Symptoms in Euthyroid Hashimoto's Thyroiditis: Is There a Role for Autoimmunity Itself?

Dear Editor:

We read with interest the recent article by Ott et al. (1) on the possible effect of autoimmunity per se on general health and overall quality of life of women with Hashimoto's thyroiditis (HT). In a cohort of 426 euthyroid women who had thyroid surgery for goiter, and whose postoperative findings ruled out malignancy, the authors evaluated either the quality of life or symptom load with regard to both the histological diagnosis of thyroiditis and the serum anti-thyroid peroxidase (anti-TPO) antibody levels.

With regard to general health, the authors found that women with positive anti-TPO titer reported a significantly higher prevalence of symptoms, such as chronic weakness, fatigue, and irritability, as compared with those without HT. Besides the histological thyroiditis grade, anti-TPO levels were positively correlated with the symptom score, being highest in patients with 6 or more symptoms. Similar results were reported regarding the questionnaire on quality of life: higher anti-TPO levels being associated with lower symptom score, even though all the patients were euthyroid.

The authors concluded that women with HT suffer from a high symptom load independently from the hypothyroidism that is often associated with this disorder. In agreement with these results, we recently reported on the presence of symptoms and signs consistent with fibromyalgia (FM) in 52 consecutive patients. Of them, 34 had subclinical hypothyroidism (SCH) either with (n=21), or without (n=13) autoimmunity. Eighteen patients were euthyroid with HT. None of the SCH patients without autoimmunity showed any clinical symptom consistent with FM. In our publication, we focused on the possibility of a role of antithyroid autoimmunity in the HT-associated clinical syndrome (2,3). Notably, there was FM comorbidity in almost one-third of our patients, all of whom were women, who had HT with or without SCH. It is noteworthy that the prevalence of FM was slightly higher in euthyroid HT patients (33.3%) than in those who also had SCH (28.5%). Interestingly, similar data were reported in three previous studies (see Supplementary Data, available online at www.liebertonline.com/thy), also supporting a relationship between thyroid autoimmunity per se and FM. The specific underlying mechanism for this, however, is not clear.

HT is generally considered a well-defined clinical entity but it is widely assumed that hypothyroidism of various degrees is the main, if not the only, cause of the clinical symptoms, or that muscle symptoms in patients who are euthyroid by conventional criteria are due to early SCH (see Supplementary Data). However, an electron microscopic study (see Supplementary Data) of skeletal muscle biopsies from euthyroid subjects suffering from HT showed capillary alterations and mononuclear cell infiltrate, suggesting a relationship between thyroid autoimmunity or a closely associated form of autoimmunity to account for muscle symptoms.

In conclusion, our data and those from the study by Ott et al. (1,2) provide new insights into the clinical symptomology of HT, suggesting a role for autoimmunity per se. This relatively novel concept also implies that the pathogenesis of clinical symptoms in HT with hypothyroidism may be even more complex, with morbidity related not only to hypothyroidism, but also to other factors.