Thyroid Hormone Resistance Syndrome
Thyroid Hormones
Receptors, Thyroid Hormone
Thyroid Hormone Receptors beta
Triiodothyronine
Pseudohypoparathyroidism
Thyroid Gland
Mutation
Insulin Resistance
Drug Resistance
Fibrous Dysplasia, Polyostotic
GTP-Binding Protein alpha Subunits, Gs
Thyroxine
Thyroid Hormone Receptors alpha
Hypothyroidism
Thyrotropin
Metabolic Syndrome X
Iodide Peroxidase
Microvascular Angina
Receptors, Somatotropin
Insulin
Drug Resistance, Neoplasm
Hyperthyroidism
Hyperactivity and learning deficits in transgenic mice bearing a human mutant thyroid hormone beta1 receptor gene. (1/56)
Resistance to thyroid hormone (RTH) is a human syndrome mapped to the thyroid receptor beta (TRbeta) gene on chromosome 3, representing a mutation of the ligand-binding domain of the TRbeta gene. The syndrome is characterized by reduced tissue responsiveness to thyroid hormone and elevated serum levels of thyroid hormones. A common behavioral phenotype associated with RTH is attention deficit hyperactivity disorder (ADHD). To test the hypothesis that RTH produces attention deficits and/or hyperactivity, transgenic mice expressing a mutant TRbeta gene were generated. The present experiment tested RTH transgenic mice from the PV kindred on behavioral tasks relevant to the primary features of ADHD: hyperactivity, sustained attention (vigilance), learning, and impulsivity. Male transgenic mice showed elevated locomotor activity in an open field compared to male wild-type littermate controls. Both male and female transgenic mice exhibited impaired learning of an autoshaping task, compared to wild-type controls. On a vigilance task in an operant chamber, there were no differences between transgenics and controls on the proportion of hits, response latency, or duration of stimulus tolerated. On an operant go/no-go task measuring sustained attention and impulsivity, there were no differences between controls and transgenics. These results indicate that transgenic mice bearing a mutant human TRbeta gene demonstrate several behavioral characteristics of ADHD and may serve a valuable heuristic role in elucidating possible candidate genes in converging pathways for other causes of ADHD. (+info)Thyroid hormone resistance and increased metabolic rate in the RXR-gamma-deficient mouse. (2/56)
Vitamin A and retinoids affect pituitary-thyroid function through suppression of serum thyroid-stimulating hormone (TSH) levels and TSH-beta subunit gene expression. We have previously shown that retinoid X receptor-selective (RXR-selective) ligands can suppress serum TSH levels in vivo and TSH-beta promoter activity in vitro. The RXR-gamma isotype has limited tissue distribution that includes the thyrotrope cells of the anterior pituitary gland. In this study, we have performed a detailed analysis of the pituitary-thyroid function of mice lacking the gene for the RXR-gamma isotype. These mice had significantly higher serum T4 levels and TSH levels than did wild-type (WT) controls. Treatment of RXR-gamma-deficient and WT mice with T3 suppressed serum TSH and T4 levels in both groups, but RXR-gamma-deficient mice were relatively resistant to exogenous T3. RXR-gamma-deficient mice had significantly higher metabolic rates than did WT controls, suggesting that these animals have a pattern of central resistance to thyroid hormone. RXR-gamma, which is also expressed in skeletal muscle and the hypothalamus, may have a direct effect on muscle metabolism, regulation of food intake, or thyrotropin-releasing hormone levels in the hypothalamus. In conclusion, the RXR-gamma isotype appears to contribute to the regulation of serum TSH and T4 levels and to affect peripheral metabolism through regulation of the hypothalamic-pituitary-thyroid axis or through direct effects on skeletal muscle. (+info)Three Japanese patients from two families with generalized resistance to thyroid hormone with mutations in exon 9 of the thyroid hormone receptor beta gene. (3/56)
Resistance to thyroid hormone (RTH) is a genetic disorder caused by mutations in the thyroid hormone receptor (TR) beta gene. The mutations are clustered in two regions: exon 9 and exon 10. To date, only one patient with an exon 9 mutation has been reported in Japan. We herein report three patients from two Japanese families with RTH and mutations in exon 9. A 52-year-old woman and her 18-year-old daughter, both with inappropriate secretion of TSH (SITSH) were diagnosed simultaneously with generalized RTH. Molecular analysis revealed a G345D mutation. An 11-year-old girl with SITSH, whose only manifestation was a goiter, had an R338W mutation, which is frequently associated with pituitary RTH. Thus, RTH with mutations in exon 9 of the TR beta gene is not so rare in Japan. (+info)Biological roles and mechanistic actions of co-repressor complexes. (4/56)
Transcriptional repression, which plays a crucial role in diverse biological processes, is mediated in part by non-DNA-binding co-repressors. The closely related co-repressor proteins N-CoR and SMRT, although originally identified on the basis of their ability to associate with and confer transcriptional repression through nuclear receptors, have been shown to be recruited to many classes of transcription factor and are in fact components of multiple protein complexes containing histone deacetylase proteins. This association with histone deacetylase activity provides an important component of the mechanism that allows DNA-binding proteins interacting with N-CoR or SMRT to repress transcription of specific target genes. Both N-CoR and SMRT are important targets for cell signaling pathways, which influence their expression levels, subcellular localization and association with other proteins. Recently, the biological importance of these proteins has been revealed by studies of genetically engineered mice and human diseases such as acute promyelocytic leukemia (APL) and resistance to thyroid hormone (RTH). (+info)Thyroid-hormone-dependent negative regulation of thyrotropin beta gene by thyroid hormone receptors: study with a new experimental system using CV1 cells. (5/56)
The molecular mechanism involved in the liganded thyroid hormone receptor suppression of the TSHbeta (thyroid-stimulating hormone beta, or thyrotropin beta) gene transcription is undetermined. One of the main reasons is the limitation of useful cell lines for the experiments. We have developed an assay system using non-pituitary CV1 cells and studied the negative regulation of the TSHbeta gene. In CV1 cells, the TSHbeta-CAT (chloramphenicol acetyltransferase) reporter was stimulated by Pit1 and GATA2 and suppressed by T3 (3,3',5-tri-iodothyronine)-bound thyroid hormone receptor. The suppression was dependent on the amounts of T3 and the receptor. Unliganded receptor did not stimulate TSHbeta activity, suggesting that the receptor itself is not an activator. Analyses using various receptor mutants revealed that the intact DNA-binding domain is crucial to the TSHbeta gene suppression. Co-activators and co-repressors are not necessarily essential, but are required for the full suppression of the TSHbeta gene. Among the three receptor isoforms, beta2 exhibited the strongest inhibition and its protein level was the most predominant in a thyrotroph cell line, TalphaT1, in Western blotting. The dominant-negative effects of various receptor mutants measured on the TSHbeta-CAT reporter were not simple mirror images of those in the positive regulation under physiological T3 concentration. (+info)Retarded bone growth in thyroid hormone resistance. A clinical study of a large family with a novel thyroid hormone receptor mutation. (6/56)
OBJECTIVE: Thyroid hormone resistance (RTH) is characterised by variable tissue hyporesponsiveness to thyroid hormone. The disorder is usually caused by mutations in the thyroid hormone receptor beta (TR beta). We describe a large family with this disorder. SUBJECTS AND MEASUREMENT: We identified 36 family members with RTH in four generations by screening relatives of patients with the diagnosis. The diagnosis was verified by identification of a mutation in the thyroid hormone receptor beta (TR beta) gene. Symptoms, clinical findings and laboratory tests of 29 affected individuals were compared with those of 16 first-degree relatives. RESULTS: Bone maturation in children with RTH was delayed. The height was lower both in children and in adults with RTH than in the controls. Children with RTH had lower birth weight than the controls, particularly when the condition was inherited from the father. We did not observe increased prevalence of neuropsychological symptoms associated with RTH in this family. Palpitations and increased pulse rate indicated mild cardiac hyperthyroidism. Direct sequence analysis of the TR beta gene revealed a novel point mutation, a heterozygous transition c.1031G>C in exon 9 theoretically substituting Gly344Ala. CONCLUSIONS: We found evidence of skeletal tissue hypothyroidism that resulted in permanent growth retardation from prenatal to adult life. We found substantial variations in thyroid hormone levels and clinical presentation, but most individuals were without symptoms of thyroid disorder. (+info)Multi-tissue gene-expression analysis in a mouse model of thyroid hormone resistance. (7/56)
BACKGROUND: Resistance to thyroid hormone (RTH) is caused by mutations of the thyroid hormone receptor beta (TRbeta) gene. To understand the transcriptional program underlying TRbeta mutant-induced phenotypic expression of RTH, cDNA microarrays were used to profile the expression of 11,500 genes in a mouse model of human RTH. RESULTS: We analyzed transcript levels in cerebellum, heart and white adipose tissue from a knock-in mouse (TRbetaPV/PV mouse) that harbors a human mutation (referred to as PV) and faithfully reproduces human RTH. Because TRbetaPV/PV mice have elevated thyroid hormone (T3), to define T3-responsive genes in the context of normal TRbeta, we also analyzed T3 effects in hyperthyroid wild-type gender-matched littermates. Microarray analysis revealed 163 genes responsive to T3 treatment and 187 genes differentially expressed between TRbetaPV/PV mice and wild-type littermates. Both the magnitude and gene make-up of the transcriptional response varied widely across tissues and conditions. We identified genes modulated in T3-dependent PV-independent, T3- and PV-dependent, and T3-independent PV-dependent pathways that illuminated the biological consequences of PV action in vivo. Most T3-responsive genes that were dysregulated in the heart and white adipose tissue of TRbetaPV/PV mice were repressed in T3-treated wild-type mice and upregulated in TRbetaPV/PV mice, suggesting the inappropriate activation of T3-suppressed genes in RTH. CONCLUSIONS: Comprehensive multi-tissue gene-expression analysis uncovered complex multiple signaling pathways that mediate the molecular actions of TRbeta mutants in vivo. In particular, the T3-independent mutant-dependent genomic response unveiled the contribution of a novel 'change-of-function' of TRbeta mutants to the pathogenesis of RTH. Thus, the molecular actions of TRbeta mutants are more complex than previously envisioned. (+info)Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. (8/56)
Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. (+info)Thyroid Hormone Resistance Syndrome, also known as Refractory Thyroid Disease or Generalized T3 Resistance, is a rare genetic disorder characterized by reduced sensitivity and impaired response of the body's tissues to thyroid hormones, despite having normal or elevated levels of these hormones in the blood. This condition is caused by mutations in the THRB gene, which encodes the thyroid hormone receptor beta.
In this syndrome, the target cells and tissues do not respond properly to thyroid hormones, leading to a wide range of symptoms similar to those seen in hypothyroidism (underactive thyroid), such as fatigue, weight gain, cold intolerance, constipation, dry skin, and depression. However, unlike hypothyroidism, patients with Thyroid Hormone Resistance Syndrome usually have normal or increased levels of thyroid-stimulating hormone (TSH) and free thyroxine (FT4) in their blood.
The diagnosis of Thyroid Hormone Resistance Syndrome is often challenging, as it requires the exclusion of other causes of hypothyroidism and the confirmation of normal or elevated thyroid hormone levels with impaired tissue response. Treatment typically involves careful monitoring and management of symptoms, as the use of additional thyroid hormones may not improve the condition and can even worsen symptoms in some cases.
Thyroid hormones are hormones produced and released by the thyroid gland, a small endocrine gland located in the neck that helps regulate metabolism, growth, and development in the human body. The two main thyroid hormones are triiodothyronine (T3) and thyroxine (T4), which contain iodine atoms. These hormones play a crucial role in various bodily functions, including heart rate, body temperature, digestion, and brain development. They help regulate the rate at which your body uses energy, affects how sensitive your body is to other hormones, and plays a vital role in the development and differentiation of all cells of the human body. Thyroid hormone levels are regulated by the hypothalamus and pituitary gland through a feedback mechanism that helps maintain proper balance.
Thyroid hormone receptors (THRs) are nuclear receptor proteins that bind to thyroid hormones, triiodothyronine (T3) and thyroxine (T4), and regulate gene transcription in target cells. These receptors play a crucial role in the development, growth, and metabolism of an organism by mediating the actions of thyroid hormones. THRs are encoded by genes THRA and THRB, which give rise to two major isoforms: TRα1 and TRβ1. Additionally, alternative splicing results in other isoforms with distinct tissue distributions and functions. THRs function as heterodimers with retinoid X receptors (RXRs) and bind to thyroid hormone response elements (TREs) in the regulatory regions of target genes. The binding of T3 or T4 to THRs triggers a conformational change, which leads to recruitment of coactivators or corepressors, ultimately resulting in activation or repression of gene transcription.
Thyroid hormone receptors (THRs) are nuclear receptor proteins that bind to thyroid hormones and mediate their effects in target cells. There are two main types of THRs, referred to as THR alpha and THR beta. THR beta is further divided into two subtypes, THR beta1 and THR beta2.
THR beta is a type of nuclear receptor that is primarily expressed in the liver, kidney, and heart, as well as in the central nervous system. It plays an important role in regulating the metabolism of carbohydrates, lipids, and proteins, as well as in the development and function of the heart. THR beta is also involved in the regulation of body weight and energy expenditure.
THR beta1 is the predominant subtype expressed in the liver and is responsible for many of the metabolic effects of thyroid hormones in this organ. THR beta2, on the other hand, is primarily expressed in the heart and plays a role in regulating cardiac function.
Abnormalities in THR beta function can lead to various diseases, including thyroid hormone resistance, a condition in which the body's cells are unable to respond properly to thyroid hormones. This can result in symptoms such as weight gain, fatigue, and cold intolerance.
Triiodothyronine (T3) is a thyroid hormone, specifically the active form of thyroid hormone, that plays a critical role in the regulation of metabolism, growth, and development in the human body. It is produced by the thyroid gland through the iodination and coupling of the amino acid tyrosine with three atoms of iodine. T3 is more potent than its precursor, thyroxine (T4), which has four iodine atoms, as T3 binds more strongly to thyroid hormone receptors and accelerates metabolic processes at the cellular level.
In circulation, about 80% of T3 is bound to plasma proteins, while the remaining 20% is unbound or free, allowing it to enter cells and exert its biological effects. The primary functions of T3 include increasing the rate of metabolic reactions, promoting protein synthesis, enhancing sensitivity to catecholamines (e.g., adrenaline), and supporting normal brain development during fetal growth and early infancy. Imbalances in T3 levels can lead to various medical conditions, such as hypothyroidism or hyperthyroidism, which may require clinical intervention and management.
Pseudohypoparathyroidism (PHP) is a rare genetic disorder characterized by the body's resistance to the action of parathyroid hormone (PTH), leading to hypocalcemia (low serum calcium levels) and hyperphosphatemia (high serum phosphate levels). Despite normal or elevated PTH levels, target organs such as the kidneys and bones do not respond appropriately to its actions.
There are several types of PHP, with the most common being type Ia, which is caused by mutations in the GNAS gene. This gene provides instructions for making a protein called the alpha-subunit of the stimulatory G protein (Gs-alpha), which plays a crucial role in transmitting signals within cells. In PHP type Ia, there is a reduced amount or functionally impaired Gs-alpha protein, leading to resistance to PTH and other hormones that use this signaling pathway, such as thyroid-stimulating hormone (TSH) and gonadotropins.
PHP type Ia patients often exhibit physical features known as Albright's hereditary osteodystrophy (AHO), including short stature, round face, obesity, brachydactyly (shortened fingers and toes), and ectopic ossifications (formation of bone in abnormal places). However, it is important to note that not all individuals with AHO have PHP, and not all PHP patients display AHO features.
PHP type Ib is another common form of the disorder, characterized by PTH resistance without the physical manifestations of AHO. This type is caused by mutations in the STX16 gene or other genes involved in the intracellular trafficking of Gs-alpha protein.
Pseudohypoparathyroidism should be differentiated from hypoparathyroidism, a condition where there is an insufficient production or secretion of PTH by the parathyroid glands, leading to similar biochemical abnormalities but without resistance to PTH action.
A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.
For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.
It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.
The thyroid gland is a major endocrine gland located in the neck, anterior to the trachea and extends from the lower third of the Adams apple to the suprasternal notch. It has two lateral lobes, connected by an isthmus, and sometimes a pyramidal lobe. This gland plays a crucial role in the metabolism, growth, and development of the human body through the production of thyroid hormones (triiodothyronine/T3 and thyroxine/T4) and calcitonin. The thyroid hormones regulate body temperature, heart rate, and the production of protein, while calcitonin helps in controlling calcium levels in the blood. The function of the thyroid gland is controlled by the hypothalamus and pituitary gland through the thyroid-stimulating hormone (TSH).
A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.
Insulin resistance is a condition in which the body's cells become less responsive to insulin, a hormone produced by the pancreas that regulates blood sugar levels. In response to this decreased sensitivity, the pancreas produces more insulin to help glucose enter the cells. However, over time, the pancreas may not be able to keep up with the increased demand for insulin, leading to high levels of glucose in the blood and potentially resulting in type 2 diabetes, prediabetes, or other health issues such as metabolic syndrome, cardiovascular disease, and non-alcoholic fatty liver disease. Insulin resistance is often associated with obesity, physical inactivity, and genetic factors.
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
Fibrous Dysplasia, Polyostotic is a rare genetic disorder that affects the bone tissue. It is characterized by the replacement of normal bone tissue with fibrous (scar-like) tissue, leading to weak and fragile bones that are prone to fractures and deformities. The term "polyostotic" refers to the involvement of multiple bones in the body.
In this condition, there is an abnormal development of the bone during fetal growth or early childhood due to a mutation in the GNAS gene. This results in the formation of fibrous tissue instead of normal bone tissue, leading to the characteristic features of Fibrous Dysplasia, Polyostotic.
The symptoms of this condition can vary widely depending on the severity and location of the affected bones. Common symptoms include:
* Bone pain and tenderness
* Bone deformities (such as bowing of the legs)
* Increased risk of fractures
* Skin pigmentation changes (cafe-au-lait spots)
* Hearing loss or other hearing problems (if the skull is affected)
Fibrous Dysplasia, Polyostotic can also be associated with endocrine disorders such as precocious puberty and hyperthyroidism. Treatment typically involves a combination of medications to manage pain and prevent fractures, as well as surgical intervention to correct bone deformities or stabilize fractures.
Thyroid neoplasms refer to abnormal growths or tumors in the thyroid gland, which can be benign (non-cancerous) or malignant (cancerous). These growths can vary in size and may cause a noticeable lump or nodule in the neck. Thyroid neoplasms can also affect the function of the thyroid gland, leading to hormonal imbalances and related symptoms. The exact causes of thyroid neoplasms are not fully understood, but risk factors include radiation exposure, family history, and certain genetic conditions. It is important to note that most thyroid nodules are benign, but a proper medical evaluation is necessary to determine the nature of the growth and develop an appropriate treatment plan.
GTP-binding protein alpha subunits, Gs, are a type of heterotrimeric G proteins that play a crucial role in the transmission of signals within cells. These proteins are composed of three subunits: alpha, beta, and gamma. The alpha subunit of Gs proteins (Gs-alpha) is responsible for activating adenylyl cyclase, an enzyme that converts ATP to cyclic AMP (cAMP), a secondary messenger involved in various cellular processes.
When a G protein-coupled receptor (GPCR) is activated by an extracellular signal, it interacts with and activates the Gs protein. This activation causes the exchange of guanosine diphosphate (GDP) bound to the alpha subunit with guanosine triphosphate (GTP). The GTP-bound Gs-alpha then dissociates from the beta-gamma subunits and interacts with adenylyl cyclase, activating it and leading to an increase in cAMP levels. This signaling cascade ultimately results in various cellular responses, such as changes in gene expression, metabolism, or cell growth and differentiation.
It is important to note that mutations in the GNAS gene, which encodes the Gs-alpha subunit, can lead to several endocrine and non-endocrine disorders, such as McCune-Albright syndrome, fibrous dysplasia, and various hormone-related diseases.
Thyroxine (T4) is a type of hormone produced and released by the thyroid gland, a small butterfly-shaped endocrine gland located in the front of your neck. It is one of two major hormones produced by the thyroid gland, with the other being triiodothyronine (T3).
Thyroxine plays a crucial role in regulating various metabolic processes in the body, including growth, development, and energy expenditure. Specifically, T4 helps to control the rate at which your body burns calories for energy, regulates protein, fat, and carbohydrate metabolism, and influences the body's sensitivity to other hormones.
T4 is produced by combining iodine and tyrosine, an amino acid found in many foods. Once produced, T4 circulates in the bloodstream and gets converted into its active form, T3, in various tissues throughout the body. Thyroxine has a longer half-life than T3, which means it remains active in the body for a more extended period.
Abnormal levels of thyroxine can lead to various medical conditions, such as hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). These conditions can cause a range of symptoms, including weight gain or loss, fatigue, mood changes, and changes in heart rate and blood pressure.
Thyroid hormone receptors (THRs) are nuclear receptor proteins that bind to thyroid hormones and mediate their effects in the body. There are two main types of THRs, referred to as THRα and THRβ.
THRα is a subtype of thyroid hormone receptor that is primarily expressed in tissues such as the heart, skeletal muscle, and brown adipose tissue. It plays an important role in regulating metabolism, growth, and development in these tissues. THRα has two subtypes, THRα1 and THRα2, which have different functions and are expressed in different tissues.
THRα1 is the predominant form of THRα and is found in many tissues, including the heart, skeletal muscle, and brown adipose tissue. It regulates genes involved in metabolism, growth, and development, and has been shown to play a role in regulating heart rate and contractility.
THRα2, on the other hand, is primarily expressed in the brain and pituitary gland, where it regulates the production of thyroid-stimulating hormone (TSH). THRα2 is unable to bind to thyroid hormones, but can form heterodimers with THRα1 or THRβ1, which allows it to modulate their activity.
Overall, THRα plays an important role in regulating various physiological processes in the body, and dysregulation of THRα function has been implicated in a number of diseases, including heart disease, muscle wasting, and neurological disorders.
Thyroid diseases are a group of conditions that affect the function and structure of the thyroid gland, a small butterfly-shaped endocrine gland located in the base of the neck. The thyroid gland produces hormones that regulate many vital functions in the body, including metabolism, growth, and development.
Thyroid diseases can be classified into two main categories: hypothyroidism and hyperthyroidism. Hypothyroidism occurs when the thyroid gland does not produce enough hormones, leading to symptoms such as fatigue, weight gain, cold intolerance, constipation, and depression. Hyperthyroidism, on the other hand, occurs when the thyroid gland produces too much hormone, resulting in symptoms such as weight loss, heat intolerance, rapid heart rate, tremors, and anxiety.
Other common thyroid diseases include:
1. Goiter: an enlargement of the thyroid gland that can be caused by iodine deficiency or autoimmune disorders.
2. Thyroid nodules: abnormal growths on the thyroid gland that can be benign or malignant.
3. Thyroid cancer: a malignant tumor of the thyroid gland that requires medical treatment.
4. Hashimoto's disease: an autoimmune disorder that causes chronic inflammation of the thyroid gland, leading to hypothyroidism.
5. Graves' disease: an autoimmune disorder that causes hyperthyroidism and can also lead to eye problems and skin changes.
Thyroid diseases are diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as ultrasound or CT scan. Treatment options depend on the specific type and severity of the disease and may include medication, surgery, or radioactive iodine therapy.
Hypothyroidism is a medical condition where the thyroid gland, which is a small butterfly-shaped gland located in the front of your neck, does not produce enough thyroid hormones. This results in a slowing down of the body's metabolic processes, leading to various symptoms such as fatigue, weight gain, constipation, cold intolerance, dry skin, hair loss, muscle weakness, and depression.
The two main thyroid hormones produced by the thyroid gland are triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating various bodily functions, including heart rate, body temperature, and energy levels. In hypothyroidism, the production of these hormones is insufficient, leading to a range of symptoms that can affect multiple organ systems.
Hypothyroidism can be caused by several factors, including autoimmune disorders (such as Hashimoto's thyroiditis), surgical removal of the thyroid gland, radiation therapy for neck cancer, certain medications, and congenital defects. Hypothyroidism is typically diagnosed through blood tests that measure levels of TSH (thyroid-stimulating hormone), T3, and T4. Treatment usually involves taking synthetic thyroid hormones to replace the missing hormones and alleviate symptoms.
Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a hormone secreted by the anterior pituitary gland. Its primary function is to regulate the production and release of thyroxine (T4) and triiodothyronine (T3) hormones from the thyroid gland. Thyrotropin binds to receptors on the surface of thyroid follicular cells, stimulating the uptake of iodide and the synthesis and release of T4 and T3. The secretion of thyrotropin is controlled by the hypothalamic-pituitary-thyroid axis: thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release of thyrotropin, while T3 and T4 inhibit its release through a negative feedback mechanism.
Metabolic syndrome, also known as Syndrome X, is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes. It is not a single disease but a group of risk factors that often co-occur. According to the American Heart Association and the National Heart, Lung, and Blood Institute, a person has metabolic syndrome if they have any three of the following five conditions:
1. Abdominal obesity (waist circumference of 40 inches or more in men, and 35 inches or more in women)
2. Triglyceride level of 150 milligrams per deciliter of blood (mg/dL) or greater
3. HDL cholesterol level of less than 40 mg/dL in men or less than 50 mg/dL in women
4. Systolic blood pressure of 130 millimeters of mercury (mmHg) or greater, or diastolic blood pressure of 85 mmHg or greater
5. Fasting glucose level of 100 mg/dL or greater
Metabolic syndrome is thought to be caused by a combination of genetic and lifestyle factors, such as physical inactivity and a diet high in refined carbohydrates and unhealthy fats. Treatment typically involves making lifestyle changes, such as eating a healthy diet, getting regular exercise, and losing weight if necessary. In some cases, medication may also be needed to manage individual components of the syndrome, such as high blood pressure or high cholesterol.
Iodide peroxidase, also known as iodide:hydrogen peroxide oxidoreductase, is an enzyme that belongs to the family of oxidoreductases. Specifically, it is a peroxidase that uses iodide as its physiological reducing substrate. This enzyme catalyzes the oxidation of iodide by hydrogen peroxide to produce iodine, which plays a crucial role in thyroid hormone biosynthesis.
The systematic name for this enzyme is iodide:hydrogen-peroxide oxidoreductase (iodinating). It is most commonly found in the thyroid gland, where it helps to produce and regulate thyroid hormones by facilitating the iodination of tyrosine residues on thyroglobulin, a protein produced by the thyroid gland.
Iodide peroxidase requires a heme cofactor for its enzymatic activity, which is responsible for the oxidation-reduction reactions it catalyzes. The enzyme's ability to iodinate tyrosine residues on thyroglobulin is essential for the production of triiodothyronine (T3) and thyroxine (T4), two critical hormones that regulate metabolism, growth, and development in mammals.
Microvascular angina, also known as cardiac syndrome X or microvascular ischemia, is a type of angina (chest pain) that results from reduced blood flow to the heart muscle due to dysfunction in the small coronary arteries (microvasculature). These vessels are too small to be visualized during conventional diagnostic tests like coronary angiography.
The medical definition of microvascular angina is:
A clinical syndrome characterized by the presence of anginal chest pain, often accompanied by evidence of myocardial ischemia (insufficient blood flow to the heart muscle), in the absence of obstructive coronary artery disease on conventional diagnostic imaging. The underlying mechanism involves dysfunction and impaired regulation of the microvasculature, leading to reduced vasodilatory capacity, increased vasoconstriction, and ultimately, inadequate oxygen supply to meet the metabolic demands of the heart muscle.
Microvascular angina is more prevalent in women, especially those with risk factors such as hypertension, diabetes, hyperlipidemia, and smoking. Diagnosis often requires specialized testing like coronary flow reserve assessment using positron emission tomography (PET) or cardiac magnetic resonance imaging (MRI). Treatment typically involves a combination of lifestyle modifications, medications to improve blood vessel function and reduce chest pain, and sometimes, invasive treatments such as transmyocardial laser revascularization.
Somatotropin receptors are a type of cell surface receptor that binds to and gets activated by the hormone somatotropin, also known as growth hormone (GH). These receptors are found in many tissues throughout the body, including the liver, muscle, and fat. When somatotropin binds to its receptor, it activates a series of intracellular signaling pathways that regulate various physiological processes such as growth, metabolism, and cell reproduction.
Somatotropin receptors belong to the class I cytokine receptor family and are composed of two subunits, a homodimer of extracellular glycoproteins that bind to the hormone and an intracellular tyrosine kinase domain that activates downstream signaling pathways. Mutations in the somatotropin receptor gene can lead to growth disorders such as dwarfism or gigantism, depending on whether the mutation results in a decrease or increase in receptor activity.
Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.
Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.
Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.
Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.
Hyperthyroidism is a medical condition characterized by an excessive production and release of thyroid hormones from the thyroid gland, leading to an increased metabolic rate in various body systems. The thyroid gland, located in the front of the neck, produces two main thyroid hormones: triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating many bodily functions, including heart rate, digestion, energy levels, and mood.
In hyperthyroidism, the elevated levels of T3 and T4 can cause a wide range of symptoms, such as rapid heartbeat, weight loss, heat intolerance, increased appetite, tremors, anxiety, and sleep disturbances. Some common causes of hyperthyroidism include Graves' disease, toxic adenoma, Plummer's disease (toxic multinodular goiter), and thyroiditis. Proper diagnosis and treatment are essential to manage the symptoms and prevent potential complications associated with this condition.
Thyroid function tests (TFTs) are a group of blood tests that assess the functioning of the thyroid gland, which is a small butterfly-shaped gland located in the front of the neck. The thyroid gland produces hormones that regulate metabolism, growth, and development in the body.
TFTs typically include the following tests:
1. Thyroid-stimulating hormone (TSH) test: This test measures the level of TSH, a hormone produced by the pituitary gland that regulates the production of thyroid hormones. High levels of TSH may indicate an underactive thyroid gland (hypothyroidism), while low levels may indicate an overactive thyroid gland (hyperthyroidism).
2. Thyroxine (T4) test: This test measures the level of T4, a hormone produced by the thyroid gland. High levels of T4 may indicate hyperthyroidism, while low levels may indicate hypothyroidism.
3. Triiodothyronine (T3) test: This test measures the level of T3, another hormone produced by the thyroid gland. High levels of T3 may indicate hyperthyroidism, while low levels may indicate hypothyroidism.
4. Thyroid peroxidase antibody (TPOAb) test: This test measures the level of TPOAb, an antibody that attacks the thyroid gland and can cause hypothyroidism.
5. Thyroglobulin (Tg) test: This test measures the level of Tg, a protein produced by the thyroid gland. It is used to monitor the treatment of thyroid cancer.
These tests help diagnose and manage various thyroid disorders, including hypothyroidism, hyperthyroidism, thyroiditis, and thyroid cancer.
Tiratricol
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Thyroid hormone receptor beta
Thyrotroph Thyroid Hormone Sensitivity Index
Hyperthyroxinemia
Thyroid hormone resistance
Thyroid disease
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Thyroid's secretory capacity
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Endocrine disease
Sum activity of peripheral deiodinases
List of Bulgarian inventors and discoverers
Alström syndrome
Acromegaly
Hypothalamic-pituitary-thyroid axis
Congenital hypothyroidism
Pattern hair loss
Maternal physiological changes in pregnancy
Sex hormone-binding globulin
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Thyroid function tests
Thyroid Feedback Quantile-based Index
Vandetanib
Chromosome 11
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Tiratricol - Wikipedia
Thyroid hormone action: insight from transgenic mouse models
JCI - A heartfelt response: new thyroid hormone-sensitive neurons in the hypothalamus
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Clinical case reports Thyroid/Others | 0035 | ECE2014 | 16th European Congress of Endocrinology | Endocrine Abstracts
Low T3 Syndrome V: Should It Be Treated with Thyroid Hormone?
Generalized resistance to thyroid hormone (Concept Id: C4722330) - MedGen - NCBI
A Case of Hypothyroxinemia with Thyroxine-Binding-Globulin Deficiency
Pituitary Diseases | Profiles RNS
Časopis Internal medicine - Článok Congenital syndromes with reduced sensitiwvity to thyroid hormones
TR alpha/NR1A1/Thyroid Hormone Receptor alpha Antibody (NBP2-22523): Novus Biologicals
MRC Epidemiology Unit - Publications Database
ТИРОНЕТ - все о щитовидной железе // Для специалистов // Журнал Тиронет // Архив журнала // 2001 год // № 3
The causes and complications of menorrhagia and how to stop or treat heavy menstrual bleeding. - Laboratory Insider
Table2 Expanding the phenotype of THRB: a range of macular dystrophies as the major clinical manifestations in patients with a...
Epiphany: OAA
N ervichny hypothyroidism | Thyroid hormones and thyroid cancer
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Research Highlights | Semnan University of Medical Sciences
Genetic disorders of thyroid development, hormone biosynthesis and signalling.
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Bamforth-Lazarus Syndrome via the FOXE1 Gene Test - PreventionGenetics
The Thyroid Gland; what it's job is and what happens when it's malfunctioning... - Dr. Dady
Pediatric Hypothyroidism Workup: Laboratory Studies, Imaging Studies, Procedures
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FERRAU', Francesco
Hypothyroidism28
- Congenital hypothyroidism, which occurs in 1 in less than 3,000 births ( 3 ), and other thyroid gland disorders are associated with defects in the maturation and function of many tissues and organ systems. (jci.org)
- We describe the clinical case of two childbearing age women with thyroid dysfunction, hypocalcemia, hyperphosphatemia, and high levels of PTH.Case 1: A 34-year-old woman with infertility for 3 years, microprolactinoma treated with low-dose dopamine agonists, autoimmune primary hypothyroidism and obesity. (endocrine-abstracts.org)
- Mutations in thyroid hormone receptor α1 (TRα1) cause Resistance to Thyroid Hormone α (RTHα), a disorder characterized by hypothyroidism in TRα1-expressing tissues including the heart. (cam.ac.uk)
- However, hypothyroidism may develop after surgery on the thyroid gland (postoperative hypothyroidism), when treating thyrostatics (medical hypothyroidism), after irradiation with iodine radioactive isotopes (post-radiation hypothyroidism) and with endemic goiter. (synthroidnews.net)
- The emergence of hypothyroidism is possible with tumors of the thyroid gland. (synthroidnews.net)
- Secondary and tertiary forms of hypothyroidism (the so-called central hypothyroidism) are associated with damage to the hypothalamic-pituitary system in diseases such as pituitary adenomas and other tumors of the sellar area, empty Turkish saddle syndrome, heart attacks and pituitary necrosis (their development is possible with DIC and massive bleeding). (synthroidnews.net)
- The decrease in the functional activity of the thyroid gland in the central forms of hypothyroidism is associated with a deficiency of thyroid stimulating hormone (TSH). (synthroidnews.net)
- Causes of congenital hypothyroidism can be: aplasia and thyroid dysplasia, genetically determined defects in thyroid hormone biosynthesis, severe iodine deficiency, autoimmune thyroid disease in the mother (due to the penetration of thyroid blocking antibodies through the placenta), treatment of thyrotoxicosis in the mother thyrothyrosytorestoherapists. (synthroidnews.net)
- Primary congenital hypothyroidism (CH) due to thyroid dysgenesis may be mediated by defects in thyroid transcription factors or impaired TSH receptor function. (cam.ac.uk)
- Here, we review the genetic basis, pathogenesis and clinical features of congenital, dysgenetic or dyshormonogenic hypothyroidism and disorders of thyroid hormone transport, metabolism and action. (cam.ac.uk)
- Bamforth-Lazarus syndrome is a congenital genetic disorder characterized by hypothyroidism due to thyroid dysgenesis, cleft palate and spiky hair. (preventiongenetics.com)
- The endocrine system produces, stores, and releases hormones into the bloodstream to be used by the body's cells.More than 10 percent of the general population in the United States, and 20 percent of women over the age of 60, have subclinical hypothyroidism. (drdady.com)
- It is important to have your thyroid function checked if you feel that you are having symptoms.Often, at first, you barely notice the symptoms of hypothyroidism, such as fatigue and weight gain. (drdady.com)
- Serum TSH is the optimal parameter to guide dosing of thyroid hormone replacement, except in patients with secondary or tertiary hypothyroidism. (medscape.com)
- Therefore, the occurrence of a normal screening result must not preclude thyroid function testing in any infant with signs or symptoms of hypothyroidism. (medscape.com)
- If total T4 is low, and serum TSH is not elevated, TBG deficiency, central hypothyroidism, or euthyroid sick syndrome should be considered, and repeat testing may be needed. (medscape.com)
- Diffuse toxic goiter is also present in other autoimmune thyroid conditions that cause hypothyroidism, most commonly Hashimoto thyroiditis. (medscape.com)
- RTHα manifests with features of hypothyroidism (skeletal dysplasia and growth retardation, neurocognitive impairment, low metabolic rate, reduced intestinal transit) reflecting hormone resistance in TRα-expressing tissues, but associated paradoxically with near-normal circulating TH levels. (endocrine-abstracts.org)
- Congenital hypothyroidism (CH), occurs with a frequency of one in 3 4000 and is most commonly due (85%) to complete or partial failure of thyroid gland development (dysgenesis). (endocrine-abstracts.org)
- Resistance to Thyroid Hormone alpha (RTHα) is characterised by tissue-selective hypothyroidism with near-normal thyroid function tests, and is due to thyroid receptor α gene mutations. (endocrine-abstracts.org)
- hypothyroidism - Diminished production of thyroid hormone, leading to clinical manifestations of thyroid insufficiency, including low metabolic rate, tendency to weight gain, somnolence and sometimes myxedema. (en-academic.com)
- From brain fog and poor memory to fertility issues, low thyroid function (hypothyroidism) can negatively affect nearly every cell in your body. (thethyroidfixbook.com)
- A condition that has been encountered very frequently in recent years is thyroid hormone deficiency, namely Hypothyroidism. (smarthealthcodes.com)
- For example, congenital hypothyroidism is part of newborn screening, autoimmune thyroid conditions are increasingly common and thyroid nodules are frequently diagnosed on ultrasound. (racgp.org.au)
- Distinguished experts provide reviews on thyroid hormone physiology, congenital hypothyroidism, impaired sensitivity on thyroid hormones, thyroid and the environment, and thyroid cancer. (racgp.org.au)
- Areas to highlight include thyroid physiology, new advances in clinical genetics of congenital hypothyroidism that lead to changes in practice guidelines for newborn screening and information on iodine deficiency in children that is becoming increasingly common in Australia. (racgp.org.au)
- This covers congenital hypothyroidism, syndromes that include thyroid disease, resistance to thyroid hormone, iodine, autoimmune thyroid diasease and thyroid tumours. (racgp.org.au)
- Reduced total triiodothyronine values are found in clinical or subclinical hypothyroidism, starvation, stress, and acute illness, as well as in the setting of reduced levels of thyroid-binding globulin. (medscape.com)
Gland26
- Development and differentiation of the thyroid gland is directed by expression of specific transcription factors in the thyroid follicular cell which mediates hormone biosynthesis. (cam.ac.uk)
- The thyroid gland plays many roles in our health and is therefore widely studied. (drdady.com)
- From regulating body weight to body temperature, the thyroid gland and its hormones are responsible for several essential functions. (drdady.com)
- HYPO-thyroidism refers to an underactive thyroid gland, one that can't make enough hormones for the body to function optimally. (drdady.com)
- From the picture above you see the thyroid gland is located in the neck. (drdady.com)
- The thyroid is a butterfly-shaped gland that sits low on the front of the neck, along the front of the windpipe. (drdady.com)
- The thyroid gland is part of the endocrine system and is responsible for several functions in the body. (drdady.com)
- Diffuse toxic goiter is an autoimmune condition characterized by a diffusely hyperplastic thyroid gland with excessive overproduction of thyroid hormone. (medscape.com)
- Diffuse toxic goiter findings on physical examination include a mildly enlarged thyroid gland (but may be normal in size, many times normal in size, or difficult to palpate) with a smooth, rubbery firm texture. (medscape.com)
- Toxic multinodular goiters generally occur when the thyroid gland is enlarged to at least two to three times the normal size. (medscape.com)
- In diffuse toxic goiter, the thyroid gland is usually enlarged to a variable degree and is vascular and diffusely affected. (medscape.com)
- Lymphocytes and plasma cells infiltrate into the thyroid gland and may aggregate into lymphoid follicles. (medscape.com)
- This condition is an autoimmune disorder whereby the thyroid gland is overstimulated by antibodies directed to the thyroid-stimulating hormone (TSH) receptor on the thyroid follicular cells. (medscape.com)
- This antibody stimulates iodine uptake, thyroid hormonogenesis and release, and thyroid gland growth. (medscape.com)
- 3] Although mainly produced within the thyroid gland, these antibodies reach the circulation and can be measured by various assays in most, but not all, cases. (medscape.com)
- The presence of Hashimoto thyroiditis (which has more of a destructive effect on the thyroid gland) or the presence of another antibody (TSH-receptor blocking antibody) results in a variable natural history of the course of diffuse toxic goiter. (medscape.com)
- Imbalance in production of Thyroid Disease hormones arises from dysfunction of the thyroid gland itself, the pituitary gland, which produces thyroid-stimulating hormone (TSH), or the hypothalamus, which regulates the pituitary gland via thyrotropin-releasing hormone (TRH). (kidneyfailed.in)
- Conventional treatment of thyroid dysfunction relies mainly on drugs and surgery whereas Homeopathic treatment improves the function of the thyroid gland through natural means. (kidneyfailed.in)
- endocrine system, human - ▪ anatomy Introduction group of ductless glands (gland) that regulate body processes by secreting chemical substances called hormones (hormone). (en-academic.com)
- A disease of the PITUITARY GLAND characterized by the excess amount of ADRENOCORTICOTROPIC HORMONE secreted. (uchicago.edu)
- When the pituitary gland does not produce enough growth hormones or the thyroid gland does not produce enough thyroid hormones, hormone therapy may be used. (lifegaines.com)
- Hashimoto's disease, especially seen in women, is an autoimmune disease and develops as a result of antibodies against the thyroid gland. (smarthealthcodes.com)
- The thyroid gland, located in the anterior neck just below the cricoid cartilage, consists of 2 lobes connected by an isthmus. (msdmanuals.com)
- Genetically inherited forms arise from defects of parathyroid gland development, defects in the parathyroid hormone (PTH) gene, defects in the calcium-sensing receptor gene, defects in PTH action, defects in the autoimmune regulator gene, and genetic syndromes. (medscape.com)
- DiGeorge syndrome (ie, hypoparathyroidism, absence of thymus gland [T-cell abnormalities], cardiac anomalies) is associated with abnormal development of the third and fourth pharyngeal pouches from which the parathyroids derive embryologically and represents an example of a defect in parathyroid gland development. (medscape.com)
- This is mediated by an enzyme called peroxidase (thyroperoxidase) and occurs at the luminal surface of the follicular cells of the thyroid gland. (medscape.com)
Receptors13
- Thyroid hormone receptors (TRs) are cellular homologues of the viral erythroblastic leukemia oncogene (v-erbA). (nih.gov)
- Thyroid hormone is a well-known regulator of metabolic and cardiovascular functions, and signaling through thyroid receptors has differential effects on cells depending on the receptor isoform that they express. (jci.org)
- provide evidence that thyroid hormone receptors are essential for the formation of a population of parvalbuminergic neurons in the anterior hypothalamus, linking, for the first time, impaired thyroid hormone signaling during development to cellular deficits in the hypothalamus. (jci.org)
- Molecular and structural biology of thyroid hormone receptors. (nih.gov)
- It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. (novusbio.com)
- Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. (novusbio.com)
- Collingwood T.N., Adams M., Tone Y., Chatterjee V.K. Spectrum of transcriptional, dimerization, and dominant negative properties of twenty different mutant thyroid hormone beta-receptors in thyroid hormone resistance syndrome. (rusmedserv.com)
- Hayashi Y., Weiss R.E., Sarne D.H., Yen P.M., Sunthornthepvarakul T., Marcocci C., Chin W.W., Refetoff S. Do clinical manifestations of resistance to thyroid hormone correlate with the functional alteration of the corresponding mutant thyroid hormone-beta receptors? (rusmedserv.com)
- Thyroid hormones regulate expression of target genes via hormone-inducible nuclear receptors (TRα, TRβ) to exert their physiological effects. (cam.ac.uk)
- These receptors are activated by hormones that leads to transcription, cell differentiation, and growth suppression. (bvsalud.org)
- Thyroid hormone receptors are encoded by two genes (GENES, ERBA): erbA-alpha and erbA-beta for alpha and beta thyroid hormone receptors, respectively. (bvsalud.org)
- These hormones act on cells in virtually every body tissue by combining with nuclear receptors and altering expression of a wide range of gene products. (msdmanuals.com)
- T4 is converted (in most tissues) to T3, the active form that binds to nuclear receptors, and to reverse T3 (rT3), an inactive form of thyroid hormone without metabolic activity. (msdmanuals.com)
Insulin22
- Introduction: Psoriasis is not only a skin disease, is a chronic inflammatory disease associated with serious comorbidities: psoriatic arthritis, metabolic syndrome (obesity, dyslipidemia and insulin resistance), Crohn s disease, depression, ocular problems, cardio-vascular diseases (myocardial infarction), cancer.Methods: 1236 patients (male 54.13% and female 45.87%) with psoriasis were seen in an Outpatient Clinic over a period of 8 years (2004. (endocrine-abstracts.org)
- A number of conditions can cause hormone imbalances, including polycystic ovary syndrome (PCOS), obesity, insulin resistance and thyroid problems. (laboratoryinsider.com)
- Insulin resistance (40-80% of those with PCOS have insulin resistance, and 40% will develop diabetes by the age of 40. (mum.org)
- The connection between insulin resistance and PCOS was not made until relatively recently however, and many physicians are only now beginning to recognise that there is a relationship between the two. (mum.org)
- first published reports of a connection between insulin resistance and PCOS in the 1980s. (mum.org)
- Insulin resistance is a rather complicated phenomenon. (mum.org)
- First, it is important to note that insulin is a very important hormone in the human body and too much or too little of it leads to problems. (mum.org)
- When a person suffers from insulin resistance however, glucose cannot enter the cells. (mum.org)
- It is important to note that insulin resistance also occurs in thin women, as does PCOS. (mum.org)
- Samuel Thatcher believes that thin women with PCOS may even have a more severe form of PCOS, with more entrenched insulin resistance and infertility. (mum.org)
- Hypoglycaemia is also a common phenomenon in people with insulin resistance. (mum.org)
- Those suffering from insulin resistance are vulnerable to bouts of hypoglycaemia due to the constant fluctuations in their blood sugar levels. (mum.org)
- Obviously, insulin resistance is a problem in and of itself, but if left unchecked it may lead to diabetes. (mum.org)
- Since insulin levels are so important in controlling weight, blood sugar and satiety, and have a knock-on effect on other hormones such as testosterone, it is vitally important that insulin levels are kept at a steady level. (mum.org)
- And what about that low carb doctor who implies that insulin resistance (or some other hormone) mucks up the equation? (mefitpro.com)
- It helps to maintain normal thyroid, adrenal, and pituitary function in horses affected by symptoms of Equine Metabolic Syndrome, Cushing's, and Insulin Resistance. (littlebitwestern.ca)
- Insulin resistance is usually linked with obesity, but women of normal weight with pcos also have an increased risk of developing insulin. (veganvan.life)
- To be hormone-related, including too much insulin and testosterone. (veganvan.life)
- Hormone imbalances caused due to conditions such as polycystic ovary syndrome (PCOS), insulin resistance, obesity, and thyroid problems can lead to heavy periods. (femhealthproject.com)
- In insulin resistance and diabetes , the sensitivity of cells to insulin decreases. (smarthealthcodes.com)
- Recent studies suggest an association between vitamin D status, metabolic syndrome, insulin resistance, and obesity among Canadians (12,13). (cdc.gov)
- In the European Region, the Eastern Mediterranean Region and the Region of the Americas this proportion exceeds 50%.1 The mean body mass index has increased over the past 20 years, leading to adverse metabolic effects on blood pressure, cholesterol and triglyceride concentrations, and insulin resistance, thereby increasing the risks of coronary heart disease, ischaemic stroke, type 2 diabetes and polycystic ovarian syndrome. (who.int)
Polycystic ovary sy2
- Polycystic ovary syndrome (PCOS). (massgeneral.org)
- Hyperandrogenism, hirsutism, and polycystic ovary syndrome. (medlineplus.gov)
Adrenal3
- Herbs that support thyroid function include ashwaganda, eleuthero and other adrenal adaptogens. (drdady.com)
- This leads to hypersecretion of cortisol (HYDROCORTISONE) by the ADRENAL GLANDS resulting in CUSHING SYNDROME. (uchicago.edu)
- In cases of chronic stress and depression, cortisol, a stress hormone, is secreted from the adrenal glands. (smarthealthcodes.com)
Secretion8
- A lack of TSH can be isolated, but more often it is combined with a violation of the secretion of other pituitary tropic hormones (in such cases, hypopituitarism is indicated). (synthroidnews.net)
- FOXE1 regulates the expression of thyroglobulin ( TG ) and thyroid peroxidase ( TPO ) and plays important roles in the maintenance of thyroid function, including the production and secretion of thyroid hormones (Cuesta et al. (preventiongenetics.com)
- Effect of pioglitazone on adrenocorticotropic hormone and cortisol secretion in Cushing's disease. (uchicago.edu)
- Inappropriate TSH secretion syndromes. (machtbranchen.com)
- Hormone replacement therapy for women is the use of hormones to either effectively replace natural hormones if your body doesn't make enough of them or to control excessive hormone secretion with medication. (lifegaines.com)
- TSH secretion is also influenced by thyrotropin -releasing hormone (TRH), which is synthesized in the hypothalamus. (msdmanuals.com)
- Hypoparathyroidism results from defective synthesis or secretion of parathyroid hormone (PTH), end-organ resistance, or inappropriate regulations that result from the activated or antibody-stimulated calcium-sensing receptor (CaSR). (medscape.com)
- Unlike other protein hormones, its production and secretion are stimulated by decreased intracellular calcium concentrations, which reflect serum calcium concentrations. (medscape.com)
Disorders7
- This article is part of a special report on Thyroid Disorders . (chriskresser.com)
- Genetic disorders of thyroid development, hormone biosynthesis and signalling. (cam.ac.uk)
- Disorders of thyroid hormone signalling encompass conditions due to defects in membrane thyroid hormone transporters, impaired hormone metabolism due to deficiency of deiodinases and syndromes of Resistance to Thyroid Hormone due to pathogenic variants in either TRα or TRβ. (cam.ac.uk)
- Acording to the American Thyroid Association guidelines for diagnosis and management of hyperthyroidism, serum thyroid-stimulating hormone (TSH) should be the initial biochemical evaluation, because it has the highest sensitivity and specificity in the diagnosis of thyroid disorders. (medscape.com)
- There are excellent remedies in Homeopathy for the patients suffering from Thyroid Disorders. (kidneyfailed.in)
- Since the hyper-androgenic syndromes are often associated with menstrual disorders, it is a valuable and easy-to-use resource, not only for endocrinologists but for gynecologists as well. (nshealth.ca)
- Dr. Soszka is a functional medicine and naturopathic physician who, for 23 years, has helped patients with thyroid disorders regain control of their lives. (thethyroidfixbook.com)
Metabolism10
- Thyroid hormone is well known for its profound direct effects on cardiovascular function and metabolism. (jci.org)
- In this work, we present the results of calcium metabolism analysis in such patients.Subjects and methods: 3929 operations of patients with different thyroid diseases were performed during 2010 2012 years. (endocrine-abstracts.org)
- Symptoms of decreased thyroid hormones include slowed metabolism, tiredness, and weight gain. (drdady.com)
- For patient education resources, see Thyroid & Metabolism Center, as well as Thyroid Problems. (medscape.com)
- Hormone Boost is blended to support horses with poor metabolism, low energy, slow hair shedding and excessive sweating. (littlebitwestern.ca)
- The constant high level of cortisol hormone in the blood also upsets the metabolism. (smarthealthcodes.com)
- Thyroid hormones are an extremely important group of hormones in terms of metabolism and they directly control energy metabolism. (smarthealthcodes.com)
- Thyroid hormone deficiency causes a slowdown in metabolism and a decrease in energy levels. (smarthealthcodes.com)
- Thyroid hormone is required for normal brain and somatic tissue development in the fetus and neonate, and, in people of all ages, thyroid hormone regulates protein, carbohydrate, and fat metabolism. (msdmanuals.com)
- Regulation of Calcium Metabolism Calcium (Ca) is required for the proper functioning of muscle contraction, nerve conduction, hormone release, and blood coagulation. (msdmanuals.com)
Triiodothyronine7
- The binding of triiodothyronine (T3), the biologically active form of thyroid hormone, induces a conformational change in the TR that leads to a dynamic exchange of associated transcriptional corepressor and coactivator complexes. (jci.org)
- It is characterized by a defective physiological resistance to thyroid hormones, resulting in the elevation of thyroxin and triiodothyronine in the serum. (nih.gov)
- Thyroid Hormone Receptor alpha is encoded by this gene is a nuclear hormone receptor for triiodothyronine. (novusbio.com)
- Hauffa B.P., De Nayer P. Metabolic and cardiovascular responses to exogenous triiodothyronine favour nontreatment of a girl with familial receptor-positive thyroid hormone resistance. (rusmedserv.com)
- Triiodothyronine (T3) levels are obtained in suspected cases of hyperthyroidism, either because the patient has typical symptoms or when the thyroid-stimulation hormone (TSH) levels are lower than normal. (medscape.com)
- Increased free T3 values are found in triiodothyronine toxicosis, hyperthyroidism, and peripheral resistance syndrome. (medscape.com)
- They are also increased in association with a daily dosage of 25 µg or more of triiodothyronine or 300 µg of thyroxine (T4) and elevation in the levels of thyroid-binding globulin. (medscape.com)
Diseases5
- These diseases usually manifest as hypersecretion or hyposecretion of PITUITARY HORMONES. (uchicago.edu)
- When it comes to hypo- vs. hyperthyroidism, the most common difference between the two diseases relates to hormone levels. (drdady.com)
- The association is high with another autoimmune thyroid disease, Hashimoto thyroiditis, and to a lesser degree with other autoimmune diseases in other endocrine glands and other systems in the same person. (medscape.com)
- Dr. Soszka explains why it's vital to correctly diagnose and treat autoimmune thyroid diseases such as Hashimoto's thyroiditis as early as possible. (thethyroidfixbook.com)
- Chronic Fatigue Syndrome negatively impacts life quality and may be sign of serious diseases! (smarthealthcodes.com)
Iodine5
- Thyroid ultrasonography and thyroid radioactive iodine uptake have similar sensitivity for the diagnosis of Graves disease. (medscape.com)
- Advantages of ultrasonography include the absence of exposure to ionizing radiation and a higher accuracy in the detection of thyroid nodules and lower cost than with radioactive iodine uptake. (medscape.com)
- Thyroid scintigraphy, imaging of the thyroid with the aid of radioactive iodine, usually iodine-123 (123I), is performed in the nuclear medicine department of a hospital or clinic. (kidneyfailed.in)
- Iodine, ingested in food and water as iodide, is actively concentrated by the thyroid and converted to organic iodine (organification) within follicular cells by thyroid peroxidase. (msdmanuals.com)
- Once iodination occurs, the iodine does not readily leave the thyroid. (medscape.com)
Serum10
- Reduced sensitivity of end organs to thyroid hormone characterized by elevated serum levels of free thyroid hormone with nonsuppressed thyroid stimulating hormone. (nih.gov)
- Selective pituitary resistance to thyroid hormone (PRTH) results in continued thyroid-stimulating hormone (TSH) production driving hypersecretion of T3 and T4 to establish a new equilibrium, with high serum levels of free thyroid hormones together with a nonsuppressed TSH. (nih.gov)
- Generalized thyroid hormone resistance is characterized by elevated serum levels of free thyroid hormones with inappropriately elevated thyroid-stimulating hormone (TSH) as well as clinical and biochemical evidence of decreased thyroid hormone action. (nih.gov)
- TBG is a major thyroid hormone transport protein in serum. (sch.ac.kr)
- We experienced a case that a man who had an abnormal thyroid function showed unexpectedly low concentrations of serum total thyroxine. (sch.ac.kr)
- Ercan-Fang S., Schwartz H.L., Mariash C.N., Oppenheimer J.H. Quantitative assessment of pituitary resistance to thyroid hormone from plots of the logarithm of thyrotropin versus serum free thyroxine index. (rusmedserv.com)
- Adequate thyroid hormone replacement results in normalization of serum TSH. (medscape.com)
- In the rare syndromes of thyroid hormone resistance, serum TSH levels are elevated in the presence of normal-to-high serum total T4 concentration. (medscape.com)
- Background: Resistance to thyroid hormone (TH) beta (RTHβ), caused by mutations in THRB, is characterized by elevated serum (F)T4 accompanied by non-suppressed TSH concentrations. (endocrine-abstracts.org)
- Approximately 0.3% of total serum T3 and 0.03% of total serum T4 are free and in equilibrium with bound hormones. (msdmanuals.com)
Thyroxine2
- The transport proteins such as thyroxine-binding-globulin (TBG), albumin and transthyretin carry over 99% of circulating thyroid hormones. (sch.ac.kr)
- Surprisingly, we report that treatment of RTHα patients with thyroxine to overcome tissue hormone resistance does not elevate their heart rate. (cam.ac.uk)
Deficiency3
- Although TBG deficiency does not have metabolic consequences, it has diagnostic implications as it can lead to an incorrect interpretation of thyroid function tests. (sch.ac.kr)
- Among the rare causes include congenital TSH deficiency, as well as the syndrome of peripheral resistance to thyroid hormones. (synthroidnews.net)
- Isolated TSH deficiency is far less common than multiple anterior pituitary hormone deficiencies. (medscape.com)
Follicular cells3
- Microscopically, the thyroid follicular cells are hypertrophic and hyperplastic, and they contain little colloid (stored hormone) and show evidence of hypersecretion. (medscape.com)
- Tyrosine in contact with the membrane of the follicular cells is iodinated at 1 (monoiodotyrosine) or 2 (diiodotyrosine) sites and then coupled to produce the 2 forms of thyroid hormone. (msdmanuals.com)
- Once inside the thyroid follicular cells, T3 and T4 are cleaved from thyroglobulin. (msdmanuals.com)
Mutations5
- Screening of nineteen unrelated families with generalized resistance to thyroid hormone for known point mutations in the thyroid hormone receptor beta gene and the detection of a new mutation. (nih.gov)
- Identification of thirteen novel mutations in the thyroid hormone receptor beta gene. (rusmedserv.com)
- Mutations in THRA, a ligand-inducible transcription factor, cause Resistance to Thyroid Hormone α (RTHα). (endocrine-abstracts.org)
- 230) different mutations in thyroid hormone receptor β (TRβ) causing Resistance to Thyroid Hormone β (RTHβ), localise to three clusters within its hormone binding domain. (endocrine-abstracts.org)
- Two intriguing studies using novel models of thyroid hormone receptor alpha ( THRA ) mutations, which cause thyroid hormone resistance syndrome (RTH), were published in 2020. (e-enm.org)
Hypothalamus2
- Here, we describe a previously unknown population of parvalbuminergic neurons in the anterior hypothalamus that requires thyroid hormone receptor signaling for proper development. (jci.org)
- Disease features arise from variable resistance to TH action in tissues expressing Thyroid Hormone Receptor (TR) β (hypothalamus, pituitary, liver) and from thyrotoxic effects in tissues expressing TRα (heart, bone, brain). (endocrine-abstracts.org)
Thyrotropin2
- Abel E.D., Kaulbach H.C., Campos-Barros A., Ahima R.S., Boers M.E., Hashimoto K., Forrest D., Wondisford F.E. Novel insight from transgenic mice into thyroid hormone resistance and the regulation of thyrotropin. (rusmedserv.com)
- In selected cases, total hormone levels, thyrotropin-releasing hormone (TRH) stimulation test, thyroglobulin levels, and thyroid antibodies may be advised. (medscape.com)
Symptoms10
- Wilson's Syndrome refers to low basal body temperature and other nonspecific symptoms occurring in the presence of normal thyroid hormones. (chriskresser.com)
- Patients with clinical symptoms consistent with Bamforth-Lazarus syndrome are candidates for this test. (preventiongenetics.com)
- However, a combination of the right nutrients and treatment with whole food supplements and herbs can help restore thyroid function and minimize your symptoms. (drdady.com)
- It stimulate the body to reactivate the hormone secretions, replenish and restore the thyroid tissue through the pituitary and other glands as a whole allowing the body to heal itself.The fundamental understanding of Homeopathy is that substances that can cause a pattern of symptoms in a healthy person can activate a cure of that pattern of symptoms in a sick person when those substances are Homeopathically potentized. (kidneyfailed.in)
- syndrome - The aggregate of symptoms and signs associated with any morbid process, and constituting together the picture of the disease. (en-academic.com)
- As we age, our changing hormones can contribute to several physical and emotional symptoms, often negatively impacting our daily lives. (drmelindasilva.com)
- This test may be done if you have symptoms of abnormal male hormone (androgen) production. (medlineplus.gov)
- If you are experiencing the following symptoms, hormone replacement therapy may be an option for you. (lifegaines.com)
- Every woman's hormone-driven bodily change is different, but an imbalance in normal hormone levels can make the symptoms seem much worse. (lifegaines.com)
- Due to the hormonal imbalance in the body, hormone levels fluctuate during the perimenopause era, often triggering the typical symptoms of menopause, such as hot flashes and severe mood swings. (lifegaines.com)
Tissues5
- It has been a long-standing challenge to decipher the mechanisms by which thyroid hormone regulates such a wide range of cellular processes in so many different tissues. (jci.org)
- Introduction: Resistance to thyroid hormone (RTH) is an inherited syndrome characterized by reduced responsiveness of target tissues to thyroid hormone (TH). (endocrine-abstracts.org)
- The presence of a variety of thyrotoxic features, including palpitations, anxiety, tremor, heat intolerance, insomnia, weight loss, and increased stool frequency, suggests that peripheral tissues are less refractory to thyroid hormones than the pituitary (summary by Adams et al. (nih.gov)
- Membrane transporters are rate-limiting for cellular entry of thyroid hormones (T4, T3) into some tissues, with selenocysteine-containing, deiodinase enzymes (DIO1, DIO2) converting T4 to the biologically active hormone T3. (cam.ac.uk)
- From the thyroid hormones released into the bloodstream, a peripheral deiodinase in target tissues such as the pituitary, kidney, and liver selectively removes iodide from the 5' position of T4 to make T3, which is a much more active molecule. (medscape.com)
Nodules2
- In case of multinodular goiter each nodule was punctured and examined separately.3929 cases (8%) were noninformative out of 49 419 FNAB of thyroid nodules performed in Nor. (endocrine-abstracts.org)
- Nodules of the thyroid may or may not be cancer. (kidneyfailed.in)
Regulates2
- Recent evidence, however, suggests that the hormone also regulates these systems indirectly through the central nervous system. (jci.org)
- In a normal menstrual cycle, a balance between the hormones estrogen and progesterone regulates the buildup of the lining of the uterus (endometrium), which is shed during menstruation. (laboratoryinsider.com)
Imbalance5
- Hormone imbalance. (laboratoryinsider.com)
- If a hormone imbalance occurs, the endometrium develops in excess and eventually sheds by way of heavy menstrual bleeding. (laboratoryinsider.com)
- This leads to hormone imbalance and may result in menorrhagia. (laboratoryinsider.com)
- If a hormone imbalance occurs, the endometrium grows excessively and eventually sheds by way of heavy menstrual bleeding. (create-health.com.au)
- As a result, hormone imbalance can appear in a variety of ways, making it difficult to spot. (lifegaines.com)
Peripheral2
- Defective thyroid hormone feedback regulation in the syndrome of peripheral resistance to thyroid hormone. (uchicago.edu)
- Peripheral resistance to thyroid hormones. (machtbranchen.com)
Protein3
- For example, the changes observed in the thyroid axis in acute illness are similar to those observed in fasting, which can be interpreted as an attempt to reduce energy expenditure and protein wasting. (chriskresser.com)
- Much of the testosterone in the blood is bound to a protein called sex hormone binding globulin (SHBG). (medlineplus.gov)
- High-sensitivity c-reactive protein, testosterone and sex hormone binding globulin. (veganvan.life)
Sensitivity to thyroid1
- Today, we know that any abnormality in the chain of processes involving the creation, transport, adequate deiodination, receptor response to the action of thyroid hormones or histone acetylation, may result in decreased sensitivity to thyroid hormones. (amedi.sk)
Intracellular2
- Thyroid hormone acts through the intracellular thyroid hormone receptor (TR), which belongs to the nuclear receptor family and acts as a ligand-regulated transcription factor ( 4 , 5 ), eliciting cellular responses by binding to and regulating the expression of target genes. (jci.org)
- This inherited condition with reduced intracellular action of thyroid hormones is accompanied by persistent elevation of fT4 and fT3 with inadequately high TSH. (amedi.sk)
Thyroiditis2
- Selenium is essential to a healthy thyroid and the first thing I recommend for those with autoimmune thyroiditis or Hashimoto's. (drdady.com)
- If the thyroid is enlarged and painful, the likely diagnosis is subacute painful or granulomatous thyroiditis. (medscape.com)
Testosterone3
- A testosterone test measures the amount of the male hormone, testosterone, in the blood. (medlineplus.gov)
- when women have too much testosterone, it throws the ratio of female to male hormones out of balance. (veganvan.life)
- Dr. Fuksina has the expertise to precisely balance bio-identical hormones such as Estrogen, Testosterone, DHEA, and Thyroid Hormone, returning the body to its optimum hormone levels, allowing it to function at peak performance, restoring health and wellness. (newjerseybioidenticalhormonedoctors.com)
Estrogen1
- Hormone replacement therapy for women can help restore the levels of estrogen your body produced in your younger years. (lifegaines.com)
TRIAC2
- Tiratricol (also known as TRIAC or triiodothyroacetic acid) is a thyroid hormone analogue. (wikipedia.org)
- Darendeliler F., Bas F. Successful therapy with 3,5,3'-triiodothyroacetic acid (TRIAC) in pituitary resistance to thyroid hormone. (rusmedserv.com)
Bioidentical Hormone7
- Thanks to advancements in medical science, it's now possible to achieve hormonal balance and regain control over your well-being through a revolutionary treatment known as bioidentical hormone replacement therapy (BHRT). (drmelindasilva.com)
- At San Diego's premier anti-aging and wellness medical spa, Dr. Melinda Silva specializes in providing customized bioidentical hormone replacement therapy treatments to help clients feel their best. (drmelindasilva.com)
- From improved energy levels and mood stability to better sleep quality and weight management, the benefits of bioidentical hormone replacement therapy are nothing short of remarkable. (drmelindasilva.com)
- Thankfully, the innovative treatment, bioidentical hormone replacement therapy (BHRT), offers a safe and effective solution to these challenges. (drmelindasilva.com)
- Bioidentical hormone replacement therapy (BHRT) involves the use of hormones that are structurally identical to those produced by your body. (drmelindasilva.com)
- New Jersey BHRT Locator® New Jersey Bioidentical Hormone Doctors Locator features a large selection of hormone doctors and anti aging clinics specializing in the use of (BHRT) Bioidentical Hormone Replacement Therapy in the state of New Jersey including North Jersey, Central Jersey, and South Jersey areas. (newjerseybioidenticalhormonedoctors.com)
- Rouzbeh Sattari, M.D. believes that not all people are the same, so an individualized Bioidentical Hormone Replacement Therapy program will be developed to meet your needs. (newjerseybioidenticalhormonedoctors.com)
Recessive2
- Forrest D., Hanebuth E., Smeyne R.J., Everds N., Stewart C.L., Wehner J.M., Curran T. Recessive resistance to thyroid hormone in mice lacking thyroid hormone receptor beta: evidence for tissue-specific modulation of receptor function. (rusmedserv.com)
- Bamforth-Lazarus syndrome is inherited in an autosomal recessive manner. (preventiongenetics.com)
Hyperthyroidism1
- As its name suggests, hyperthyroidism occurs when your body makes too much of the thyroid hormones. (drdady.com)
Patients with thyroid cancer2
- It is indicated in the management of thyroid hormone resistance syndrome and is used, in combination with levothyroxine, to suppress thyroid-stimulating hormone production in patients with thyroid cancer. (wikipedia.org)
- Could circulating thyroglobulin autoantibodies be an indicator of treatment response to lenvatinib among patients with thyroid cancer? (medscape.com)
Gene3
- Data analysis identified a novel spliceogenic variant (c.283 + 1G>A) in the thyroid hormone receptor beta gene (THRB) as the candidate disease-associated variant. (figshare.com)
- Ala248Gly) in the FOXE1 gene has also been observed in a family with non-medullary thyroid carcinoma (FNMTC) (Pereira et al. (preventiongenetics.com)
- We first showed that the FKHL15 gene is the human homologue of TTF-2, identifying a homozygous, loss-of-function, mutation in two siblings with CH, thyroid agenesis, clef. (endocrine-abstracts.org)
Biosynthesis2
- The thyroid is the only tissue that can oxidize iodide to a higher valence state that is essential for iodide organification and thyroid hormone biosynthesis. (medscape.com)
- An enzyme called deiodinase removes iodide from the inactive monoiodothyronine and diiodothyronine molecules in the thyroid, which restores most of the iodide used in the biosynthesis of T4 and T3. (medscape.com)
Nodule1
- Background: It is disputable whether to repeat FNAB after the first one was nondiagnostic, or to submit the patient to operation.Methods: Indication for FNAB was a thyroid nodule of ≥1 cm or of a less size with clinical or ultrasound features of malignancy. (endocrine-abstracts.org)
Androgen1
- Androgen insensitivity syndrome is caused by a mutation in the androgen receptor, and it affects 1 in 100,000 chromosomal males. (medquizzes.net)
Mutation in thyroid2
- Furthermore, the findings may be beneficial for treatment of the recently identified patients that have a mutation in thyroid hormone receptor α1. (jci.org)
- Resistance to thyroid hormone due to a mutation in thyroid hormone receptor alpha (RTHα) is a syndrome whose features include delayed growth and neurocognitive development. (endocrine-abstracts.org)
Clinical manifestations1
- A better understanding of the various clinical manifestations and presentations of Van Wyk Grumbach syndrome could lead to earlier diagnoses and treatment. (medscape.com)
Disease7
- When it comes to thyroid disease, there are several ways the thyroid can malfunction. (drdady.com)
- Using high resolution cryo-electron microscopy, the fine functional structure of thyroglobulin was demonstrated, and new insights into the pathogenesis of thyroid disease were achieved, with a focus on research into thyroid-disrupting chemicals and the gut microbiome. (e-enm.org)
- Polycystic ovarian syndrome was first identified by Irving Stein and Michael Leventhal in 1935, and the condition was originally called Stein-Leventhal disease. (mum.org)
- Thyroid Disease is a medical condition impairing the function of the thyroid. (kidneyfailed.in)
- General practitioners (GPs) are frequently dealing with cases of paediatric thyroid disease. (racgp.org.au)
- Paediatric thyroidology is a special edition in the 'Endocrine development' series dedicated to thyroid disease in children. (racgp.org.au)
- and advancements in science in developed countries have made it possible for people affected by this syndrome to live longer, but an extended life span has brought with it Alzheimer's disease (AD), which exacerbates the cognitive decline in these individuals. (bvsalud.org)
Menstrual2
- If your ovaries don't release an egg (ovulate) during a menstrual cycle (anovulation), your body doesn't produce the hormone progesterone, as it would during a normal menstrual cycle. (laboratoryinsider.com)
- As a result, the body does not produce adequate levels of a hormone called progesterone during menstrual periods. (femhealthproject.com)
Thyroglobulin1
- Thyroid hormones thus formed are stored in the thyroglobulin until it is degraded and the hormones are released into the circulation. (medscape.com)
Receptor alpha2
- Western Blot: TR alpha/NR1A1/Thyroid Hormone Receptor alpha Antibody [NBP2-22523] - Analysis of 25 ug of mouse thyroid (lane 1), NIH-3T3 (lane 2) and A431 (lane 3) cell lysates onto an SDS polyacrylamide gel. (novusbio.com)
- 1 ] demonstrated the essential actions of thyroid hormone receptor alpha (TRα) on the normal development of the human cerebral cortex. (e-enm.org)
Abnormal1
- The lack of clear-cut, abnormal thyroid function tests. (endocrine-abstracts.org)
Hirsutism1
- But high levels of these hormones can lead to hirsutism. (massgeneral.org)