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[Long-term effects of high iodine intake: inhibition of thyroid iodine uptake and organification in Wistar rats]Man N, Guan HX, Shan ZY, Li YS, Fan CL, Guo XJ, Chen W, Tong YJ, Chong W, Mao JY, Teng WP. Zhonghua Yi Xue Za Zhi. 2006 Dec 26;86(48):3420-4. Chinese. [abstract only]
"OBJECTIVE: To investigate the effects of chronic iodine excess on thyroid function, thyroid peroxidase (TPO) activity, and expression of sodium-iodide symporter (NIS).
METHODS: 500 Wistar rats were randomly exposed to 4 doses of iodine 4 microg/d (G0, control), 6 microg/d (G1), 12 microg/d (G2), and 24 microg/d (G3) for 1, 2, 4 and 8 months. The urine iodine and tissue iodine was determined by arsenic/cerium catalyzing spectrophotography. Radioimmunoassays were used to detect thyrotropin (TSH), free thyroxin (FT4), free triiodothyronine (FT3), total thyroxin (TT4), and total triiodothyronine (TT3). Guaiacol reaction method and potassium iodide oxygenation method were used to determine the activity of TPO. Suspension of single cells from thyroid tissue was made and the positive rate of NIS was determined by flow cytometry. The expression of NIS protein was assayed by immunohistochemistry.
RESULTS: The urine iodine levels of G1, G2, and G3 were 1.5, 3, and 6 times of G0 respectively. FT4, FT3, and total iodine were found progressively accumulated in thyroid tissue with the elevation of iodine intake. The TPO activities of G2 and G3 at the 8th month were 0.17 +/- 0.04 and 0.15 +/- 0.03 respectively, both significantly lower than that of G0 (0.4 +/- 0.23, P < 0.05). The levels of iodine intake at different time points of G1-3 were significantly reduced in a iodine-dose dependent manner (r = -0.63 to -0.78, P < 0.01). The 131I intake at month 8 of G1, G2, and G3 were 56%, 49%, and 39% that of G0 respectively. At month 8 the NIS positive rates of G2 and G3 were significantly lower than that of G0 (both P < 0.05). The NIS protein positive rate was positively correlated with NIS protein expression intensity (r = 0.7-0.72, P < 0.01). The iodine content of thyroid tissue was negatively correlated with TPO activity, iodine intake rate, NIS protein positive rate and expression intensity (r = -0.62 to -0.88, P < 0.05).
CONCLUSION: Moderate iodine excess continuously suppresses the thyroid iodine uptake and organification, which presents a mechanism for iodine-induced thyroid failure."
Effect of iodine intake on thyroid diseases in China.Teng W, Shan Z, Teng X, Guan H, Li Y, Teng D, Jin Y, Yu X, Fan C, Chong W, Yang F, Dai H, Yu Y, Li J, Chen Y, Zhao D, Shi X, Hu F, Mao J, Gu X, Yang R, Tong Y, Wang W, Gao T, Li C. N Engl J Med. 2006 Jun 29;354(26):2783-93.
"BACKGROUND: Iodine is an essential component of thyroid hormones; either low or high intake may lead to thyroid disease. We observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake: mildly deficient (median urinary iodine excretion, 84 microg per liter), more than adequate (median, 243 microg per liter), and excessive (median, 651 microg per liter). Participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, we examined the effect of regional differences in iodine intake on the incidence of thyroid disease.
METHODS: Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured and B-mode ultrasonography of the thyroid was performed at baseline and follow-up.
RESULTS: Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the cumulative incidence of overt hypothyroidism was 0.2 percent, 0.5 percent, and 0.3 percent, respectively; that of subclinical hypothyroidism, 0.2 percent, 2.6 percent, and 2.9 percent, respectively; and that of autoimmune thyroiditis, 0.2 percent, 1.0 percent, and 1.3 percent, respectively. Among subjects with euthyroidism and antithyroid antibodies at baseline, the five-year incidence of elevated serum thyrotropin levels was greater among those with more than adequate or excessive iodine intake than among those with mildly deficient iodine intake. A baseline serum thyrotropin level of 1.0 to 1.9 mIU per liter was associated with the lowest subsequent incidence of abnormal thyroid function.
CONCLUSIONS: More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis."
[Effect of chronic mild and moderate iodine excess on thyroid anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats]Zhang N, Tong YJ, Shan ZY, Teng WP. Zhonghua Yi Xue Za Zhi. 2006 May 16;86(18):1274-8. Chinese. [abstract only]
"OBJECTIVE: To investigate the effects of chronic mild and moderate iodine excess on thyroid oxidative injury and anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats.
METHODS: Four-week-old Wistar rats were fed with iodine deficient diet for three months to make iodine deficient goiter models, then divided randomly into three groups: iodine deficient control group (Group IDC) fed with double distilled water, iodine-supplement group I (Group IS I) fed with potassium iodate solutions with the iodine concentrations of 100 microg/L, and iodine-supplement group II (Group IS II), fed with potassium iodate solution with the iodine concentrations of 330 microg/L. Another four-week-old Wistar rats were fed with normal diet for three months, and then divided randomly into three groups: normal control group (NC) fed with double distilled water, iodine-excess group I (IEI) fed with potassium iodate solution with the iodine concentration of 300 microg/L, and iodine-excess group II (Group IEII), fed with potassium iodate solution with the iodine concentration of 660 microg/L. 1, 2, 4, 8, and 24 weeks after treatment samples of urine were collected to detect the median urine iodine (MUI), samples of plasma were collected from the hearts of 8-14 rats from each group and then rats were killed. Their thyroid glands were taken out to measure the wet weight and made into homogenate. Biochemical method was used to measure the activities of glutathione-peroxidase (GSH-P(X)) and superoxide dismutase (SOD) as well as the contents of malonyldialdehyde (MDA) and H2O2 in the homogenates of thyroid glands.
RESULTS: The GSH-P(X) activity 2 weeks after treatment of Group IS II was significantly lower than that of Group IDC (P < 0.05), and the GSH-P(X) activity 4 weeks after treatment of Group IS I was significantly lower than that of Group IDC (P < 0.001). The activities of GSH-P(X) 4, 8, and 24 weeks after treatment of Groups IS I and IS II were all lower than those of Group C at the same time points significantly (P < 0.001, < 0.01, and < 0.05 respectively). The activities of SOD were decreased gradually in Groups IS I and IS II and were significantly lower than those of Group IDC since 8 weeks after treatment (P < 0.001 or < 0.05). The SOD activities in thyroid glands of Groups IEI and IEII since 8 weeks after treatment decreased significantly in comparison with Group NC (all P < 0.01 or < 0.001). The contents of H2O2 in thyroid glands of Groups IS I and IS II were significantly lower than those of Group IDC at different time points (P < 0.001, < 0.01, or < 0.05), and were significantly lower than those of Group NC 8 and 24 weeks after treatment (P < 0.001 or < 0.01). The contents of MDA in thyroid glands since 2 weeks after treatment of Group IEI were all significantly lower than those of Group IDC at the same time points (all P < 0.05), and the content of MDA in thyroid glands since 1 week after treatment of Groups IS II were all significantly lower than those of Group IDC at the same time points (all P < 0.05).
CONCLUSION: Supplementation of 100 microg/L and 330 microg/L iodine on iodine deficiency Wistar rats may alleviate the oxidative injury but weaken the anti-oxidative protection of thyroid. The anti-oxidative protection of thyroid glands of non-iodine deficiency Wistar rats may also be weakened by supplementation of 300 microg/L and 660 microg/L iodine."
[The relationship between serum thyroid autoantibodies, iodine intake, development and prognosis of Graves' disease]Chen W, Man N, Li YS, Shan ZY, Teng WP. Zhonghua Nei Ke Za Zhi. 2006 Feb;45(2):95-9. Chinese. [abstract only]
"OBJECTIVE: To investigate the relationship of thyroid autoantibodies including serum thyroid stimulating antibody (TSAb), thyroid stimulation blocking antibody (TSBAb) and iodine intake with the development and prognosis of Graves' hyperthyroidism.
METHODS: A total of 63 subjects with overt hyperthyroidism were screened out from 3 Chinese rural communities with different iodine intakes at first survey. Serum TSAb, TSBAb, thyrotropin binding inhibitory immunoglobulin (TBII), thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) were detected. The patients were followed up 2 years later. TSAb and TSBAb were measured with recombinant human thyrotropin receptor (rhTSHR)-Chinese hamster ovary cell (rhTSHR-CHO cell) bioassay.
RESULTS: At the first survey, the prevalences of positive TSAb, TBII and TSBAb were found in 80.9%, 61.7% and 6.4% of the patients with Graves' disease respectively. TSAb and/or TBII were positive in 91.5% of the patients. The consistent rate of TSAb and TBII was 59.6% in the cases. All indexes mentioned above were higher in the patients than in healthy controls. Positive correlations were found between TSAb and TBII (r = 0.407), TSAb and thyroglobulin (r = 0.301), TSAb and thyroid volume (r = 0.317) respectively. The prevalence of positive TSAb (91.7%) in Graves' patients in iodine excessive area are significantly higher than those in iodine mildly deficient area (66.7%). The positive rates and the titers of TBII, TPOAb and TGAb were not different statistically among the patients in the three communities. At follow-up, the patients with Graves' hyperthyroidism were classified into euthyroid group (G1) and hyperthyroid group (G2) according to their outcomes of the disease. The TSAb titers and the thyroid volume in the cases of G1 decreased significantly, whereas the patients with highly positive TPOAb titers in the first survey and the follow-up were hard to become euthyroid and TSAb may be the secondary factor influencing the thyroid as compared with TPOAb.
CONCLUSION: TSAb is more significant than TBII in diagnosing and predicting the outcomes of Graves' hyperthyroidism. The application of both TSAb and TBII could raise the positive rates of thyrotrophin receptor antibody tests. TSAb, TPOAb titers and thyroid volume were factors influencing the prognosis of Graves' hyperthyroidism."
High iodine intake is a risk factor of post-partum thyroiditis: result of a survey from Shenyang, China.Guan H, Li C, Li Y, Fan C, Teng Y, Shan Z, Teng W. J Endocrinol Invest. 2005 Nov;28(10):876-81. [abstract only]
"The aim of the present study is to obtain the epidemiological data on post-partum thyroiditis (PPT) firstly in Chinese women, and to tryto evaluate whether excessive intake of iodine in post-partum women imposes any danger of occurring PPT. Sixty hundred and ten pregnant women were involved in the cohort just before delivery. Four hundred and eighty-eight (80%) of them accepted taking part in follow-ups more than 6 months post-partum. A blood sample was taken from participants before delivery and every 3 months post-partum for testing of serum TSH, thyroid autoantibodies. Free T3 (FT3), free T4 (FT4) and TSH receptor antibody (TRAb) were detected if TSH was abnormal. The iodine nutrition was evaluated according to the mean level of the fasting urinary iodine excretions at different times during the studying period, and participants were subgrouped into 3 categories with low, adequate and high iodine intake. For those participants who had thyroid dysfunction within 6 months post-partum, the follow-up persisted for 1 yr. Of 488 pregnant women, PPT developed in 11.9% (58/488). Given overt and subclinical PPT, the prevalence was 7.17% (no.=35) and 4.71% (no.=23), respectively. There was a strong association between the presence of thyroid peroxidase antibody (TPOAb) at delivery and the risk of developing PPT [RR=6.76, 95% (CI) 4.42-10.34]. Overt cases had much higher titers of TPOAb than subclinical patients (all p<0.05). The median urinary iodine (MUI) of patients with PPT was significantly higher than that of healthy women (231.93 vs 199.88 microg/l p=0.00153). Both the prevalence of PPT and positive TPOAb rise with the increment of iodine intakes. Pregnant women with high iodine intake had more risk of developing PPT when compared with those with low iodine intake (RR=2.92, 95%CI 1.31-6.50). We concluded that positive TPOAb was of value for predicting the occurrence and severity of PPT, and a high iodine intake was a risk factor triggering PPT."
Effect of different iodine intake on the prevalence of hypothyroidism in 3 counties in China.Shan ZY, Li YS, Wang ZY, Jin Y, Guan HX, Hu FN, Teng XC, Yang F, Gao TS, Wang WB, Shi XG, Tong YJ, Chen W, Teng WP. Chin Med J (Engl). 2005 Nov 20;118(22):1918-20.
"We conducted a cross-sectional epidemiological study in three counties (rural communities) in 1999 to investigate the effect of iodine intake on the prevalence of hypothyroidism.... These results demonstrate that elevating iodine intake could increase the risk for development of overt and subclinical hypo-thyroidism. The fact that TSH level was higher in TPOAb (+) group than in TPOAb (-) group in Huanghua in this study indicates that excessive iodine intake may easily induce hypothyroidism in subjects with autoimmune diseases."
Multivariate analysis of relationships between iodine biological exposure and subclinical thyroid dysfunctions.Chong W, Shan ZY, Sun W, Teng WP. Chin Med Sci J. 2005 Sep;20(3):202-5. [abstract only]
"OBJECTIVE: To assess the relationships between iodine biological exposure and subclinical thyroid dysfunctions.
METHODS: The cross-sectional survey was performed to obtain the epidemiologic data of population in three communities with different iodine biological exposure: mild iodine deficiency [median urinary iodine concentration (MUI) of 50-99 microg/L], more than adequate iodine intake (MUI of 200-299 microg/L), and excessive iodine intake (MUI over 300 microg/L). Univariate and multivariate analysis (logistic regression analysis) were used to analyze the risk factors of subclinical hypothyroidism and subclinical hyperthyroidism.
RESULTS: Logistic regression analysis with sex and age controlled suggested that more than adequate iodine intake (OR = 3.172, P = 0.0004) and excessive iodine intake (OR = 6.391, P = 0.0001) increased the risk of subclinical hypothyroidism, while excessive iodine intake decreased the risk of subclinical hyperthyroidism (OR = 0.218, P = 0.0001). Logistic regression analysis including interaction of iodine intake and antibodies [thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb)] suggested that excessive iodine intake was an independent risk factor of subclinical hypothyroidism (OR = 6.360, P = 0.0001), but independent protect factor of subclinical hyperthyroidism (OR = 0.193, P = 0.0001). More than adequate iodine intake and it's interaction with TgAb increased the risk of subclinical hypothyroidism independently, in addition, it decreased the risk of subclinical hyperthyroidism at the present of TPOAb.
CONCLUSION: Both excessive iodine intake and more than adequate iodine intake could increase risk of subclinical hypothyroidism, supplement of iodine should be controlled to ensure MUI within the safe range."
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