Hashimoto Thyroiditis Hashimoto thyroiditis, or chronic lymphocytic thyroiditis, was first described in 1912 by Dr. Hakaru Hashimoto. Hashimoto thyroiditis can manifest as hyperthyroidism, hypothyroidism, euthyroid goiter, or diffuse goiter. High levels of antimicrosomal and antithyroglobulin antibody are usually present, and TSHRAb may be present (353,375,376). Typically, glandular hypertrophy is found, but atrophic forms are also present. Three classic types of autoimmune injury are found in Hashimoto thyroiditis: (i) complement-mediated cytotoxicity, (ii) antibody-dependent cell-mediated cytotoxicity, and (iii) stimulation or blockade of hormone receptors, which results in hypo-or hyperfunction or growth (Fig. 31.11).
The histologic picture of Hashimoto thyroiditis includes cellular hyperplasia, disruption of follicular cells, and infiltration of the gland by lymphocytes, monocytes, and plasma cells. Occasionally, adjacent lymphadenopathy may be noted. Some epithelial cells are enlarged and demonstrate oxyphilic changes in the cytoplasm (Askanazy cells or H¨urthle cells, which are not specific to this disorder). The interstitial cells show fibrosis and lymphocytic infiltration. Graves disease and Hashimoto thyroiditis may cause very similar histologic findings manifested by a similar mechanism of injury.
Clinical Characteristics and Diagnosis of Hashimoto Thyroiditis
Patients with Hashimoto thyroiditis may present with typical symptoms of hypothyroidism or may be relatively asymptomatic. Patients often present with a goiter, which can involve the parietal lobe. At later stages of the disease, hypothyroidism can be found without a goiter. Notable clinical manifestations associated with Hashimoto thyroiditis include fatigue, weight gain, hyperlipidemia, dry hair, dry skin, cold intolerance, depression, menstrual irregularities, bradycardia, and or memory impairment. Hashitoxicosis, the hyperthyroid manifestation of
Table 31.13 Potential Causes of Hypothyroidism
Congenital absence of thyroid gland
Ingestion of antithyroid drugs
Surgical removal of thyroid gland
Hashimoto thyroiditis, may occur after a hypothyroid state and development into a euthyroid or hyperthyroid state and is thought to be the result of development of TSH-stimulating antibodies (TSI) associated with Graves disease (368). This variant is estimated to occur in 4% to 8% of patients with Hashimoto thyroiditis. In the setting of Hashitoxicosis, the patient requires frequent follow-up and the potential for adjustments in thyroid supplementation. These patients often become hypothyroid during the course of treatment.
In many cases, an elevated serum TSH is detected during routine screening. Elevated serum anti-TPO antibodies confirm the diagnosis, and free T4 and T3 document overt or subclinical hypothyroidsim. The sedimentation rate may be elevated, depending on the course of the disease at the time of recognition. Other causes of hypothyroidism should be considered, as listed in Table 31.13. Progression from subclinical to clinically overt hypothyroidism is reported to vary from 3% to 20%, with a higher risk noted in patients with goiter or thyroid antibodies (329,377). Treatment of subclinical hypothyroidism is somewhat controversial, but clinical studies suggested treatment of subclinical hypothyroidism is associated with a reduction in neurobehavioral abnormalities, a reduction in cardiovascular risk factors, and an improvement in lipid profile (378,379).