Urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in patients with Graves' disease, subacute thyroiditis, and silent thyroiditis: a longitudinal study.

Urinary N-acetyl-beta-D-glucosaminidase (NAG) activity was measured longitudinally in 12 patients with Graves' disease, 5 patients with subacute thyroiditis, and 1 patient with silent thyroiditis, and compared with that of 36 normal controls. The patients with Graves' disease and subacute thyroiditis were treated with anti-thyroid drug (methimazole or propylthiouracil) and prednisolone, respectively. On the other hand, no treatment was given to the patient with silent thyroiditis. Since two patients with Graves' disease clearly showed transient deterioration of the thyroid function during the treatment period, data from these two patients were separately investigated. Urinary levels of NAG in the remaining ten patients with Graves' disease before, 1, 3, 6 and 12 months after the treatment were 15.59 +/- 7.93 (SD), 8.96 +/- 6.82, 4.39 +/- 2.33, 3.46 +/- 2.24, and 3.63 +/- 2.38 U/g.creatinine (g.Cr.), respectively. Those obtained before, 1 and 3 months after the treatment were significantly higher than those of the controls (2.85 +/- 1.12 U/g.Cr.). Free thyroid hormone levels became normal or low 3 months after the treatment. The two Graves' patients mentioned above showed a transient increase in urinary NAG with concomitant changes in free thyroid hormone levels. Urinary NAG levels in the patients with subacute thyroiditis before, 2, 4, and 6 weeks after the treatment were 16.56 +/- 10.97, 6.76 +/- 2.79, 3.14 +/- 0.48 and 3.70 +/- 1.44 U/g.Cr., respectively. Those obtained before and 2 weeks after the treatment were significantly higher than those of the controls. Free thyroid hormones were normal 2 weeks after therapy. Urinary NAG in the patient with silent thyroiditis was 9.60 U/g.Cr. on the first visit and gradually decreased.(ABSTRACT TRUNCATED AT 250 WORDS)     

A case of Graves' disease with false hyperthyrotropinemia who developed silent thyroiditis.

We encountered a patient who developed silent thyroiditis during the course of Graves' disease. The diagnosis of silent thyroiditis was made on the basis of a low thyroidal 131I uptake, no response to the thyrotropin releasing hormone (TRH) test, and subsequent hypothyroidism despite the presence of high titers of thyrotropin (TSH) receptor antibody (TRAb) and thyroid stimulating antibody (TSAb). The patient, in addition, had a discrepancy between serum TSH and thyroid hormone values. This was due to the presence of interfering substances that react to mouse IgG in the sera since serum TSH levels were decreased in a dose dependent manner by the addition of increasing amounts of mouse IgG to the sera. It should therefore be noted that silent thyroiditis can develop in patients with Graves' disease. Furthermore, clinicians should be aware that two-site immunoassay kits that use mouse monoclonal antibodies are subject to interference by some substances, possibly antibodies which react to mouse IgG.     

Experimental autoimmune thyroiditis in mice chronically treated from birth with anti-IgM antibodies

The role of T lymphocytes in the pathogenesis of experimental autoimmune thyroiditis in mice is well established while the role of B lymphocytes is unclear. Mice with thyroid lesions have thyroglobulin antibodies whereas these antibodies can occur in mice immunized with Tg that do not develop thyroid lesions. To determine whether thyroglobulin antibodies are necessary for the development of the thyroid infiltrates with mononuclear cells, which are characteristic for experimental autoimmune thyroiditis, AKR mice chronically treated from birth with goat anti-mouse IgM antibodies were immunized with mouse thyroglobulin in Freund's complete adjuvant when they were 7 weeks old. Control mice, similarly immunized, were chronically injected from birth with normal goat gamma-globulin. Three weeks after immunization, all mice were sacrificed, thyroglobulin antibodies in the serum were measured by hemagglutination assay and enzyme-linked immunosorbent assay, and thyroid pathology was assessed. The serum concentration of IgG and IgM, the percentage of B and T lymphocytes in the spleen (flow cytometry), and the in vitro proliferative response of spleen lymphocytes to stimulation by PHA, LPS, and Tg were also measured. All mice treated with anti-IgM antibodies did not have detectable thyroglobulin antibodies but 63% of these mice and 88% of control mice (all of which had thyroglobulin antibodies) had thyroid lesions. Mice treated with anti-IgM antibodies that did not have thyroid lesions had a more pronounced depression of B lymphocytes than similarly treated mice that had thyroid lesions. These experiments suggest that thyroglobulin antibodies are not necessary for the development of thyroid infiltrates with mononuclear cells. B lymphocytes could still participate in the production of experimental autoimmune thyroiditis by presenting thyroglobulin to helper T lymphocytes.     

TSH and prolactin secretions in Hashimoto's thyroiditis following withdrawal of thyroid hormone therapy

Changes in the pituitary-thyroid axis in patients with Hashimoto's thyroiditis following withdrawal of thyroid suppressive therapy were analyzed. The group of patients with thyroid adenoma served as control (group I). Patients with Hashimoto's thyroiditis were divided into 2 groups on the basis of serum TSH levels 8 weeks after discontinuing the exogenous thyroid hormone (group II, less than 10 microunits/ml; group III, more than 10 microunits/ml). During treatment with L-T4(200 micrograms/day) or L-T3(50 micrograms/day), there was no significant difference in serum T4-I and T3 levels among the three groups. Following L-T4 withdrawal, basal serum TSH levels were higher at 2 to 8 weeks in groups II and III than in group I. Serum TSH response to TRH was greater at 4 to 8 weeks in groups II and III than in group I. Following L-T3 withdrawal, basal serum TSH levels were higher at 1 and 2 weeks in group II than in group I, while those of group III were consistently higher during the study. Higher TSH responses to TRH were observed at 1 to 8 weeks in groups II and III. Neither basal nor TRH-induced prolactin (PRL) secretion differed significantly among the three groups. We have demonstrated that pituitary TSH secretion in patients with Hashimoto's thyroiditis is affected more by withdrawal of thyroid hormone therapy than in patients with thyroid adenoma. In addition, the present findings suggest a difference between the sensitivity of thyrotrophs and lactotrophs in Hashimoto's thyroiditis after prolonged thyroid therapy is discontinued.     

Detection of the novel autoantibody (anti-UACA antibody) in patients with Graves' disease

Uveal autoantigen with coiled coil domains and ankyrin repeats (UACA) is an autoantigen in patients with panuveitis such as Vogt-Koyanagi-Harada disease. The prevalence of IgG anti-UACA antibodies in patients with uveitis is significantly higher than healthy controls, suggesting its potential role as an autoantigen. Originally, UACA was cloned from dog thyroid tissue following TSH stimulation. So, we presumed UACA could be a novel autoantigen in autoimmune thyroid diseases. We measured serum anti-UACA antibody titer using ELISA in patients with autoimmune thyroid diseases (Graves' disease, Hashimoto's thyroiditis, subacute thyroiditis, and silent thyroiditis). The prevalence of anti-UACA antibodies in Graves' disease group was significantly higher than that in healthy group (15% vs. 0%). Moreover, the prevalence of anti-UACA antibodies in Graves' ophthalmopathy was significantly higher than that in Graves' patients without ophthalmopathy (29% vs. 11%). Especially, 75% of severe ocular myopathy cases showed high UACA titer. Immunohistochemical analysis revealed that UACA protein is expressed in eye muscles as well as human thyroid follicular cells. Taken together, UACA is a novel candidate for eye muscle autoantigens in thyroid-associated ophthalmopathy.     

Seasonal recurrence of transient hypothyroidism in a patient with autoimmune thyroiditis

Two postpartum and 7 spontaneous episodes of transient hypothyroidism developed during 5 years of observation in a florist with autoimmune thyroiditis and seasonal allergic rhinitis. The spontaneous episodes recurred twice a year regularly in spring and in autumn, the seasons of her allergic rhinitis. In most of these episodes as well as in the postpartum ones, hypothyroidism was preceded by transient thyrotoxicosis. In addition to the similarity in the clinical course, the changes in antimicrosomal antibody titers in pregnancy-unrelated episodes were almost identical to those in postpartum episodes. Throughout the observation periods, she had supranormal serum total immunoglobulin (Ig) E concentrations and high antigen-specific Ig E levels for various pollen extracts such as cedar and ragweed. However, we failed to demonstrate a correlation between thyroid function and total or any antigen-specific Ig E level. The present findings suggest that the pregnancy-unrelated thyroid dysfunction in our patient developed as a result of silent thyroiditis and through similar immunological mechanisms to those in postpartum thyroiditis. And it is suspected, though unproved, that the seasonal recurrence of pregnancy-unrelated thyroiditis has some causal relation to her allergic disease.     

Subacute thyroiditis associated with systemic multi-organ disorders

Subacute thyroiditis is generally thought to be a self-limited inflammatory disease of the thyroid gland. This paper describes serial observations on the clinical course of a typical patient with subacute thyroiditis. This patient showed specific features of destructive thyrotoxicosis with increases in the serum levels of acute phase reactants and in the erythrocyte sedimentation rate. She also showed signs of liver dysfunction [slightly increased alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), and leucine aminopeptidase (LAP)], slight anemia, glucose intolerance, increased pancreatic enzymes, splenomegaly, and an increase in peripheral Leu 7 positive (NK/K) cells. These abnormalities all improved with recovery from disease. These findings indicate that in this patient with subacute thyroiditis inflammation is not limited to the thyroid gland but also involves the liver, pancreas and spleen. Thus the subacute thyroiditis in this patient may be a systemic multi-organ disease.     

Silent thyroiditis following rubella

A 40-year-old housewife was referred to our hospital for evaluation of a thyrotoxic state. A month after rubella infection, she developed heat intolerance. Physical examination revealed a hard and non-tender goiter with no signs or symptoms of inflammation. Free thyroid hormones were high and TSH was undetectable. 123I-thyroidal uptake was suppressed. Antithyroglobulin and anti-microsomal antibodies were negative throughout the course. A serologic study revealed high levels of anti-rubella antibodies. After a month without any treatment, she became euthyroid. Free thyroid hormones and TSH gradually became normal and the antibodies to rubella decreased. 123I-thyroidal uptake increased. From the clinical course, the patient was diagnosed as having silent thyroiditis. We suggest that viral infection such as rubella could cause the development of silent thyroiditis.     

A case of progressive systemic sclerosis (PSS) with silent thyroiditis and anti-bovine thyrotropin antibodies.

We have examined a patient with progressive systemic sclerosis (PSS) who had increased serum T3 (235 ng/dl) and T4 (13.2 micrograms/dl) and low 24-h thyroidal 123I-uptake (1.2%). A diagnosis of silent thyroiditis was made on the basis of the clinical course and laboratory and histopathologic findings. Simultaneous measurement of serum anti-thyrotropin receptor antibody (TRAb) showed a negative value (-49.0%) which suggested the presence of anti-TSH antibody. Further examination by immune precipitation with 125I-bovine TSH (bTSH) and also with 125I-human TSH (hTSH) revealed the presence of anti-bTSH antibody but not anti-hTSH antibody in his serum gamma-globulin. The significance of the association of PSS, silent thyroiditis, and anti-bTSH in one individual is discussed.     

Tg in Adults as a Sensitive Biomarker of Iodine Status: A 5-Year Follow up Population Study in Different Levels of Iodine Intake Regions

This study was to evaluate the usefulness of serum thymoglobulin (Tg) in adults to assess iodine status through a 5-year cohort study which was conducted in three regions with different levels of iodine intake: mild deficiency, more than adequate, and excess, from 1999 to 2004 in China. A total of 3099 subjects over 14 years old with normal serum levels of Tg in 1999 were eligible, of whom 2448 were followed in 2004. Serum levels of thyroid hormones and thyroid autoantibodies as well as urine iodine were measured, and B-mode ultrasonography of the thyroid was performed. A general linear model was performed to determine the determinant factors of serum Tg. Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the baseline levels of serum Tg were substantially different (7.5μg/L, 5.9μg/L, and 6.8μg/L respectively, P<0.01), which were associated with age, sex, the rate of positive TgAb, abnormal thyroid volume, abnormal TSH, and positive personal history of thyroid diseases. The data from 1856 subjects with normal range of thyroid parameters but no personal history of thyroid diseases were analyzed to clarify the effect of iodine intake on Tg. Among these three regions, the serum Tg levels were substantially different in both 1999 and 2004, with a similar pattern for increased Tg (ΔTg) (3.1μg/L, 2.5μg/L and 3.5μg/L respectively, P<0.01). The general linear model analysis revealed that age, Tg, and baseline TSH levels were the determinants of ΔTg besides iodine intake. In conclusion, serum Tg in adults, resulting from a time-accumulative effect of iodine exposure, is a useful biomarker of regional iodine intake.     

Tall cell variant of papillary carcinoma coexisting with chronic lymphocytic thyroiditis. A case report.

BACKGROUND: Recent studies have shown a correlation between lymphocytic thyroiditis and papillary carcinoma of the thyroid. It is thought that autoimmune thyroiditis could be a risk factor for the development of thyroid carcinoma, mainly for the papillary variant. CASE: A 59-year-old female presented with a history of enlargement in the neck and five months of dysphagia. Clinical examination showed generalized expansion and an increase in the hardness of the thyroid gland. Hormonal outline showed subclinical hypothyroidism with serum levels of TSH slightly elevated (5 micrograms/dL; range, 0.25-4). Thyroglobulin antibodies and thyroperoxidase titers were moderately positive. Given these results, a diagnosis of chronic thyroiditis was made. Thyroid ultrasound scan showed diffuse gland irregularity and the presence of a solitary nodule (2.3 cm in diameter) localized in the right lobe. Fine needle aspiration biopsy (FNAB) of the nodule was performed under ultrasound guidance. CONCLUSION: Although clinical and laboratory results supported the diagnosis of autoimmune thyroiditis only, FNAB of the nodular lesion provided evidence of a rare case of papillary carcinoma, tall cell variant, confirmed by histologic results.     

桥本氏病合并甲状腺乳头状癌患者血清甲状腺相关激素水平的变化及意义

目的:探究桥本氏病(HT)合并甲状腺乳头状癌(PTC)患者血清甲状腺相关激素水平的变化及意义。方法:对我院148例HT患者的临床资料进行回顾性分析,根据其是否合并PTC分为HT合并PTC组(n=68)和单纯HT组(n=80)。比较两组患者性别、年龄及血清促甲状腺激素(TSH)、甲状腺功能指标[游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)]、抗甲状腺抗体[甲状腺球蛋白抗体(TGAb)、甲状腺过氧物酶抗体(TPOAb)]水平等临床资料差异,分析血清TSH水平变化及意义。结果:HT合并PTC组患者男性比例、年龄、病程及血清TSH水平均大于单纯HT组,血清TGAb、TPOAb水平则均小于单纯HT组(P0.05);血清FT3、FT4水平比较差异无统计学意义(P0.05)。HT合并PTC患者组血清TSH4.2 m IU/L患者占比高于血清TSH正常组(P0.05)。血清TSH4.2 m IU/L患者中HT合并PTC患者的占比大于血清TSH水平正常的患者(P0.05)。HT合并PTC患者中,血清TSH水平4.2 m IU/L患者中央区淋巴结转移发生率高于血清TSH水平正常患者(P0.05);血清TSH4.2 m IU/L与血清TSH正常患者多灶癌发生率比较差异无统计学意义(P0.05)。结论:HT患者血清TSH水平升高可能促进其甲状腺组织癌变,HT合并PTC患者血清TSH水平升高可能促进其中央区淋巴结转移。     

Subacute thyroiditis manifesting as a thyroid mass, vocal cord paralysis, and hypercalcemia

ObjectiveTo report a case of subacute thyroiditis manifesting as a thyroid mass, vocal cord paralysis, and hypercalcemia.MethodsWe describe the clinical, laboratory, and radiologic findings in a patient with an unusual clinical course of subacute thyroiditis.ResultsA 65-year-old woman presented with a hoarse voice and an enlarging tender mass in the right side of the neck. On admission, thyroid function was consistent with thyrotoxicosis from subacute thyroiditis. Laboratory studies showed a corrected serum calcium concentration of 11.4 mg/dL, intact parathyroid hormone of 125 pg/mL, 25-hydroxyvitamin D of 12 ng/mL, and creatinine of 1.8 mg/dL. Computed tomography of the neck without use of a contrast agent showed a heterogeneous mass in the right side of the neck in conjunction with deviation of the trachea from right to left but without invasion of the trachea. Thyroid ultrasonography disclosed a heterogeneous mass in the right thyroid lobe measuring 4.7 cm by 5.5 cm by 4.5 cm. Flexible laryngoscopy revealed right vocal cord paralysis. Treatment with a course of prednisone yielded normalization of the serum calcium level, improvement in her voice, and a decrease in size of the thyroid mass. Four months after initial presentation of the patient, thyroid hormone levels became normal, she was clinically euthyroid, and she had a full recovery of her voice. Her serum calcium concentration was normal (9.8 mg/dL) in association with a near-normal parathyroid hormone level of 90 pg/mL. The 25-hydroxyvitamin D and creatinine values were also normal. Repeated thyroid ultrasonography showed a smaller right thyroid lobe with a dominant nodule measuring 2.0 cm by 1.3 cm by 1.4 cm in the right upper pole.ConclusionThis case illustrates that subacute thyroiditis can have the unusual initial manifestations of a thyroid mass, vocal cord paralysis, and hypercalcemia. In similar patients, a trial of corticosteroid therapy may be warranted in an effort to improve clinical symptoms and thus avoid unnecessary surgical treatment. (Endocr Pract. 2012;18:e17-e20)     

Changes in serum anion gap and sodium level in monoclonal gammopathies

In a group of patients with monoclonal gammopathies a decrease in the serum anion gap was seen with increasing serum concentrations of monoclonal IgG and IgM but not monoclonal IgA. This was probably related to the fact that IgG and IgM are cationic but IgA is a anionic at a physiologic pH. The serum sodium level decreased by 0.7 mmol/l for every increase of 1 g/dl in the serum level of the monoclonal immunoglobulin, likely because of the volume displacement effect of the monoclonal protein.     

Recent Canadian court decisions on consent.

A 51-year-old woman presented with a painful, rapidly enlarging thyroid gland. The serum concentrations of the thyroid hormones were initially at the upper limit of normal, and the uptake of radioactive iodine by the thyroid was completely depressed. Although subacute thyroiditis was suspected, a biopsy specimen from the thyroid showed malignant disease and no evidence of inflammation. At the time of right subtotal lobectomy metastatic breast carcinoma was diagnosed. Thus, primary or secondary malignant disease of the thyroid can simulate thyroiditis and present a serious problem in differential diagnosis.     

Characterization of a rapid and reliable method for iodide biomonitoring in serum and urine based on ion chromatography–ICP-mass spectrometry

An appropriate and controlled supply of thyroid hormones is vital for proper body function. In turn, an appropriate synthesis of T3 and T4 in the thyroid gland is dependent on a sufficient and balanced iodide concentration in blood serum. Due to widespread iodine deficiency or some cases of iodine over exposure, iodide biomonitoring in serum is important and it is that biomonitoring approach being closest to the bioavailable I⁻ supply for the thyroid gland. Therefore, this paper describes a biomonitoring method for iodide determination in serum based on ion chromatography–inductively coupled plasma mass spectrometry (IC–ICP-MS). Since in literature only very few data are available on iodide in serum but many in urine the method is also extended to I⁻ monitoring in urine. The method was additionally designed to have short analysis time (8 min) for increased sample throughput, good precision in serial measurement (serum: 4.86%; urine: 1.4%), and day-to-day determination (serum: 5.7%; urine: 2.28%), high accuracy (serum: 105%; urine: 101%) and good recovery (serum: 102%; urine: 99%) even in matrix-rich samples at low I⁻ concentration. Also, investigations were performed to elucidate whether internal standardization during chromatography, sample preparation for protein-matrix removal or matrix-matched calibration are advantageous for analytical performance. Finally, limits of detection (3σ) of 0.12 μg/L or 0.05 μg/L (serum or urine) and limit of quantification (10σ) of 0.39 μg/L or 0.17 μg/L (serum or urine) were achieved.     

Transient hypothyroidism associated with increased anti-microsomal antibodies.

An unusual case of transient hypothyroidism during the course of chronic thyroiditis was reported. A 25 years old female noticed the remarkable enlargement of thyroid gland 3 months after paturition and was developed to be hypothyroidism with decreased blood thyroid hormone and increased serum TSH. The patient recovered to be euthyroid spontaneously in association with the decrement of goiter size. Anti-thyroid microsomal antibody increased concomitantly with hypothyroid period and decreased parallel with the recovery of thyroid function. The ratio of TSH potency estimated by bioassay to that by immunoassay changed during the course. Possible etiologic factors of this transient changes were discussed.     

Using Hashimoto thyroiditis as gold standard to determine the upper limit value of thyroid stimulating hormone in a Chinese cohort

Background

Subclinical hypothyroidism, commonly caused by Hashimoto thyroiditis (HT), is a risk factor for cardiovascular diseases. This disorder is defined as merely having elevated serum thyroid stimulating hormone (TSH) levels. However, the upper limit of reference range for TSH is debated recently. This study was to determine the cutoff value for the upper normal limit of TSH in a cohort using the prevalence of Hashimoto thyroiditis as “gold” calibration standard.

Methods

The research population was medical staff of 2856 individuals who took part in health examination annually. Serum free triiodothyronine (FT3), free thyroxine (FT4), TSH, thyroid peroxidase antibody (TPAb), thyroglobulin antibody (TGAb) and other biochemistry parameters were tested. Meanwhile, thyroid ultrasound examination was performed. The diagnosis of HT was based on presence of thyroid antibodies (TPAb and TGAb) and abnormalities of thyroid ultrasound examination. We used two different methods to estimate the cutoff point of TSH based on the prevalence of HT.

Results

Joinpoint regression showed the prevalence of HT increased significantly at the ninth decile of TSH value corresponding to 2.9 mU/L. ROC curve showed a TSH cutoff value of 2.6 mU/L with the maximized sensitivity and specificity in identifying HT. Using the newly defined cutoff value of TSH can detect patients with hyperlipidemia more efficiently, which may indicate our approach to define the upper limit of TSH can make more sense from the clinical point of view.

Conclusions

A significant increase in the prevalence of HT occurred among individuals with a TSH of 2.6–2.9 mU/L made it possible to determine the cutoff value of normal upper limit of TSH.

     

Serum thyroglobulin as a biomarker of iodine excess and thyroid disease occurrence in adults

BackgroundThyroglobulin (Tg) is considered a sensitive indicator of iodine deficiency. However, the usefulness of Tg as a biomarker of excess iodine is uncertain. The present study aimed to determine the influence of different iodine intake on serum Tg levels, evaluate the influence of thyroid diseases on the distribution of Tg, and identify the factors that may affect Tg levels.MethodsA cross-sectional survey with a total of 1208 adults was conducted in different water iodine areas in China. Urinary iodine concentration (UIC), water iodine concentration (WIC), serum Tg, thyroid-stimulating hormone (TSH), and thyroid antibodies were measured. The thyroid volumes and nodules were measured by B-scan ultrasound.ResultsBased on the WIC data, subjects were divided into three groups. Based on the median urinary iodine concentration (MUIC) data, the iodine levels were adequate, more than adequate, and excess for the WIC < 10 μg/L group, 10 μg/L ≤ WIC ≤ 100 μg/L g, and WIC > 100 μg/L groups, respectively. The median Tg was significantly higher in the excess iodine group than in the adequate iodine group and the more than adequate iodine group (14.6 μg/L vs.12.7 μg/L, P = 0.042; 14.6 μg/L vs.12.5 μg/L, P = 0.004). Multiple linear regression analysis showed that excess iodine intake, goitre, thyroid nodules, and hypothyroidism were significantly related to higher serum Tg levels.ConclusionSerum Tg level can be a promising biomarker of excessive iodine intake, but other factors, especially the presence of thyroid disease, should be considered when using this parameter.     

Safe Range of Iodine Intake Levels: A Comparative Study of Thyroid Diseases in Three Women Population Cohorts with Slightly Different Iodine Intake Levels

Iodine excess may lead to thyroid diseases. Our previous 5-year prospective survey showed that the prevalence and incidence of hypothyroidism or autoimmune thyroiditis increased with iodine intake. The aim of the present study was to investigate the optimal range of iodine intake by comparing the prevalence of thyroid diseases in three areas with slightly different levels of iodine intake. In 2005, 778 unselected women subjects from three areas with different iodine intake levels were enrolled. Levels of serum thyroid hormones, thyroid autoantibodies, and urinary iodine were measured, and thyroid B ultrasounds were performed. Among the subjects with mildly deficient iodine intake, those with adequate intake, and those with more than adequate intake, the prevalence of clinical and subclinical hypothyroidism was 0, 1.13, and 2.84%, respectively (P = 0.014); that of thyroid goiter was 24.88, 5.65, and 11.37%, respectively (P < 0.001); that of serum thyrotropin values was1.01, 1.25, and 1.39 mIU/l, respectively; and that of serum thyrotropin/thyroglobulin ratio was 7.98, 6.84, and 5.11, respectively (P < 0.001). In conclusion, median urinary iodine 100~200 μg/l may reflect the safe range of iodine intake levels. Serum thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine status.