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It could be more than just stress and fatigue.
Find out if it could be Graves’ Disease.
btns:
Check your symptoms
Learn about the test
The symptoms are common and easy to explain away – but a simple blood test can provide an effective and possibly life-savings diagnosis.
• Low or suppressed Thyroid Stimulating Hormone (TSH), along with symptoms, is an early indicator of Hyperthyroidism.
• At least 70% of Hyperthyroid patients suffer from an autoimmune disorder called Graves’ disease.
• Thyroid Stimulating Immunoglobulins (TSIs) are antibodies that cause Graves’ disease.
Thyretain® TSI Reporter BioAssay is for the specific detection of thyroid-stimulating immunoglobulin (TSI) in the bloodstream, the antibodies directly linked to Graves’ disease.
A timely, accurate diagnosis is crucial.
• Symptoms alone aren’t enough for diagnosis. To really know for sure, you have to measure for TSI antibodies.
• Thyretain is the only FDA-cleared assay specifically designed to detect the TSI antibodies directly linked with Graves’ disease.
• With a simple blood sample, a positive TSI result can lead to diagnostic confidence in pursuing the desired treatment plan with the patient
• This result is commercially available in large reference laboratories and regional centers of excellence
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Diagnosing Graves’ Disease.
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Phy page:
The most common autoimmune disorder is one of the most difficult to diagnose.
Early visual symptoms aren’t enough. Thyretain is the only FDA-approved assay specifically designed to detect the TSI antibodies directly linked with Graves’ disease.
See how Thyretain works
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Diagnosing Graves’ Disease
TSI Function
How can thyretain help?
Detecting TSI using Thyretain
Treatment options
Diagnosing Graves’ disease
• Hyperthyroidism is typically characterized by signs like low or suppressed thyroid stimulating hormone (TSH) levels and elevated T4 and/or T3 values.
• Over 70% of these hyperthyroid patients have the autoimmune disease called Graves’ disease.
• The causative agent of Graves’ disease is thyroid stimulating immunoglobulin (TSI).
• Elevated levels of TSI in a patient’s bloodstream can be detected using the Thyretain TSI Reporter BioAssay. Positive results can provide physicians with an important specific aid in the diagnosis of Graves’ disease.
*References
The Most Common Autoimmune Disorder in the United States
[un_chart]
[mapcalpeop]
3 million
People in the U.S.
12,000
cases per month
8:1
women to men
[acc]
Signs and Symptoms of Graves’ Disease
Low TSH and symptoms usually begin the investigation
Hyperthyroidism suspected … why?
70% of Hyperthyroid patients are TSI positive
Which Thyroid antibodies are specific?
Antibody Specificity Disease Association
TSH-Receptor (TSI): Graves’ Disease 90-99%
TSH-Receptor: Hashimoto’s Thyroiditis 0-10%
Peroxidase TPOAb: Graves’ Disease 70-80%
Peroxidase TPOAb: Hashimoto’s Thyroiditis 90-95%
Thyroglobulin TgAb: Graves’ Disease 20-40%
Thyroglobulin TgAb: Hashimoto’s Thyroiditis 30-50%
1 Mariotti S, et al. Clin Exp Immunol 1978
2 Amino N, et al. Clin Endocrinol 1976
3 Miles J, et al. Ann Clin Biochem 1998
4 Feldt-Rasmussen U. Clin Chem 1996
Why not TRAb
Specificity and Functionality
• Stimulating (TSI) cause hyperthyroidism
• Blocking (TBI) cause hypothyroidism TRAb assays cannot differentiate between the TSHr types
• Neutral (binding)
[acc]
Diagnostic Dilemma
There are classic symptoms that are usually definitive and associated with Hyperthyroidism and Hypothyroid. But as is true of many autoimmune disorders, there are many earlier symptoms are not mutually exclusive to one diagnosis.
What else affects the diagnosis?
• Age
• Gender
• Ethnicity
• Genetics
• Medical History
• Smoking
• Contraceptives
• Current Medications
• Others…
*References
TSI Function
In normal thyroid metabolism, thyroid hormone production is tightly regulated by the hypothalamic-pituitary-thyroid axis.
Normal Thyroid Function
Negative feedback loop
[un_diagram01]
Graves’ disease is an autoimmune disorder that primarily affects the thyroid. The Thyroid is responding to the stimulation of TSI and is not “malfunctioning” per se. Thyroid Stimulating Immunoglobulin (TSI) mimics the action of TSH on the TSH receptor, in that it causes T4 to be over produced. TSI of course is not regulated by the same negative feedback system.
Effects of TSI – Patients with Graves’ Disease
[un-diagram02]
How can Thyretain help?
Find the specific culprit behind the disease. Based on a novel genetically engineered cell line, Thyretain detects only stimulating immunoglobulins. The engineered cell technology also enhances the sensitivity for detecting TSI , providing improved results over currently available non-specific assays.
Graves’ Disease is an Autoimmune Disorder
Thyretain Can Quickly Help Differentiate Graves’ Disease Induced Autoimmune Hyperthroidism from Non-Autoimmune Hyperthroidism
[un_diagram03]
• TSI is the autoantibody that stimulates TSH receptors – and is the cause of Graves’ Disease.1
• Quidel’s TSI Reporter Assay (Thyretain) is the only FDA-cleared test that specifically identifies TSI.2
• If a positive TSI result, patient has autoimmune disease; a differential diagnosis of Graves’ can be confirmed.
Detecting TSI using Thyretain
Thyretain is a living bioassay system. It has been genetically engineered with chimeric human TSH receptors that are linked to a luciferase gene (firefly light) and will produce light indicating the presence or absence of TSI antibodies.
As a living system, these cells respond to TSI and have been shown to correlate with disease severity and extrathyroidal manifestations (i.e., eye or skin disease associated with TSI).
[phy_diagram01]
Treatment options
(Treatment is a personal choice and Quidel does not advocate one therapy over another)
Medical Management Therapy
Antithyroid drugs (ATD) are suppressive drugs meant to inhibit the production of thyroid hormones T4 and/or T3 in an effort to treat the symptoms of Graves’ disease. These medications include Methimazole (MMI), and propylthiouracil (PTU). Methimazole or MMI, and propylthiouracil act by inhibiting the synthesis (the production) of thyroid hormone though PTU use has been stopped especially in children, due to effects on liver function. MMI is widely used and does not carry this restriction. Medical management has a success rate of ~45-50% using current medical management guidelines. Patients can retain their thyroid and may have remission of the autoimmune response. For those who do not respond to the ATD therapy, those patients can either continue the ATD or chose the definitive cure options listed below.
There are some side effects for ATD that could occur and most are mild (rash ~3-4%) one in particular is severe; agranulocytosis (~0.3%). This is extremely rare and corrected by stopping the ATD therapy.
*References
Definitive Therapies
Radiodine Ablation Therapy
Iodine-131 (Radioiodine) is given orally to destroy the function of a hyperactive gland. Usually one dose is sufficient but some patients might require more than one treatment. The radioactive iodine is picked up by the active cells in the thyroid, which use iodine to produce T4, and destroys these cells.
Radioiodine is an ablative approach and is considered the definitive cure for hyperthyroidism brought about by eliminating most if not all of the target organ, however, >80% of patients develop permanent hypothyroidism soon after treatment and require lifelong synthetic hormone replacement. Hypothyroidism is believed to be an easier disease to manage than hyperthyroidism.
Theoretically the radioiodine could be dosed to only destroy part of the thyroid gland, but the dosage is extremely difficult to determine, and if thyroid tissue remains, the body can still produce TSI against any remnant tissue. These antibodies can still cause Graves’ eye disease even after ablative therapy. . Although widely used and relatively safe, for incompletely ablated women in their child bearing years these antibodies could be passed across the placenta during pregnancy, leading to the child developing Graves’ disease. This has been addressed in the ATA and AACE guidelines for treating patients with a history of thyroid disease in pregnant women and those considering pregnancy who have undergone this treatment. (see Graves’ disease and Pregnancy)
Surgery
This option is also considered a definitive cure for Graves’ disease. For patients who cannot tolerate medicines or who are allergic to or decline iodine-131, a surgical treatment option is available. Full or partial thyroidectomy is used uncommonly in the US and is not considered a primary option for Graves’ disease treatment, due to risks from surgery and anesthesia. If this option is chosen it is important to select a surgeon with sufficient skill in thyroid surgery specifically.
*References
Treatment can vary by region
Percentage choosing treatment as primary therapy
[un_diagram05]
[acc]
Graves' Disease and Pregnancy
TSI antibodies can pass through the placenta and affect the fetus. As a result, the ATA/AACE issued the following guidance:
• Recommendation 74: TSH receptor (TSH-R) antibody levels should be measured to differentiate the etiology of hyperthyroidism in pregnancy
• Recommendation 75: Patients who were treated for Graves’ disease prior to pregnancy should have TSH-R antibody levels initially during the first trimester and, if elevated, again at 22-26 weeks of gestation
• Recommendation 76: Patients diagnosed with Graves’ disease during pregnancy should have TSH-R antibody levels measured at diagnosis and again at 22-26 weeks of gestation
• Recommendation 77: TSH-R antibody levels measured at 22-26 wks of gestation should be used to guide decisions regarding neonatal monitoring
The American Thyroid Association recommends that the following high-risk women be screened for thyroid disease either prior to becoming pregnant, or as soon as feasible once a woman becomes pregnant:
• Women with a history of thyroid disease or thyroid surgery.
• Women with a family history of thyroid disease
• Women with a goiter
• Women with known thyroid antibodies
• Women with symptoms or clinical signs of hyperthyroidism or hypothyroidism
• Women with Type I diabetes mellitus
• Women with other autoimmune disorders
• Women with infertility
• Women with previous therapeutic head or neck irradiation
• Women with a history of miscarriage or preterm delivery
[org_twin_btns]
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sign up to learn more
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Don’t explain away your symptoms. It could be the most common autoimmune disease.
Learn about the symptoms and how to talk to your doctor.
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What is Graves' Disease?
How can Thyretain help?
What is Graves' Disease?
Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism).
Named for Sir Robert Graves (1796-1853), Graves’ disease is the most common cause of hyperthyroidism.
Graves’ is an autoimmune disease and not necessarily a thyroid disease. With an autoimmune disorder, such as Graves’ disease, your immune system mistakenly turns against your body.
In the matter of Graves’ disease, the antibodies are against the receptors on your thyroid causing your metabolism to speed up.
[pat_ad]
[graves_foun_logo]
The Most Common Autoimmune Disorder in the United States
[un_chart]
[acc]
Signs and Symptoms of Graves’ Disease
Low TSH and symptoms usually begin the investigation
[com_sign_01 -04]
[acc]
Causes of Graves' Disease
For unknown reasons your immune system creates antibodies called thyroid-stimulating immunoglobulins (TSIs). These antibodies cause your thyroid gland to produce more thyroid hormone than your body needs.
The TSIs fool the thyroid gland into over-producing thyroid hormone, which causes hyperthyroidism.
Family history and gender may also be factors.
Effects of TSI
In normal thyroid metabolism, thyroid hormone production is tightly regulated by the hypothalamic-pituitary-thyroid axis. The pituitary gland releases TSH in response to thyroid releasing hormone (TRH) from the hypothalamus, which monitors T4 and T3 levels in the blood stream. TSH binds to its receptor on the thyroid gland and stimulates production and release of T4 and T3. If T4 and T3 levels fluctuate outside of a normal range, TSH production is increased or lowered to compensate.
Normal Thyroid Function
Negative feedback loop
[un_diagram01]
Thyroid Stimulating Immunoglobulin (TSI) mimics the action of TSH on the thyroid gland in that it causes T4 to be over produced, but TSI is not regulated by the same negative feedback system. As a result TSI continues to stimulate the thyroid even after hormone levels are elevated, leading to an overabundance of hormones, and thus hyperthyroidism.
Effects of TSI – Patients with Graves’ Disease
[un_diagram02]
[acc]
Graves' Disease and Pregnancy
TSI antibodies can pass through the placenta and affect the fetus. As a result, the ATA/AACE issued the following guidance:
• Recommendation 74: TSH receptor (TSH-R) antibody levels should be measured to differentiate the etiology of hyperthyroidism in pregnancy
• Recommendation 75: Patients who were treated for Graves’ disease prior to pregnancy should have TSH-R antibody levels initially during the first trimester and, if elevated, again at 22-26 weeks of gestation
• Recommendation 76: Patients diagnosed with Graves’ disease during pregnancy should have TSH-R antibody levels measured at diagnosis and again at 22-26 weeks of gestation
• Recommendation 77: TSH-R antibody levels measured at 22-26 wks of gestation should be used to guide decisions regarding neonatal monitoring
The American Thyroid Association recommends that the following high-risk women be screened for thyroid disease either prior to becoming pregnant, or as soon as feasible once a woman becomes pregnant:
• Women with a history of thyroid disease or thyroid surgery.
• Women with a family history of thyroid disease
• Women with a goiter
• Women with known thyroid antibodies
• Women with symptoms or clinical signs of hyperthyroidism or hypothyroidism
• Women with Type I diabetes mellitus
• Women with other autoimmune disorders
• Women with infertility
• Women with previous therapeutic head or neck irradiation
• Women with a history of miscarriage or preterm delivery
How can Thyretain help?
Thyretain TSI Reporter BioAssay detects TSI, the causative agent of Graves’ disease, in patient serum. Other thyroid receptor antibody (TRAB) assays are nonspecific in that they cannot differentiate between blocking, binding and stimulating antibodies (immunoglobulins). Based on a novel genetically engineered cell line, Thyretain detects only stimulating immunoglobulins. The engineered cell technology also enhances the sensitivity for detecting TSI , providing improved results over currently available non-specific assays.
Thyretain Can Quickly Help Differentiate Graves’ Disease Induced Autoimmune Hyperthroidism from Non-Autoimmune Hyperthroidism
[un_diagram013]
• TSI is the autoantibody that stimulates TSH receptors – and is the cause of Graves’ Disease.1
• Quidel’s TSI Reporter Assay (Thyretain) is the only FDA-cleared test that specifically identifies TSI.2
• If a positive TSI result, patient has autoimmune disease; a differential diagnosis of Graves’ can be confirmed.
[acc]
How does Thyretain work?
The assay is a living system and responds similarly to TSI.
The genetically engineered cell line in Thyretain has a version of the TSH receptor that is naturally found on your own thyroid. When test serum is allowed to incubate with these cells any TSI binds to this receptor and a cyclic AMP triggers the production of firefly luciferase. Just like Fireflies you might see flashing light on a summer evening, the cells emit light that can then be detected using a special device.
[phy_diagram02]
[acc]
Treatment Options
(Treatment is a personal choice and Quidel does not advocate one therapy over another)
Medical Management Therapy
Antithyroid drugs (ATD) are suppressive drugs meant to inhibit the production of thyroid hormones T4 and/or T3 in an effort to treat the symptoms of Graves’ disease. These medications include Methimazole (MMI), and propylthiouracil (PTU). Methimazole or MMI, and propylthiouracil act by inhibiting the synthesis (the production) of thyroid hormone though PTU use has been stopped especially in children, due to effects on liver function. MMI is widely used and does not carry this restriction. Medical management has a success rate of ~45-50% using current medical management guidelines. Patients can retain their thyroid and may have remission of the autoimmune response. For those who do not respond to the ATD therapy, those patients can either continue the ATD or chose the definitive cure options listed below.
There are some side effects for ATD that could occur and most are mild (rash ~3-4%) one in particular is severe; agranulocytosis (~0.3%). This is extremely rare and corrected by stopping the ATD therapy.
*References
Definitive Therapies
Radiodine Ablation Therapy
Iodine-131 (Radioiodine) is given orally to destroy the function of a hyperactive gland. Usually one dose is sufficient but some patients might require more than one treatment. The radioactive iodine is picked up by the active cells in the thyroid, which use iodine to produce T4, and destroys these cells.
Radioiodine is an ablative approach and is considered the definitive cure for hyperthyroidism brought about by eliminating most if not all of the target organ, however, >80% of patients develop permanent hypothyroidism soon after treatment and require lifelong synthetic hormone replacement. Hypothyroidism is believed to be an easier disease to manage than hyperthyroidism.
Theoretically the radioiodine could be dosed to only destroy part of the thyroid gland, but the dosage is extremely difficult to determine, and if thyroid tissue remains, the body can still produce TSI against any remnant tissue. These antibodies can still cause Graves’ eye disease even after ablative therapy. . Although widely used and relatively safe, for incompletely ablated women in their child bearing years these antibodies could be passed across the placenta during pregnancy, leading to the child developing Graves’ disease. This has been addressed in the ATA and AACE guidelines for treating patients with a history of thyroid disease in pregnant women and those considering pregnancy who have undergone this treatment. (see Graves’ disease and Pregnancy)
Surgery
This option is also considered a definitive cure for Graves’ disease. For patients who cannot tolerate medicines or who are allergic to or decline iodine-131, a surgical treatment option is available. Full or partial thyroidectomy is used uncommonly in the US and is not considered a primary option for Graves’ disease treatment, due to risks from surgery and anesthesia. If this option is chosen it is important to select a surgeon with sufficient skill in thyroid surgery specifically.
*References
Treatment can vary by region
[un_chart]
[org_twin_btn]
view Resources
sign up to learn more
++++++++++++++++++++++++++++++++++
resources page:
Resources
side:
Organizations and General Information
Health Economics
TSI Clinical and Analytical Papers
TSI/TBI (Blocking Antibodies) Papers
Management
Pregnancy
Other Disorders
Thyroid Disease; Organizations and General Information
Link to the ATA home page
http://www.thyroid.org/
http://online.liebertpub.com/doi/full/10.1089/thy.2011.0087
American Journal of Medicine Thyroid Disease On-line Library
http://www.amjmed.com/
Go to CME Tab to find the Thyroid Library
Journal of Nurse Practitioners
http://www.npjournal.org/#
Go to the CME tab (coming in September)
Graves’ disease and Thyroid Foundation
http://www.gdatf.org/
American Autoimmune Related Disease Association (AARDA)
http://www.aarda.org/about-aarda/autoimmune-coalition/
PubMed Health Site for Hyperthyroidism
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024711/
Hyperthyroidism
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(03)14073-1/abstract
Epidemiology and Estimated Population Burden of Selected Autoimmune Disease in the United States
http://www.ncbi.nlm.nih.gov/pubmed/9281381
Thyroid Disease; Health Economics
TSI assay utilization: impact on costs of Graves' hyperthyroidism diagnosis
http://www.ncbi.nlm.nih.gov/pubmed/?term=Utilization%3A+Impact+on+Costs+of+Graves'+Hyperthyroidism+Diagnosis
Thyroid Disease; TSI Clinical and Analytical Papers
Novel chimeric thyroid-stimulating hormone-receptor bioassay for thyroid-stimulating immunoglobulins
http://www.ncbi.nlm.nih.gov/pubmed/21070207
A novel thyroid stimulating immunoglobulin bioassay is a functional indicator of activity and severity of Graves' orbitopathy
http://www.ncbi.nlm.nih.gov/pubmed/20237164
Standardization of a bioassay for thyrotropin receptor stimulating autoantibodies
http://www.ncbi.nlm.nih.gov/pubmed/25317659
Clinical relevance of thyroid-stimulating immunoglobulins in Graves' Opthalmopathy
http://www.ncbi.nlm.nih.gov/pubmed/21684605
Graves' orbitopathy activation after radioactive iodine therapy with and without steroid prophylaxis
http://www.ncbi.nlm.nih.gov/pubmed/19567525
Thyroid Disease; TSI/TBI (Blocking Antibodies) Papers
A novel bioassay for anti-thyrotrophin receptor autoantibodies detects both thyroid-blocking and stimulating activity
http://www.ncbi.nlm.nih.gov/pubmed/?term=A+novel+bioassay+for+anti-thyrotrophin+receptor+autoantibodies
Prevalence and functional significance of thyrotropin receptor blocking antibodies in children and adolescents with chronic lymphocytic thyroiditis
http://www.ncbi.nlm.nih.gov/pubmed/19850692
Thyroid Disease; Management
Guidelines for TSH-receptor antibody measurements in pregnancy: results of an evidence-based symposium organized by the European Thyroid Association
http://www.ncbi.nlm.nih.gov/pubmed/9916861
TSH-receptor autoimmunity in Graves' disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study.
http://www.ncbi.nlm.nih.gov/pubmed/18166819
The utility of radioiodine uptake and thyroid scintigraphy in the diagnosis and management of hyperthyroidism
http://www.ncbi.nlm.nih.gov/pubmed/19453641
Diagnosis and Treatment of Graves’ disease
http://www.ncbi.nlm.nih.gov/pubmed/25905403
Thyroid Disease; Pregnancy
Clinical relevance of thyroid-stimulating autoantibodies in pediatric Graves ‘disease-a multicenter study
http://www.ncbi.nlm.nih.gov/pubmed/24517152
Thyroid diseases during pregnancy: A number of important issues
http://www.ncbi.nlm.nih.gov/pubmed/25885104
Spontaneous abortion, stillbirth and hyperthyroidism: a Danish population-based study.
http://www.ncbi.nlm.nih.gov/pubmed/25538898
Autoimmune thyroid disease in pregnant women and their offspring
http://www.ncbi.nlm.nih.gov/pubmed/15251562
Early severe fetal Graves’ disease in a mother after thyroid ablation and thyroidectomy
http://www.ncbi.nlm.nih.gov/pubmed/25710616
A case of fetal hyperthyroidism treated with maternal administration of Methimazole
http://www.ncbi.nlm.nih.gov/pubmed/25421129
Thyroid dysfunction and thyroid autoimmunity in Euthyroid women in achieving fertility
http://www.ncbi.nlm.nih.gov/pubmed/25855922
Thyroid Disease; Other Disorders
Successful surgical treatment of cardiac complication of Graves’ disease
http://www.ncbi.nlm.nih.gov/pubmed/25207231
Cardiovascular involvement in patients with different causes of hyperthyroidism
http://www.ncbi.nlm.nih.gov/pubmed/20585347
Meta-Analysis of the Association between Vitamin D and Autoimmune Thyroid Disease
http://www.ncbi.nlm.nih.gov/pubmed/25854833
Peculiarities of autoimmune thyroid diseases in children with Turner or Down syndrome: an overview.
http://www.ncbi.nlm.nih.gov/pubmed/25971674
Role of the family physician in the care of children with Down’s syndrome
http://www.ncbi.nlm.nih.gov/pubmed/25591185
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