Hashitoxicosis

What happens in hashitoxicosis

In Hashimoto's thyroiditis, the immune system makes antibodies and white cells that attack the thyroid gland. Usually this slowly destroys the gland and causes an underactive thyroid. In some people, especially early on, the attack causes a burst of inflammation that breaks open thyroid follicles. The hormone stored inside (thyroxine, T4, and triiodothyronine, T3) spills into the blood all at once.

The result is thyrotoxicosis, too much thyroid hormone in the blood, even though the gland is not making more hormone. Once the stored hormone is used up, levels fall. The gland then either recovers or, if damage is extensive, becomes underactive.

The word combines Hashimoto's and thyrotoxicosis. Some endocrinologists use it more loosely for any hyperthyroid phase in someone with Hashimoto's antibodies, including rare cases where TSH receptor antibodies (the Graves' type) are also present.

Symptoms

Symptoms are the same as other overactive thyroid states, often milder:

• palpitations or a fast resting heart rate
• anxiety, irritability, restlessness and poor sleep
• shaky hands (tremor)
• sweating and feeling too hot
• weight loss despite a normal appetite
• more frequent bowel movements
• tiredness and muscle weakness
• in women, lighter or irregular periods

The thyroid is usually painless. It may be slightly enlarged and firm (a goiter). Eye bulging, typical of Graves' disease, does not occur in hashitoxicosis.

Hashitoxicosis vs Graves' disease

This is the key distinction, because the treatment is very different.

Diagnosis

1. Thyroid blood tests: low TSH with raised free T4 and/or T3 confirms thyrotoxicosis. A T3 to T4 ratio that is not very high favors a leak rather than overproduction.
2. Antibodies: high thyroid peroxidase (TPO) antibodies point to Hashimoto's. Negative TSH receptor antibodies make Graves' unlikely.
3. Radioactive iodine uptake scan: low uptake shows the gland is not actively making hormone. This test is not done in pregnancy or while breastfeeding.
4. Ultrasound: shows the patchy, darker (hypoechoic) texture typical of Hashimoto's.

Your doctor will also consider other causes of a low uptake picture: postpartum thyroiditis, painful subacute thyroiditis, too much thyroid hormone medicine, and iodine exposure from contrast dye or amiodarone.

Treatment

Because the phase resolves on its own, the aim is to control symptoms and monitor:

• Beta-blockers such as propranolol or atenolol slow the heart rate and reduce tremor, anxiety and sweating. They are stopped as levels normalize.
• Antithyroid drugs (methimazole, propylthiouracil) are generally not helpful, because the gland is not overproducing hormone. They may be used if testing suggests a Graves' component.
• Radioactive iodine and surgery are not used for hashitoxicosis.
• Follow-up blood tests every 4 to 6 weeks track the return to normal and catch the hypothyroid phase that may follow.

If thyroid levels fall low and stay low, or cause symptoms, levothyroxine is started. Many people with Hashimoto's eventually need it long term.

Outlook

Hashitoxicosis typically lasts weeks to a few months. Afterward, thyroid function may return to normal for a time, but because Hashimoto's is a lifelong condition, hypothyroidism develops in many people over the following years. Some people have more than one hashitoxic episode. Yearly TSH checks, or sooner if symptoms change, are sensible.

Frequently asked questions

What is hashitoxicosis?

Hashitoxicosis is a temporary overactive thyroid phase in Hashimoto's thyroiditis. Immune damage to the thyroid releases stored hormone into the blood, causing hyperthyroid symptoms such as palpitations, anxiety and weight loss. It resolves on its own, often followed by normal or underactive thyroid function.

How long does hashitoxicosis last?

It usually lasts about 1 to 3 months, occasionally longer. Thyroid blood tests are repeated every 4 to 6 weeks to confirm when levels are returning to normal and to watch for a hypothyroid phase afterward.

Can you have Hashimoto's and hyperthyroidism at the same time?

Yes. Hashitoxicosis is exactly that: a hyperthyroid phase in someone with Hashimoto's. Rarely, a person has both Hashimoto's antibodies and the TSH receptor antibodies of Graves' disease, and their thyroid can swing between overactive and underactive.

Is hashitoxicosis treated with methimazole?

Usually not. Methimazole stops the thyroid from making new hormone, but in hashitoxicosis the excess comes from stored hormone leaking out. Beta-blockers to control symptoms and monitoring are the standard approach, unless tests point to Graves' disease as well.

Can hashitoxicosis come back?

It can. Because Hashimoto's thyroiditis is ongoing, some people have repeated episodes of inflammation with short hyperthyroid phases, especially in the early years or after pregnancy. Most eventually develop stable hypothyroidism.