Painful Hashimoto’s Thyroiditis
Kanji Kasagi
Key words: painful Hashimoto’s thyroiditis, subacute thyroiditis, acute inflammation, Graves’ disease, corticosteroids (DOI: 10.2169/internalmedicine.45.0144)

The acute inflammatory changes in the thyroid observed in patients with painful Hashimoto’s thyroiditis were introduced first by Doniach et al (1) and Suzuki et al (2) in 1960 and 1964, respectively. From that time, no detailed descriptions of similar cases were found until 1986, when Ishihara et al (3) reported a case of known Hashimoto’s thyroiditis with 12 episodes of acute exacerbation, characterized by high fever and spontaneous pain of the thyroid. Thereafter, these authors reported 6 additional cases in 1987 (4). Zimmerman et al (5) reported 8 cases of thyroid tenderness secondary to Hashimoto’s thyroiditis. Painful Hashimoto’s thyroiditis (pHT) has also been referred to as acute exacerbation of Hashimoto’s thyroiditis or painful variant of Hashimoto’s thyroiditis. The patients exhibit inflammatory symptoms and signs such as fever, neck pain, and increased CRP and ESR values. The cause of thyroid tenderness is unknown. Capsular stretching by rapid thyroid enlargement may be contributory in some (3) but clearly not in all patients. If fever is predominant and pain is equivocal, other diagnostic possibilities causing fever should be ruled out. If neck pain is predominant, one should consider other diseases such as gastro-esophageal reflux disease, esophageal spasms, dental problems with referred pain, angina with referred pain, several posterior pharyngeal problems, etc (6). Pain and tenderness of the thyroid are most commonly caused by subacute thyroiditis (SAT), and less frequently caused by hemorrhage into a thyroid cyst or an enlarged malignant tumor. The differential diagnosis from SAT is often difficult, because both diseases present symptoms resulting from acute inflammation. Considering the different clinical courses and treatment responses, the differential diagnosis is important. Preexisting goiter or autoimmune thyroid diseases and high titers of TgAb and/or TPOAb (TGHA and/or MCHA) are helpful clues to diagnose painful pHT. History of a preceding upper respiratory tract infection is frequent in SAT but infrequent in pHT (5/11 in SAT and 1/8 in pHT) (7). Patients with SAT are usually thyrotoxic, while the thyroid function is variable in the case of pHT [thyro-

toxic/euthyroid/hypothyroid; 2/2/2 (4); 0/5/2 (5); 6/2/0 (7); 1/3/0 (8)]. Radioactive iodine or Tc-99m uptake is very low in case of SAT, but variable in case of pHT [high/normal/ low; 0/3/4 (4), 1/5/1 (5); 0/0/6 (7)]. Differentiation from SAT by histological examination is easy. As a typical pathological finding of pHT, Ishihara et al described an edematous inflammation with loosely arranged collagen fibers (3, 4). Zimmerman et al, on the other hand, found no difference in pathology from the more common non-painful Hashimoto’s thyroiditis (5). Granulomatous change and giant cell formation, histological features consistent with SAT, are not observed in pHT. The clinical course and treatment responses in patients with pHT are somewhat different from those in SAT patients. Aspirin, corticosteroids and l-thyroxine are used for treatment of pHT. Corticosteroids are not effective in some patients, or the pain is relieved only by a large dose. Surgical treatment by an experienced surgeon is recommended in such cases. Ohye et al recently reported that total thyroidectomy was successful in relieving the symptoms completely in 4 cases of pHT (8). Risk of developing hypothyroidism is high in pHT, but rare in SAT. Blocking-type TSH receptor antibodies seem not to play a role in the development of hypothyroidism (7), although destruction of the thyroid due to pHT may cause TSH receptor leakage, resulting in enhanced production of antibodies against the TSH receptor (TRAb). In this issue, Ohye et al reported 4 cases of Graves’ disease which developed after pHT (9). See also p 385. DOI: 10.2169/internal medicine.45.1506 Destruction-induced development of hyperthyroidism due to Graves’ disease has been reported following painless thyroiditis, subacute thyroiditis, external head and neck irradiation, etc. (9). Appearance of TRAb and development of Graves’ disease after pHT have never been reported before. Surprisingly, these authors have seen as many as 102 patients with pHT. The incidence of Graves’ disease (4/102; 3.9%) was much higher than that after subacute thyroiditis

Department of Internal Medicine, Takamatsu Red Cross Hospital, Takamatsu Correspondence to Kanji Kasagi, Department of Internal Medicine, Takamatsu Red Cross Hospital, 4-3-1 Bancho, Takamatsu 760-0017


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