Background A lifelong thyroxine therapy is indicated in all patients who have hypothyroidism as a result of autoimmune thyroiditis. However, it has been reported that some hypothyroid patients with autoimmune thyroiditis have spontaneous remission with restriction of iodine intake instead of thyroxine therapy. The purpose of study was to investigate how many hypothyroid patients with autoimmune thyroiditis can recover from hypothyroidism with restriction of iodine intake instead of thyroxine therapy and which factors predict recovery from hypothyroidism. Methods: We studied 64 patients with autoimmune thyroiditis(goitrous autoimmune thyroiditis 56, atrophic autoimmune thyroiditis 8). Thyroxine therapy was discontinued in patients with goitrous autoimmune thyroiditis on the way(group 1, n=32) or from the beginning(group 2, n=24) and atrophic autoimmune thyroiditis on the way(group 3, n-8). All patients were asked to avoid iodine-rich foods and thyroid function was monitored every one to two months for up to 35 months. Serum T3, T4, TSH concentrations, antithyroglobulin and antimicrosomal antibodies were measured by radioimmunoassay(RIA). TSH binding inhibitor immunoglobulin(TBII) was measured in serum using radioreceptor assay. Two hundred micrograms of thyrotropin releasing hormone (TRH) were given as intravenous bolus and TSH levels were measured in blood samples taken at 0, 30, and 60 minutes. All values were expressed as mean+-SEM. Statistical analysis was done with paired or non-paired t-test, ANOVA, and the Chi-square test. Statistical significance was defined as p-value below 0.05. Results: Thirteen(40.6%) of 32 patients in group 1 remained euthyroid after 12-35 months of discontinuation of thyroxine therapy. The other 19(59.4%) patients in group 1 had recurrences of hypothyroidism within 3 months after discontinuation of thyroxine therapy. In 11(45.8%) out of 24 patients in group 2, serum TSH concentrations declined below 5 mU/L within 3 months without thyroxine therapy. The other 13(54.2%) patients in group 2 remained hypothyroid till 2-16 months and the thyroxine was given. In contrast, all 8 patients in group 3 had recurrences of hypothy- roidism within 3 months after stopping thyroxine therapy. When we compared the recovered patients of goitrous autoimmune thyroiditis with the non-recovered patients of goitrous autoimmune thyroiditis, regardless of thyroxine therapy from the beginning, age at onset of disease of the 24 recovered patients was significantly younger than the 32 non-recovered patients(30.1+2.0 years vs. 40.2+ 2.4 years; p=0.004). Concl#usion: These findings suggest that 42.9% of hypothyroid patients with goitrous autoim- mune thyroiditis remain or become spontaneously euthyroid with restriction of iodine intake instead of thyroxine therapy. Young age may be a predicting factor of recovery from hypothyroidism in goitrous autoimmune thyroiditis.
Combination treatment with pegylated interferon and ribavirin has been established as a standard therapy for chronic hepatitis C. Although interferon therapy is relatively safe, an important side effect is the induction of autoantibodies and autoimmune disease, especially autoimmune thyroid disease. Interferon associated autoimmune thyroid disease can consist of autoimmune hypothyroidism, Graves' disease, and destructive thyroiditis. Thyroid disease may lead to dose reduction or discontinuation of therapy.
BACKGROUND Painless thyroiditis is characterized by painless, destructive inflammation of the thyroid gland. Although thyroid autoantibodies are frequently detected in patients suffering from this condition, the clinical significance of these antibodies is not well understood. Therefore, this study was conducted to investigate the relationship between thyroid function and thyroid autoantibodies in painless thyroiditis according to clinical course. METHODS: Patients proven to have painless thyroiditis were retrospectively included in this study. We analyzed their clinical features, thyroid function and titers of thyroid autoantibodies according to clinical course, which was divided into three phases; thyrotoxic, hypothyroid and recovery. RESULTS: Of the 21 patients included in this study, 2 were male and 19 were female. During the thyrotoxic phase, the mean free T4 concentration was 4.03 (2~6.8) ng/mL and the mean concentration of thyroid stimulating hormone (TSH) was 0.02 (0.01~0.07) U/mL. In addition, the titer of antithyroglobulin antibody and antithyroid peroxidase antibody was 298 (4.8~995) U/mL and 3318 (0.1~25280) U/mL, respectively during this phase. During the hypothyroid phase, the mean TSH was 16.3 (4.3-49.5) U/mL and was found to be positively correlated with the level of free T4 observed during the thyrotoxic phase (r = 0.523, P = 0.031). During the recovery phase, the titer of antithyroglobulin antibody was significantly reduced to 180 (38~487) U/mL when compared with the titer taken during the thyrotoxic phase (P = 0.016). Additionally, during the hypothyroid phase, patients found to have antithyroid peroxidase antibody had a higher titer of TSH than those that did not (23.9 (6.5~49.5) vs. 11.2 (5.3~18.2) U/mL, P = 0.004). CONCLUSION: The titer of free T4 and the presence of antithyroid peroxidase observed during the thyrotoxic phase were related to the titer of TSH during hypothyroid phase. Additionally, the titer of antithyroglobulin antibody was significantly reduced during the recovery phase.
A primary thyroid lymphoma is rare among all types of thyroid malignancy. Usually, a thyroid lymphoma is associated with underlying chronic autoimmune thyroiditis. Recently, we experienced a primary thyroid mucosa-associated lymphoid tissue(MALT) lymphoma, with an incidental micropapillary thyroid carcinoma, but lacking evidence of autoimmune thyroiditis. A female patient visited our hospital for further evaluation of a rapidly enlarging, painless thyroid mass which had been stable for 8 years. Lymphocytic thyroiditis or a lymphoma was suspected from fine needle aspiration performed at another hospital. The thyroid function test and other routine laboratory tests were normal. The histopathological findings after a total thyroidectomy revealed a MALT lymphoma with a micropapillary thyroid carcinoma. There was no evidence of chronic autoimmune thyroiditis. This is, to the best of our knowledge, the first case report of a MALT lymphoma arising from the thyroid gland without evidence of chronic autoimmune thyroiditis in Korea
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Primary Mucosa-Associated Lymphoid Tissue Lymphoma of Thyroid with the Serial Ultrasound Findings Eon Ju Jeon, Ho Sang Shon, Eui Dal Jung Case Reports in Endocrinology.2016; 2016: 1. CrossRef
Autoimmune Thyroid Diseases Jong Ryeal Hahm Hanyang Medical Reviews.2012; 32(4): 219. CrossRef
The polyglandular autoimmune syndrome is constellation of multiple endocrine insufficiencies often associated with diseases of nonendocrine organs occurring in individual patients and their families. In 1980, Neufeld classified this syndrome into three major types. Type II is characterized by adrenocortical insufficiency, autoimmune thyroiditis, and insulin-dependent diabetes mellitus. We experienced a case characterized by adrenocortical insufficiency, autoimmune thyroiditis, and ovarian failure and report with the review of the literature. A 38-year-old woman visited our clinic because of progressing brown colored pigmentation of skin and mucosa which is developed a year ago. Nine years ago prior to visit, amenorrhea was developed after right oophrectomy. Three years ago, she revealed feature of hyperthyroidism such as palpitation, loss of body weight (8kg/1-2years), heat intolerance, and sweating, so received antithyroid therapy for 14 months. Brown colored pigmentation of skin and mucosa, especially scar and gingiva, has been progressively aggravated during last year. She had no past or family history of other endocrine disease. Diffuse pigmentation of skin, loss of axillary and pubic hair, and diffuse enlargement of both thyroid glands were shown on physical examination. Blood cell count, serum chemistry and blood sugar test were all within normal range. Basal hormone levels were T3-uptake 29.7% (30~40), T3 153 ng/dL (85~185), T4 7.5ug/dL (5.5~11.5), TSH 2.4 IU (0.34~3.5), anti-TG antibody <100 U/mL (0~100), anti-microsome antibody <50 U/mL (0~100), TBII (thyrotropin binding inhibiting immunoglobulin) 2.2% ( (-15)~15), ACTH 989 pg/mL (0~37), cortisol 0.1 ug/dL (5~25), renin 7.1ng/mL/hr (1~2.5), aldosterone 81.0pg/mL (50~194), LH 115.2 mIU/mL (0.6~16.8), FSH 122 mIU/mL (1.6~19.0), and estradiol <10.0pg/mL (30~120). In ACTH stimulation test, levels of basal cortisol, 30 minutes, and 60 minutes were <0.1, <0.1, and <0.1 g/dL respectively. And, in glucagon stimulation test, levels of basal C-peptide, 5 minutes, 10 minutes, and 15 minutes were 0.9, 5,1, 6.3, and 5.5 ng/dL respectively. Thyroid scan showed diffuse enlargement of bilateral thyroid glands and pelvic ultrasonogram showed atrophy of left ovary. We administered corticosteroid, estrogen, and progesterone which were deficient to the patient, and has followed up the clinical course of the patient.