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When your thyroid gland shrinks, shrivels up and becomes less functional due to an antibody attack, that’s known as “atrophy.” Atrophy can be caused by Hashimoto’s thyroiditis or a separate condition known as atrophic thyroiditis. Ahead, a look at atrophy of the thyroid gland and its treatments.
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The term “thyroid atrophy” refers to a shriveled and shrunken thyroid gland that is reduced in size. Atrophy typically results in the thyroid failing to produce the thyroid hormones needed for metabolism and bodily functions, a condition known as hypothyroidism.
Most commonly, thyroid atrophy is seen in elderly thyroid patients who have had decades of autoimmune Hashimoto’s thyroiditis.
Atrophic thyroiditis is considered a rare but distinct form of autoimmune thyroid disease – apart from Hashimoto’s and Graves’ disease. The three conditions are considered distinct diseases.
According to research, atrophic thyroiditis can occur alongside other autoimmune thyroid diseases and is estimated to occur in around 10% of Hashimoto’s patients and 25% of Graves’ disease patients. Atrophic thyroiditis is more common in women, especially those over 40, with the risk rising in older women.
While researchers have concluded that atrophic thyroiditis is a “hypothyroid form of Graves’ disease” and has more in common with Graves’ than Hashimoto’s, the course and outcomes of all three conditions are different.
Hashimoto’s thyroiditis is diagnosed primarily by an elevation in thyroid peroxidase antibodies (TPOAb). These antibodies prevent the thyroid from effectively producing thyroid hormones and cause hypothyroidism. Graves’ disease is characterized by elevated thyroid receptor stimulating antibodies. Graves’ antibodies stimulate the gland to overproduce thyroid hormone and cause hyperthyroidism.
The antibodies most associated with atrophic thyroiditis are thyroid receptor blocking antibodies, abbreviated as TBAb. According to Science Direct,
“[Thyroid receptor] blocking antibodies bind to the receptor and prevent activation by TSH, inhibiting the receptor and resulting in chronic autoimmune hypothyroidism and, in some patients, thyroid atrophy.”
Atrophy is not common in most Hashimoto’s patients, and when it occurs, it typically takes decades and only develops when patients are at an advanced age. In atrophic thyroiditis, however, thyroid atrophy can occur at any age and can happen quickly.
Another difference: TPOAb in Hashimoto’s patients doesn’t interfere with the effectiveness of thyroid hormone replacement medications. In atrophic thyroiditis, TBAb antibodies can both stimulate the thyroid and block thyroid receptors. These competing antibodies cause the TSH, Free T4, and Free T3 levels tend to fluctuate wildly, causing overt hypothyroidism.
Atrophic thyroiditis can sometimes go into remission after periods of severe but temporary hypothyroidism. In this situation, permanent thyroid atrophy may not occur. In longer-standing atrophic thyroiditis, however, the atrophy of the gland causes permanent destruction, resulting in permanent hypothyroidism.
In some cases, even when advanced, there are no symptoms. This situation is known as asymptomatic atrophic thyroiditis.
In the earlier stages of symptomatic atrophic thyroiditis, the fluctuations in thyroid levels and function of the thyroid gland usually cause patients to experience changing periods of hypothyroidism, hyperthyroidism, and normal thyroid function. But the predominant symptoms of the condition typically track with the symptoms of hypothyroidism, including fatigue, weight gain, cold intolerance, depression, hair loss, and dry skin.
Patients treated for hypothyroidism with underlying atrophic thyroiditis may also experience periods of hyperthyroidism – weight loss, anxiety, excessive sweating, and heat intolerance, among other symptoms.
In the later stage of atrophic thyroiditis, additional symptoms may appear, including reduced sweating, thinning skin, and a yellow tinge to the skin. It’s also common to see conditions caused by nerve entrapment, such as carpal tunnel or tarsal tunnel syndrome.
In its later stages, atrophic thyroiditis is also sometimes called primary myxedema due to the appearance of myxedema. This condition results in thickened skin, with pitting and swelling due to tissue oversaturation and fluid retention.
While there are no formal diagnostic criteria for atrophic thyroiditis, experts have proposed three factors that should be present to make an accurate diagnosis.
- Laboratory tests showing clinical or subclinical hypothyroidism (i.e., borderline or elevated TSH and low or low-normal Free T4 and Free T3 levels.)
- A positive TBAb antibodies test
- Thyroid ultrasound results show a reduced thyroid volume.
Because the TBAb block the ability to stimulate the thyroid gland to produce thyroid hormone, some patients with atrophic thyroiditis have extremely elevated TSH levels.
The primary treatment for hypothyroidism with thyroid atrophy is thyroid hormone replacement therapy. This can include levothyroxine (synthetic T4) drugs, combination T4/T3 treatment, or natural desiccated thyroid (NDT).
- Growth hormone, when atrophic thyroiditis occurs in children and teenagers and inhibits growth
- Low-dose steroid therapy and anti-inflammatory drugs
- Iodine restriction
When you’re looking for a more accurate thyroid diagnosis and optimal thyroid treatment, consider partnering with Paloma Health. Paloma offers online video visits with expert thyroid doctors, at-home thyroid tests, prescription medications, and personalized care plans. Paloma is a comprehensive, one-stop practice to help manage your hypothyroidism.
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