Hashimoto thyroiditis: Clinical sciences

Hashimoto thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, is the most common cause of primary hypothyroidism in patients who are not iodine deficient.

In Hashimoto thyroiditis, the immune system produces antithyroid and antithyroglobulin antibodies that destroy thyroid cells, eventually reducing thyroid hormone production and causing hypothyroidism.

In fact, the presence of either of these autoantibodies confirms the diagnosis of Hashimoto thyroiditis!

Now, if your patient presents with a chief concern suggesting Hashimoto thyroiditis, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

If the patient is unstable, stabilize the airway, breathing, and circulation. Some patients might even require intubation and mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, pulse oximetry, as well as cardiac telemetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now, here are some high-yield facts to keep in mind! If your patient presents with hypothermia, bradycardia, hypoventilation, and lethargy, you should suspect myxedema coma, which is a severe, life-threatening form of hypothyroidism.

Myxedema coma typically occurs later in the disease course of Hashimoto thyroiditis, when long-term thyroid damage results in profound hypothyroidism.

Treatment consists of supportive care, which in some patients means ventilatory or circulatory support, as well as corticosteroids, and thyroid hormone and electrolyte replacement. Any underlying precipitant such as an infection should be identified and treated as well.

On the flip side, some patients with Hashimoto can initially present with tachycardia, heat intolerance, sweating, increased appetite and weight loss. In this case, you should suspect Hashitoxicosis, which is a phase of hyperthyroidism that can occur during the early stages of Hashimoto thyroiditis, when a lot of thyroid cells are destroyed at once by autoantibodies, releasing thyroid hormones into the circulation. During the Hashitoxicosis phase, treatment relies on antithyroid drugs to lower serum thyroid hormone concentration, as well as beta-blockers to control the heart rate.

Now that we're done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones.

First, obtain a focused history and physical examination. Your patient will likely report fatigue, weight gain, depression, dry skin, and sometimes cold intolerance. Remember that Hashimoto thyroiditis can be associated with other autoimmune conditions like alopecia areata, vitiligo, Addison disease, and type 1 diabetes mellitus. When at least one other of these conditions is present, that’s called multiple autoimmune endocrinopathy.

On the other hand, physical exam findings typically include bradycardia, delayed relaxation of the deep tendon reflexes, and peripheral edema. Sometimes you could notice a palpable goiter, which is a smooth, non-tender, and diffusely enlarged thyroid gland as well as isolated diastolic hypertension. At this point, you should suspect hypothyroidism,

Your next step is to order TSH and free T4 levels.

If TSH is high and free T4 is low, diagnose primary hypothyroidism, and if TSH is high and free T4 is normal, diagnose subclinical hypothyroidism. In both cases, order antithyroid peroxidase antibodies or TPOAb and antithyroglobulin antibodies or TgAb.

If neither antithyroid peroxidase, nor antithyroglobulin antibodies are not present, diagnose non-autoimmune hypothyroidism.

However, if either antithyroid peroxidase or antithyroglobulin antibodies, or both, are present, diagnose Hashimoto thyroiditis.

Keep in mind that antithyroid peroxidase antibodies are present in approximately 95% of patients with Hashimoto thyroiditis, while antithyroglobulin antibodies are present in 60 to 80% of patients.