.Materials and Methods: This cross sectional study sampling based on inclusion and exclusion criteria which obtained 50 adult hyperthyroid patients at the Clinic of the Magelang Health Research and Development Center. Data of TSH and FT4 levels were measured by the ELISA method, serum zinc was measured with the ICP-MS method, dietary zinc intake’s data was collected using the 24 hour dietary recall and it was analyzed based on the table of Indonesian food composition 2017. Statistical analysis used in this study were spearman correlation and multivariate linear regression with 95% confidence level.Results : Dietary zinc intake did not correlate with both TSH and FT4 levels (p>0.05). Serum zinc had no correlation with TSH level (p>0.05), while serum zinc had a positive correlation with FT4 level (r=0.327; β=0.054; p<0.05).Conclusion: Serum zinc concentrations in adult hyperthyroid patients must be maintained because abnormal zinc status in the body’s metabolism will affect FT4 level.International Journal of Human and Health Sciences Vol. 05 No. 03 July’21 Page: 341-346

Stress hormones mediate developmental plasticity in vertebrates with complex life cycles

The environment experienced by developing organisms can shape the timing and character of developmental processes, generating different phenotypes from the same genotype, each with different probabilities of survival and performance as adults. Chordates have two basic modes of development, indirect and direct. Species with indirect development, which includes most fishes and amphibians, have a complex life cycle with a free-swimming larva that is typically a growth stage, followed by a metamorphosis into the adult form. Species with direct development, which is an evolutionarily derived developmental mode, develop directly from embryo to the juvenile without an intervening larval stage. Among the best studied species with complex life cycles are the amphibians, especially the anurans (frogs and toads). Amphibian tadpoles are exposed to diverse biotic and abiotic factors in their developmental habitat. They have extensive capacity for developmental plasticity, which can lead to the expression of different, adaptive morphologies as tadpoles (polyphenism), variation in the timing of and size at metamorphosis, and carry-over effects on the phenotype of the juvenile/adult. The neuroendocrine stress axis plays a pivotal role in mediating environmental effects on amphibian development. Before initiating metamorphosis, if tadpoles are exposed to predators they upregulate production of the stress hormone corticosterone (CORT), which acts directly on the tail to cause it to grow, thereby increasing escape performance. When tadpoles reach a minimum body size to initiate metamorphosis they can vary the timing of transformation in relation to growth opportunity or mortality risk in the larval habitat. They do this by modulating the production of thyroid hormone (TH), the primary inducer of metamorphosis, and CORT, which synergizes with TH to promote tissue transformation. Hypophysiotropic neurons that release the stress neurohormone corticotropin-releasing factor (CRF) are activated in response to environmental stress (e.g., pond drying, food restriction, etc.), and CRF accelerates metamorphosis by directly inducing secretion of pituitary thyrotropin and corticotropin, thereby increasing secretion of TH and CORT. Although activation of the neuroendocrine stress axis promotes immediate survival in a deteriorating larval habitat, costs may be incurred such as reduced tadpole growth and size at metamorphosis. Small size at transformation can impair performance of the adult, reducing probability of survival in the terrestrial habitat, or fecundity. Furthermore, elevations in CORT in the tadpole caused by environmental stressors cause long term, stable changes in neuroendocrine function, behavior and physiology of the adult, which can affect fitness. Comparative studies show that the roles of stress hormones in developmental plasticity are conserved across vertebrate taxa including humans.

Current approach to surgical management of hyperthyroidism.

Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland, which leads to thyrotoxicosis. The most common forms of hyperthyroidism include diffuse toxic goiter (Graves' disease), toxic multinodular goiter (Plummer disease), and a solitary toxic adenoma. The most reliable screening measure of thyroid function is the thyroid-stimulating hormone (TSH) level. Options for treatment of hyperthyroidism include: antithyroid drugs, radioactive iodine therapy (the preferred treatment of hyperthyroidism among US thyroid specialists), or thyroidectomy. Massive thyroid enlargement with compressive symptoms, a suspicious nodule, Graves' orbitopathy, and patient preference are indications for surgical treatment of thyrotoxicosis. This paper reviews the current literature and controversies on the surgical approach to the management of hyperthyroidism.

Normal thyroid volume in subjects evaluated in a primary ambulatory setting in Liguria.

Ultrasonography (US) is the simplest method of evaluating thyroid volume (TV). The current normal TV in Liguria is not known. The aim of this study was to obtain normative data on TV in Liguria. From 3552 files of endocrine evaluations registered in a primary outpatient setting, we selected 483 files on euthyroid subjects (383 females and 100 males) with a normal echoic pattern on US. The inclusion criterion was the absence of thyroperoxidase autoantibodies and drugs known to interfere with thyroid hormone secretion or metabolism. TV was calculated by means of US. Anthropometric characteristics, smoking habits and the district where subjects lived were registered. Less than 50% of patients were not taking any drug. The percentage of obesity was similar in both sexes. TSH levels were similar in males and females. Median TV was 8.0 ml (IQR 6.7 - 9.8 ml) in females and 11.8 ml (9.3 - 15.6 ml) in males (P<0.0001). In females, TV was greater (P=0.01) in smokers than in non-smokers. In both sexes, the right lobe was significantly (P<0.0001) larger in volume than the left. Post-hoc analysis did not show any differences among age-groups in either females or males. In females, but not in males, TV differed significantly (P=0.0002) according to the district of residence. A significant positive correlation was found in both groups between TV and weight, height, BMI and BSA. Reference values of TV in the Ligurian population are now available. TV in the general population could be compared with these normative data.

MicroRNA Dysregulation in the Hippocampus of Rats with Noise-Induced Hearing Loss.

Although hippocampal changes due to noise-induced hearing loss have been suggested, little is known about the miRNA levels due to these hippocampal changes. Three-week-old Sprague-Dawley rats were divided into noise and control groups (n = 20 per group). The noise group rats were exposed to white Gaussian noise (115 dB SPL, 4 hours per day) for three days. One day after noise exposure, the hippocampi of rats were harvested and miRNA expressions were analyzed using the Affymetrix miRNA 4.0 microarray (n = 6 per group). The predicted target genes of each miRNA were retrieved, and the pathways related to the predicted target genes were analyzed. miR-758-5p, miR-210-5p, miR-370-5p, miR-652-5p, miR-3544, miR-128-1-5p, miR-665, miR-188-5p, and miR-874-5p expression increased in the hippocampal tissue of the noise group compared to that in the control group. The overlapping predicted target genes included Bend4, Creb1, Adcy6, Creb5, Kcnj9, and Pten. The pathways related to these genes were the estrogen signaling pathway, vasopressin-regulated water reabsorption, thyroid hormone synthesis, aldosterone synthesis and secretion, insulin secretion, circadian entrainment, insulin resistance, cholinergic synapse, dopaminergic synapse, cGMP-PKG signaling pathway, cAMP signaling pathway, PI3K-Akt signaling pathway, TNF signaling pathway, and AMPK signaling pathway. miR-448-3p, miR204-5p, and miR-204-3p expression decreased in the hippocampal tissue of the noise group compared to that in the control group. The overlapping predicted target genes of these three miRNAs were Rps6kas, Nfactc3, Rictor, Spred1, Cdh4, Cdh6, Dvl3, and Rcyt1b. Pathway analysis suggested that the Wnt signaling pathway is related to Dvl3 and Nfactc3. Noise-induced hearing loss dysregulates miR-758-5p, miR210-5p, miR370-5p, miR-652-5p, miR-3544, miR-128-1-5p, miR-665, miR-188-5p, miR-874-5p, miR-448-3p, miR-204-5p, miR-204-3p, and miR-140-5p expression in the hippocampus. These miRNAs have been predicted to be associated with hormonal, inflammatory, and synaptic pathways.

Thyroid hormone mediates cardioprotection against postinfarction remodeling and dysfunction through the IGF-1/PI3K/AKT signaling pathway

AimsSevere cardiovascular diseases, such as myocardial infarction or heart failure, can alter thyroid hormone (TH) secretion and peripheral conversion, leading to low triiodothyronine (T3) syndrome. Accumulating evidence suggests that TH has protective properties against cardiovascular diseases and that treatment with TH can effectively reduce myocardial damage after myocardial infarction (MI). Our aim is to investigate the effect of T3 pretreatment on cardiac function and pathological changes in mice subjected to MI and the underlying mechanisms. Main methodsAdult male C57BL/6 mice underwent surgical ligation of the left anterior descending coronary artery (LAD) (or sham operation) to establish MI model. T3, BMS-754807 (inhibitor of insulin-like growth factor-1 receptor (IGF-1R)) or vehicle was administered before surgery. Key findingsCompared with the MI group, the T3 pretreatment group exhibited significant attenuation of the myocardial infarct area, inhibition of cardiomyocyte apoptosis and fibrosis, and improved left ventricular function after MI. In addition, T3 exhibited an enhanced potency to stimulate angiogenesis and exert anti-inflammatory effects by reducing the levels of serum inflammatory cytokines after MI. However, all of these protective effects were inhibited by the IGF-1R inhibitor BMS-754807. Moreover, the protein expression of IGF-1/PI3K/AKT signaling-related proteins, such as IGF-1, IGF-1R, phosphorylated PI3K (p-PI3K) and p-AKT was significantly upregulated in MI mice that received T3 pretreatment, and BMS-754807 pretreatment blocked the upregulation of the expression of these signaling-related proteins. SignificanceT3 pretreatment can protect the heart against dysfunction post-MI, which may be mediated by the activation of the IGF-1/PI3K/AKT signaling pathway.

The Association of Obesity with Autoimmune Thyroiditis and Thyroid Function-Possible Mechanisms of Bilateral Interaction.

A growing number of patients suffer from autoimmune diseases, including autoimmune thyroid disease. There has simultaneously been a significant increase in the prevalence of obesity worldwide. It is still an open question whether adiposity can directly influence activation of inflammatory processes affecting the thyroid in genetically predisposed individuals. Adipokines, biologically active substances derived from the adipocytes, belong to a heterogenic group of compounds involved in numerous physiological functions, including the maintenance of metabolism, hormonal balance, and immune response. Notably, the presence of obesity worsens the course of selected autoimmune diseases and impairs response to treatment. Moreover, the excess of body fat may result in the progression of autoimmune diseases. Nutritional status, body weight, and energy expenditure may influence thyroid hormone secretion. Interestingly, thyroid hormones might influence the activity of adipose tissue as metabolic alterations related to fat tissue are observed under pathological conditions in which there are deficits or overproduction of thyroid hormones. Functioning TSH receptors are expressed on adipocytes. Thermogenesis may presumably be stimulated by TSH binding to its receptor on brown adipocytes. There could be a bilateral interaction between the thyroid and adipose. Obesity may influence the onset and course of autoimmune disease.

Clinical Profiles of Thyroid Dermopathy: A Dermato-Endocrinological Perspective

Abstract Thyroid disorders sometimes have extra-thyroidal manifestations. Hyperthyroidism is a clinical syndrome resulting from excessive secretion of thyroid hormones. The most common cause is Graves’ disease. About 0.5–4.3% of patients with Graves’ disease have an infiltrative dermopathy called thyroid dermopathy, which is due to excessive deposition of glycosaminoglycans from activated fibroblasts. Skin fibroblasts are activated by thyroid stimulating hormone receptor antibodies the whole process being initiated by T lymphocytes. Rarely, thyroid dermopathy is also found in other thyroid disorders such as Hashimoto thyroiditis. The diffuse non-pitting edema variant is the most common clinical presentation. Other variants include the nodular, plaque, mixed, and elephantiasis types. Usually, the main concerns of the patients are cosmetic, discomfort, and difficulty in wearing shoes. Thyroid dermopathy usually presents after the diagnosis of Graves’ disease, but it may also present together or sometime after this condition. Rarely, thyroid dermopathy presents before the diagnosis of Graves’ disease is made. Apart from the shin and feet, other sites that can be affected include the arms, forearms, back, thighs, pinna, and nose. The management is multidisciplinary, involving dermatologists and endocrinologists. Usually, controlling the thyroid dysfunction does not translate into regression of the skin lesions. However, many patients have their thyroid dermopathy regress spontaneously, while others usually require local therapy. Other therapeutic options include systemic therapy such as pentoxifylline, compressive physiotherapy, and surgery.

Review of European Thyroid Association Guideline (2018) for the Manage-ment of Graves’ Hyperthyroidism

Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T-cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.

Prevalence of Suspected Cases of Hyperthyroidism in Jeddah by Using Wayne's Scoring Index.

IntroductionHyperthyroidism is one of the primary dysfunctional thyroid diseases that results from abnormally high thyroid hormone secretion. It leads to metabolic derangement that manifests as heightened vital functions and metabolism and hyperdynamic blood circulation. Hyperthyroidism jeopardizes one’s quality of life and hampers the patient’s job performance. The disease is chronic but diagnosable and treatable and can be kept under control medically. We aimed to estimate the prevalence of suspected hyperthyroidism cases among a population sample in Jeddah city by using Wayne’s scoring and delineation of factors associated with the disease.Materials and methodsA cross-sectional study design was used. A total of 346 participants were conveniently selected from two shopping malls in Jeddah city during a five-day health awareness campaign. The data were collected by certified physicians, according to Wayne’s score inventory.ResultsThe study included 194 women (56.1%) and 152 men (43.9%). The participants’ ages ranged from 16 to 56 years. The Wayne’s scores showed 80.6% were euthyroid, 18.2% equivocal, and 1.2% have hyperthyroidism. Bronchial asthma was significantly associated with hyperthyroidism in men, while obesity was significantly associated with hyperthyroidism in women. Age, gender, level of education, and family history of chronic diseases, including thyroid disorders, were not significantly associated with hyperthyroidism.ConclusionsWayne’s scoring for hyperthyroidism, which is a noninvasive tool, in addition to its detection of hyperthyroidism cases, can predict patients with equivocal results or those that might be subclinical for further medical assessment and follow-up. A Wayne’s score can give the results of hyperthyroidism comparable to the results obtained by biochemical investigations. This tool is not in common use, but it is quite useful and should be put into broader usage.

Clinical profiles of thyroid dermopathy: a dermato-endocrinology minireview

Background: Thyroid disorders sometimes have extra-thyroidal manifestations. Hyperthyroidism is a clinical syndrome resulting from excessive secretion of thyroid hormones. The commonest cause is Graves’ disease. About 0.5 – 4.3% of patients with Graves’ disease have an infiltrative dermopathy called thyroid dermopathy. It is due to excessive deposition of glycosaminoglycans from activated fibroblasts. Skin fibroblasts are activated by thyroid stimulating hormone receptor antibodies and the whole process is initiated by T lymphocytes. Thyroid dermopathy is rarely also found in other thyroid disorders such as Hashimoto thyroiditis. The diffuse non-pitting oedema variant is the commonest clinical presentation. Other variants include the nodular, plaque, mixed and elephantiasis types. The main concerns of the patients usually are cosmetic, discomfort and difficulty in wearing shoes. Thyroid dermopathy usually presents after the diagnosis of Graves diseases but it may present together or sometime after. Rarely, thyroid dermopathy presents before the diagnosis of Graves’ disease is made. Apart from the shin and feet, other sites that can be affected include arms, forearms, back, thighs, pinna and nose. Conclusion: The management is multidisciplinary, involving Dermatologists and Endocrinologists. Usually, controlling the thyroid dysfunction does not translate into regression of the skin lesion. However, many patients have their thyroid dermopathy regressing spontaneously while others usually require local therapy. Other therapeutic options include systemic therapy such as pentoxifylline, compressive physiotherapy and surgery.

The role of hypothyroidism in weaning patients from mechanical ventilation: a clinical trail

Objective: Hypothyroidism is a relatively common disease around the world; and as a clinical condition due to the lack of secretion of thyroid hormone from the thyroid gland, due to some structural and/or functional disorders, thyroid hormone production is defined. The purpose of this study is to investigate the isolation of the problem of mechanical ventilation caused by hypothyroidism in hospitalized patients. Methods: In this clinical trial, 80 patients admitted to the ICU ward of Imam Reza Hospital and intubated for more than one week were studied. Patients were classified into two subgroups (each subgroup was 40). Levothyroxine was prescribed for the case group 0.1 mg of the first morning; while no Levothyroxine was prescribed to the patients in the control group. Differences between the two groups is evaluated in the time of weaning. Results: There was a significant difference between two groups regarding TSH, T3 and T4. There was also a significant difference between final outcome of the patients and time of weaning from the mechanical ventilation between the two groups; which can be attributed to the effect of the role of levothyroxine on the recovery of patients and the reduction of weaning from mechanical ventilation. Conclusion: The thyroid function of intubated patients should be monitored to be kept in normal levels to accelerate the recovery of these patients or in some cases prevent them from deterioration.

Leukotriene A4 hydrolase deficiency protects mice from diet-induced obesity by increasing energy expenditure through neuroendocrine axis.

Obesity is a health problem worldwide, and brown adipose tissue (BAT) is important for energy expenditure. Here, we explored the role of leukotriene A4 hydrolase (LTA4 H), a key enzyme in the synthesis of the lipid mediator leukotriene B4 (LTB4 ), in diet-induced obesity. LTA4 H-deficient (LTA4 H-KO) mice fed a high-fat diet (HFD) showed a lean phenotype, and bone-marrow transplantation studies revealed that LTA4 H-deficiency in non-hematopoietic cells was responsible for this lean phenotype. LTA4 H-KO mice exhibited greater energy expenditure, but similar food intake and fecal energy loss. LTA4 H-KO BAT showed higher expression of thermogenesis-related genes. In addition, the plasma thyroid-stimulating hormone and thyroid hormone concentrations, as well as HFD-induced catecholamine secretion, were higher in LTA4 H-KO mice. In contrast, LTB4 receptor (BLT1)-deficient mice did not show a lean phenotype, implying that the phenotype of LTA4 H-KO mice is independent of the LTB4 /BLT1 axis. These results indicate that LTA4 H mediates the diet-induced obesity by reducing catecholamine and thyroid hormone secretion.

New Therapeutic Horizons for Graves' Hyperthyroidism.

Graves’ hyperthyroidism is characterized by the presence of autoantibodies that stimulate the thyroid-stimulating hormone receptor (TSHR), resulting in uncontrolled secretion of excessive thyroid hormone. Conventional treatments, including antithyroid medication, radioiodine, or surgery have remained largely unchanged for the past 70 years and either lack efficacy for many patients, or result in lifelong thyroid hormone replacement therapy, in the case of the latter 2 options. The demand for new therapeutic options, combined with greater insight into basic immunobiology, has led to the emergence of novel approaches to treat Graves’ hyperthyroidism. The current therapies under investigation include biologics, small molecules, and peptide immunomodulation. There is a growing focus on TSHR-specific treatment modalities, which carry the advantage of eliciting a specific, targeted approach, with the aim of avoiding disruption of the functioning immune system. These therapies present a new opportunity to supersede the inadequate treatments currently available for some Graves’ patients, offering hope of successful restoration of euthyroidism without the need for ongoing therapy. Several of these therapeutic options have the potential to translate into clinical practice in the near future. This review provides a comprehensive summary of the recent advances and various stages of development of the novel therapeutic approaches to treat Graves’ hyperthyroidism.

Efficacy of Vitamin-D Supplement on Thyroid Profile in Children with Graves’ Disease

BACKGROUND: Many studies have shown low Vitamin-D level as a risk factor for autoimmune diseases, especially multiple sclerosis and thyroid disease. Graves’ disease (GD) is an autoimmune disease caused by autoantibodies that stimulate thyroid-stimulating hormone (TSH) receptors by increasing thyroid hormone synthesis and secretion. Several studies report that many patients with autoimmune thyroid disease including GD have low Vitamin-D status.&#x0D; AIM: The objective of the study was to evaluate the effect of Vitamin-D supplement on GD patients on improvement in thyroid hormone levels.&#x0D; METHODS: Open random clinical trial was conducted in GD patients to determine changes in thyroid hormone to achieving normal levels between those receiving methimazole plus Vitamin-D supplementation compared with those who only received methimazole. Patients were checked for TSH receptor antibody, thyroid profile and Vitamin-D level before treatment and rechecked for thyroid profile and Vitamin-D level 3 months after treatment. t-test used to compare the drug efficacy (p &lt; 0.05) in two groups.&#x0D; RESULTS: From 25 children with GD accompanied by Vitamin-D deficiency with an average value of Vitamin-D was 16 ng/mL. GD children who receive methimazole with Vitamin-D supplement had elevated TSH levels in the 3rd month of therapy that was significantly different compared to GD children who received methimazole only (p = 0.00), and the increase of TSH was also followed by an increase in Vitamin-D levels.&#x0D; CONCLUSION: All children with GD had Vitamin D deficiency, and the addition of Vitamin-D supplement to GD therapy would improve TSH faster than children who did not receive Vitamin-D supplement.