Endocrine Abstracts

Silent thyroiditis is characterized by the destructive thyroid inflammation and is considered to be a chronic autoimmune thyroid disease, although the etiology could not have been fully explained. On the other hand, Graves’ disease is autoimmune phenomena as well as silent thyroiditis and silent thyroiditis has been classified as part of the spectrum of Graves’ disease. Although, the thyroid stimulating antibody (TSAb) are found positive in most of Graves’ disease but rarely in silent thyroiditis cases and the role of TSAb in the pathogenesis of these diseases has still been unknown. In this case report, we aimed to present a rare case in which repeated thyrotoxicosis as a silent thyroiditis was followed by Graves’ disease. A 40 year old woman admitted to outpatient clinic with the complaint of palpitations, sweating and weight loss 3 years ago. Laboratory results were TSH: 0.005 μIU/ml (normal:0.56–5.57), sT3: 8.5 pg/ml (normal:2.3–4.2), sT4: 4.05 ng/dl (normal:0.93–1.7) and anti-thyroid peroxidase and anti-thyroglobulin antibodies were positive. Thyroid scintigraphy showed homogeneous increased uptake involving the whole thyroid gland and the patient was diagnosed with Graves’ disease. Treatment of the patient with propylthiouracil was stopped at the 18th month of treatment. After the 18 months of untreated follow-up, she was referred to our hospital with complaints of palpitation, tremor and sweating. On the physical examination of the patient the painless thyroid gland was palpable. Laboratory findings were as follows; TSH: 0.006 mU/l, sT3: 3.54 ng/l, sT4: 1.6 ng/dl and ESR was normal. Thyroid scintigraphy revealed a decreased uptake in the thyroid gland. The patient was diagnosed with silent thyroiditis and propranolol was started for symptoms. One month later, laboratory findings were TSH: 10.08 mU/l, sT4: 0.894 ng/dl, sT3:2.59 ng/l and the propranolol therapy was withdrawn and low-dose levothyroxine therapy was started. In a study with the patients who were followed up Graves’ disease in remission that developed thyrotoxicosis during pregnancy and postpartum period, postpartum thyroiditis was diagnosed in 44% of patients, and 28% of patients were evaluated as Graves’ exacerbation. Although the relationship between Graves’ remission and silent/postpartum thyroiditis is not fully demonstrated. In conclusion, other thyrotoxicosis causes should be excluded before the patient is accepted as Graves’ recurrence after the thyrotoxicosis in patients who are followed up due to Graves’ disease in remission.