Graves’ disease: A classic case of diffuse toxic goiter and hyperthyroidism

Oct 20, 2014 Ruchira Dhoke Lifestyle & Health, Women's Health 0

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Diffuse toxic goiter also commonly known as Graves’ disease is a classic case of hyperthyroidism, a generalized hyperactivity of the entire thyroid gland and diffuse goiter associated with a unique manifestation infiltrative orbitopathy and ophthalmopathy and less commonly with an infiltrative dermopathy.

It is named for Robert James Graves, an Irish physician, who described this form of hyperthyroidism in 3 females about 150 years ago.

What are the risk factors for Graves’ disease?

Being a multifactorial disease genetic, environmental, and hormonal factors play important role as predisposing factors of the Graves’ disease:

Genetic factors

High prevalence of Graves’ disease in immediate family members and relatives support that genetic factors are involved. Polymorphism is expressed in HLA-DR, CTLA-4 and PTPN-22 genes which are associated with increased risk of Graves’ disease

Environmental Factors

1. Infection: Graves’ disease is associated with infectious agents who have molecular resemblance with the self-antigen.
2. Stress: Stressful life events are found to precede the onset of Graves’ disease.
3. Gender: 5-10 times more prevalent in females than males.
4. Pregnancy: Postpartum period is an important risk factor for both the onset and relapse of Graves’ disease.
5. Smoking: Smoking is considered as a minor risk factor for Graves’ disease but a major risk factor for Graves’ ophthalmopathy
6. People with other autoimmune diseases have found to be at greater risk of developing Graves’ disease. Conditions associated with Graves’ disease include type 1 diabetes, rheumatoid arthritis, and vitiligo—a disorder in which some parts of the skin are not pigmented.

Pathogenesis of Graves’ disease 

Humoral and cell mediated immunity directed against different thyroid auto-antigens can be seen in in Graves’ disease, an organ specific autoimmune disorder. The immune system of the body makes an antibody called thyroid-stimulating immunoglobulin (TSI) also called TSH receptor antibody that attaches to thyroid cells. TSI behaves like TSH and stimulates the production of the thyroid hormone in large quantities. The TSI antibody sometimes blocks the thyroid hormone production which leads to mixed symptoms thereby making the diagnosis more difficult.

Auto-antigens involved are: TSHR as a primary auto-antigen, other auto-antigens like thyroglobulin and thyroid peroxidase are secondary

What are the symptoms of Graves’ disease?

Graves’ disease symptoms resemble those of hyperthyroidism which include:

1. Nervousness or irritability
2. Fatigue or muscle weakness
3. Heat intolerance
4. Trouble sleeping
5. hand tremors
6. Rapid and irregular heartbeat
7. Frequent bowel movements or diarrhea
8. Weight loss
9. Goiter, which is an enlarged thyroid, neck looks swollen and interferes with normal breathing and swallowing
10. Thick and red skin on their shins which is usually painless called pretibial myxedema or Graves’ dermopathy.
11. Graves’ ophthalmopathy (GO): the eyes appear enlarged as their eyelids get retracted and bulge out from the eye sockets. About 25 to 30 percent of people with Graves’ disease develop mild GO, and 2 to 5 percent develop severe GO.

How is Graves’ disease diagnosed?

Diagnosis of Graves’ disease is based on physical examination and a medical history. Blood tests and other diagnostic tests can confirm the diagnosis.

Blood tests:

1. TSH test: below-normal levels of TSH
2. T3 and T4 test:  normal to elevated levels of T4, and elevated levels of T3

Radioactive iodine uptake test: High levels of iodine uptake by the thyroid gland indicate Graves’ disease.

Thyroid scan: The scan shows how and where iodine is distributed in the thyroid. In case of Graves’ disease the entire thyroid gland is involved.

How is Graves’ disease treated?

An endocrinologist might recommend:

Radioiodine Therapy

The therapy involves uptake of radioactive iodine¹³¹ by mouth. Iodine¹³¹ gradually destroys the cells that make up the thyroid gland but other body tissues remain unaffected.

Medications

Beta blockers: To reduce symptoms of hyperthyroidism, such as tremors, rapid heartbeat, and nervousness.  

Antithyroid medications:  Interferes with thyroid hormone production

It is important to keep in mind that iodine is an essential mineral for the thyroid gland and its normal functioning. However, people with autoimmune thyroid disease are found to be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodine may cause or worsen hyperthyroidism. 

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• auto-antibodies, auto-antigen, autoimmune disorder, Goiter, Graves’ disease, hyperthyroidism, Iodine, myxedema, ophthalmopathy

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