Conditions Related to Hashimoto's Thyroiditis

Complications from Thyroid Autoimmunity

Aug 8, 2009 Jim Lowrance

Hashitoxicosis and Hashimoto's Encephalopathy are potentially serious conditions associated with Hashimoto's thyroiditis, that require specific treatments.

Hashimoto’s thyroiditis, an autoimmune disease of the thyroid gland that causes eventual hypothyroidism, can potentially cause other related conditions. Some of these possible complications are more common than others and some can be severe or even life threatening but each of them have treatments available once they are recognized and diagnosed. In the subheadings below, the related conditions called “Hashitoxicosis” and “Hashimoto's Encephalopathy” will be addressed.

Hashitoxicosis

Some patients with Hashimoto’s thyroiditis, experience phases of hyperthyroidism, before progressive hypothyroidism sets in. These spells of hyperthyroid symptoms are referred to as Hashitoxicosis and the condition can cause moderate to full-blown hyperthyroidism that is short term. If these phases were not short term but permanent and progressive, a diagnosis of Graves’ disease (autoimmune caused hyperthyroidism) would instead be given. The cause of Hashitoxicosis is the same as in other hyperthyroid conditions and that is an abnormally high increase in thyroid hormone levels. While some medical sources state that this condition is not common, it may be more common in less severe cases and mild manifestations of Hashitoxicosis may be responsible for anxiety symptoms in some patients.

The cause and Manifestation of Hashitoxicosis

There are two medical opinions as to why these hyperthyroid phases occur before hypothyroidism takes over. One being, that it occurs in some Hashimoto’s patients who are mildly positive for “TSI” antibodies (Thyroid Stimulating Immunoglobulins) that typically cause Graves’ disease hyperthyroidism. The second being that thyroid gland cell-death from the antibodies found in higher titers in Hashimoto’s patients (anti-TPO and Anti-TG) cause release of stored hormone from these dying cells at a faster rate, early into the onset of hypothyroidism. Once this faster phase of cell death levels-off to a slower rate, due to the thyroid gland being unable to generate new cells as quickly, hypothyroidism will then take over. During the hyperthyroid phases, a patient will experience hyperthyroid symptoms including, nervousness, trembling, sweating, increased bowel movements and temporary rapid weight loss.

Treatment for Hashitoxicosis

If a Hashimoto’s patient is already taking thyroid hormone replacement, a treating doctor may need to discontinue their thyroid dose if Hashitoxicosis is experienced. The patient would also need monitored to make sure the hyperthyroid phase is not a permanent transition over to Graves’ disease. Short-term use of a low-dose beta-blocker or anti-thyroid medication might also be administered and/or an anti-anxiety medication. Some patients rarely will continue to phase back and forth between hypothyroidism and hyperthyroidism and in these cases it becomes difficult to administer either thyroid hormone replacement or anti-thyroid drugs. Highly skilled thyroid specialists may chose to administer a combination of both, which is referred to as “block and replace” however, in most cases of highly unstable thyroid function, the patient is referred for thyroidectomy (surgical thyroid removal) or radioactive iodine destruction of the gland (ablation).

Hashimoto's Encephalopathy

The majority of Hashimoto’s patients test positive for thyroid antibodies, the killer cells created by the immune system to attack thyroid proteins that are responsible for the manufacture of thyroid hormone from iodine. While this is a misdirected immune response that causes damage to thyroid gland cells, it occurs due to an incorrect recognition of these natural thyroid cells as threats within the body. As this auto-antibody attack occurs, the body produces an inflammatory response that can contribute to a goiter and according to some medical research opinions, can also contribute to rheumatic symptoms in the body, affecting joints and muscles. With Hashimoto's Encephalopathy, this inflammatory response to these antibodies called the anti-thyroidperoxidase/Anti-TPO, also referred to as “anti-microsomal antibodies”, causes severe inflammation that begins affecting the brain. While the condition is very rare, it can occur in Hashimoto’s patients who are only sub-clinically hypothyroid or even those who are euthyroid (normal hormone levels).

Symptoms of Hashimoto's Encephalopathy

For reasons not fully understood, these high levels of inflammation, affect tissues and nerves in the brain that control motor responses and other brain-signals sent throughout the body. The resulting symptoms of interrupted brain function can result in severe neurological symptoms, including difficulty with walking and speech, involuntary movements, seizures, psychotic episodes (hallucinations and delusions) and stroke type symptoms. Without treatment, brain damage will occur and eventual coma or death may result as well. It is an emergency situation and treatment must be administered immediately once Hashimoto's Encephalopathy has been recognized and diagnosed.

Treatment for Hashimoto's Encephalopathy

Treatment for this inflammatory condition is by administering corticosteroid drugs to reduce the inflammation affecting the brain. These drugs are a type of synthetic cortisol steroid that is commonly available in the brand name Prednisone. The drug is usually only required for a two to three week period and will bring down the inflammation and resolve the neurological symptoms. Some patients require no further treatment once the initial drug therapy is completed while others may need the corticosteroid treatment repeated if the condition relapses.

Hashimoto's Encephalopathy-PubMed

The copyright of the article Conditions Related to Hashimoto's Thyroiditis in General Medicine is owned by Jim Lowrance. Permission to republish Conditions Related to Hashimoto's Thyroiditis in print or online must be granted by the author in writing.

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