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Objective To investigate the expression of sialic acid-binding immunoglobulin-like-lectin-1 (Siglec-1)in the peripheral blood mononuclear cell (PBMC) of patients with autoimmune thyroiditis ( AIT) and its relationship with AIT. To explore the moduratory role of activated Siglec-1 on the differentiation of T cells and the promotion of in flammation after PBMC culture. Methods The peripheral whole blood and serum samples were collected from 30 AIT patients with normal thyroid function and 30 sex-and age-matched controls. The expression of sSiglec-1 in serum was detected by ELISA. The expression of Siglec-1 in PBMC was detected by RT-PCR and WB. The expression of Siglec-1 in CD14+ monocytes and the proportion of Th1 and Th17 cells in each group were detected by flow cytometry. The PBMC in AIT or control was stimulated with NaI in the presence or absence of LPS for 72 h. The expression of Siglec-1 in CD14+ monocytes and the proportion of Th1 and Th17 cells were detected by flow cytometry. Results sSiglec-1 in serum, Siglec-1 mRNA, and Siglec-1 protein in AIT patients'PBMC were higher than those in control group ( P<0. 01). The expression of Siglec-1 in CD14+ monocytes by flow cytometry and differentiation of Th1 and Th17 cells were significantly higher than that in control group ( both P<0. 01). The expression of Siglec-1 in control and AIT patients was up-regulated by 5×10-5 mmol/L to 1×10-2 mmol/L stimulated with NaI in the presence or absence of LPS for 72 h (P<0.01), but the differentiation of Th1 and Th17 cells was up-regulated only in patients (P<0.01), and in a dose-dependent manner. Conclusion Elevated Siglec-1 expression in PBMCs and monocytes can potentially serve as a biomarker for AIT. Iodine may affect Th1 and Th17 cell differentiation by activating Siglec-1 to adjust the AIT immune response.
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Objective To analyze the effects of valproic acid(VPA),a histone deacetylase(HDAC)inhibitor,on macrophage polarization in?duced by paraquat(PQ)or lipopolysaccharide(LPS). Methods Mouse RAW264.7 cells were cultured at 37℃with 5%CO2,passaged,and then given one of the following treatments:(1)PQ;(2)PQ+VPA(classⅠandⅡa HDAC inhibitor);(3)PQ+apicidin(classⅠHDAC inhibitor);(4)PQ+MC1568(classⅡa HDAC inhibitor);(5)LPS;(6)LPS+VPA;(7)LPS+apicidin;(8)LPS+MC1568. The cells and culture supernatants were harvested after 8 h of treatment. RT?PCR,ELISA,and flow cytometry were conducted to assess the expression levels of macrophage phenotyp?ic markers. Results Both PQ and LPS skewed the macrophage functional polarity toward proinflammatory phenotype. VPA,apicidin,and MC1568 all inhibited PQ?and LPS?induced macrophages polarizing toward pro?inflammatory phenotype ,but the inhibitory effects were different in some ways. Conclusion VPA inhibits the proinflammatory function of macrophages induced by PQ and LPS ,but the effect of VPA on PQ?and LPS?induced macrophages has its own characteristics.
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Objective To investigate the effect of VPA and molecular hydrogen(H2)on phenotypes of microglia treated with hypoxia. Methods Mouse hypoxic BV2 microglia were treated with VPA or H2. The levels of phenotypic markers of supernatant and cells were detected by ELISA, flow cytometry and real?time PCR,respectively. Results Hypoxia significantly increased mRNA level of M1 marker(iNOS)and reduced mRNA levels of M2 markers(CD206 and TGF?β)in BV2(P<0.05). Besides,the ratio between the mRNA levels of M1 increased(P<0.05). VPA significantly reduced protein level(CD16/32)and mRNA production(iNOS)of M1 markers in hypoxia?treated BV2(P<0.05). The ratio be?tween the mRNA levels of M1 markers and M2 markers(CD16:CD206,CD32:CD206,iNOS:CD206 and iNOS:TGF?β)were also significantly decreased(P<0.05). H2 significantly reduced both protein levels(TNF?α,CD16/32 and iNOS)and mRNA production(iNOS)of M1 markers and increased secretion of M2 marker(IL?10)in hypoxia?treated BV2(P<0.05). The ratio between the mRNA levels of M1 markers and M2 markers(CD16:CD206,iNOS:CD206 and iNOS:TGF?β)were also highly declined(P<0.05). Conclusion Hypoxia can induce microglial cells toward pro?inflammatory phenotype. Both VPA and H2 can inhibit hypoxia?induced inflammatory effect on microglia.
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Objective To investigate the changes and related factors of maternal thyroid autoantibodies during early pregnancy. Methods Urinary iodine concentration( UIC) , serum thyroid stimulating hormone( TSH) , free thyroxine ( FT4 ) , thyroid-peroxidase antibody ( TPOAb ) , thyroglobulin antibody ( TgAb ) concentrations were determined in 7 190 women during early pregnancy in an iodine-sufficient region of China. Results The prevalence of TPOAb positivity and TgAb positivity were 8. 7% and 12. 0% respectively. The prevalence of overt hypothyroidism and subclinical hypothyroidism increased significantly in group of thyroid antibody positivity. The prevalence of TPOAb positivity and TgAb positivity presented a U-shaped curve, ranging from mild iodine deficiency to iodine excess, especially increased significantly in the group with UIC<100 μg/L. Conclusion Prevalence of thyroid antibodies positivity became higher during early pregnancy. The positive thyroid autoantibodies during pregnancy were significantly associated with maternal hypothyroidism. Both iodine excess and iodine deficiency are risk factors of positive thyroid antibodies.
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Objective To investigate the effect of subclinical hypothyroidism during pregnancy on hippocampus insulin-like growth factor Ⅰ (IGF-Ⅰ) signaling pathway in rat offspring.Methods A total of 60 female Wistar rats were evenly divided into control(CON),subclinical hypothyroidism(SCH),and clinical hypothyroidism (CH) groups.The hippocampus of progenies were collected on the postnatal day 3,postnatal day 7 to measure protein kinase B (Akt) and phosphorylated-Akt (p-Akt) by Western blot,IGF-Ⅰ and insulin-like growth factor Ⅰ receptor (IGF-Ⅰ R) by Elisa.Morris water maze and field excitatory postsynaptic potential long-term potentiation were measured at the postnatal 40 day.Results Western blot and Elisa revealed that levels of IGF-Ⅰ,IGF-Ⅰ R,and p-Akt of pups from SCH group were lower than that of CON group and were higher than CH group on day 3 (P < 0.05).On day 7,the levels of IGF-Ⅰ,IGF Ⅰ R,and p-Akt of pups from SCH group were lower than CON group (P< 0.05),but no difference was observed in p-Akt and IGF-Ⅰ R level between SCH group and CH group (P > 0.05).Latencies of all groups had shortened in Morris water maze test with increasing of training trials.The slope of field excitatory postsynaptic potenial was increased in all groups after Theta burst stimulation.The amplification percentage of slope of field excitatory postsynaptic potenial in SCH group's was lower than control group's but was higher than CH group's(all P values<0.05).Conclusions Maternal subclinical hypothyroidism impairs long-term potentiation induction in hippocampus of rat might be associated with the levels of IGF-Ⅰ,IGF-Ⅰ R,and p-Akt.
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A total of 1151 subjects were enrolled in this study.Metabolic syndrome (MS) was diagnosed according to the International Diabetes Federation (IDF) criteria.Significant differences in waist circumference,body mass index(BMI),diastolic blood pressure(DBP),systolic blood pressure(SBP),fat mass,Fat% in different serum TSH levels were found.There were positive relation between fasting plasma glucose,DBP,SBP,and serum FT4 levels,between high density lipoprotein-cholesterol,DBP,SBP,waist circumference,fat mass,Fat%,and serum FT3 levels,even after adjustment for age and sex.Serum FT3 and FT4 levels were higher in the MS group than those in the control group.
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Objective To investigate the efficacy and optimal time of levothyroxine (L-T4) treatment in pregnant rats with subclinical hypothyroidism.Methods Female adult Wistar rats were divided into six groups (n =10 per group):control,hypothyroid (H),subclinical hypothyroid (SCH),and SCH treated with L-T4 starting from the tenth,thirteenth,and seventeenth gestational day (GD10,GD13 and GD17),to restore normal thyroid hormone levels.Spatial learning was assessed in progenies by a water maze test and fEPSPs recording.Results Progenies from the SCH and H groups demonstrated significantly longer mean latency in the water maze test and a lower amplification percentage of the fEPSPs' amplitude and slope compared with the offspring of the control group.L-T4 treatment in the GD10 and GD13 groups significantly shortened mean latency and increased the amplification percentage of the fEPSPs' amplitude and slope as compared with the progeny of rats with subclinical hypothyroidism.However,L-T4 treatment in the GD17 group showed only minimal effect on spatial learning of offspring.Conclusion Maternal subclinical hypothyroidism may impair spatial learning in the offspring; L-T4 treatment started early during pregnancy may alleviate this adverse effect.
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Data were collected through questionnaire from 505 women enrolled during early pregnancy.Based on soy intake frequency,the subjects were divided into three groups:frequent (three or more times per week),conventional ( more than twice per month but less than three times per week),and occasional ( two or fewer times per month).Serum TSH and FT4 were measured by chemiluminescence immunoassay.The urinary concentrations of two primary isoflavones (daidzein and genistein) and creatinine were further assessed in 95 subjects from the three groups.The percentages of frequent,conventional,and occasional consumers were 18.6%,62.6%,and 18.8%,respectively.No difference was found in age,medical records,family history of thyroid diseases,serum FT4,TSH,and prevalence of thyroid dysfunctions among three groups. Both urinary daidzein and genistein levels were significantly higher in the frequent consumers compared with the other two groups.No correlations were found between urinary isoflavone levels and serum FT4 or TSH.These findings suggest that dietary soy consumption during early pregnancy seems not to be associated with the development of thyroid dysfunction.
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To explore the dose- and time- dependent relationship between the chronic iodine excess and thyroid structure, ultrastructure, and thyroid function in autoimmune-prone NOD. H-2h4 mice. Chronic iodine excess leads to iodine-induced goiter with an ultrastructure of follicle epithelial cells injury in a dose and time dependent way.
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Objective To verify the criteria proposed by National Academy of Clinical Biochemistry(NACB)guidelines in investigating the factors that affect serum TSH determination, and to determine the reference range of serum TSH in iodine-sufficient areas of China. Methods In 2007, 5 348 inhabitants were enrolled from 3 iodine-sufficient areas of Liaoning Province, and were asked to fulfill the questionnaire. Serum TSH, thyroid peroxidase antibody(TPOAb), and thyroglobulin antibody(TgAb)were determined, and thyroid ultrasonography was carried out. Results The distribution of TSH levels was skewed in healthy people and closely fit the curve of Gaussian distribution after logarithmic transformation. The levels of TSH in subjects of 12-19 years of age were significantly higher than those of other age groups(P<0.01), and no significant difference was found among the latter groups. TSH level in females [(1.68±1.90)mIU/L] was higher than in males[(1.45±1.92)mIU/L, P<0.01]. The reference range of TSH was 0.43-4.74 mIU/L in males, and 0.48-5.39 mIU/L in females. Family history of thyroid disease, abnormal thyroid ultrasonography, and positive thyroid antibodies were the factors that influenced TSH level. Conclusion The reference range of serum TSH in iodine-sufficient areas of China is established.
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Objective To use the first trimester-specific reference intervals of thyroid-related hormones to explore the prevalence of thyroid dysfunction during early pregnancy and to analyze effectiveness of different screening strategies. Methods In this study 2 899 pregnant women were enrolled during the first trimester of gestation. TSH, FT4, FT3, and thyroid peroxidase antibody (TPOAb) were measured and thyroid disorders of pregnant women were diagnosed based on the first trimester-specific reference intervals. Results The prevalence of hypothyroidism was significantly higher in the high-risk group than in the non-high risk group ( 16.3% vs 5.3%,RR = 3.1,95% CI 2.4-4.0, P<0.01 ). TPOAb ( RR = 4.7, 95 % CI 3.6-6.0, P<0.01 ), and personal history of thyroid diseases ( RR=3.2, 95% CI 1.9-5.4, P<0.01 ) increased the risk of hypothyroidism. The prevalence of hyperthyroidism was higher in the high-risk group (3.1% vs 1.4%, P = 0. 006, RR = 2.2, 95% CI 1.2-3.9, P=0.006). TPOAb (RR=2.6, 95%CI 1.3-5.0, P=0.007), and presence of personal history of thyroid diseases( RR=4.7, 95% CI 1.7-12.5, P=0.006) also increased the risk of hyperthyroidism. 56.7% women with hypothyroidism and 64. 7% women with hyperthyroidism were in the non-high risk group. Conclusion We recommend that screening all pregnant women for thyroid disorders in the first trimester with TSH, FT4, and TPOAb is more effective than the case-finding approach.
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Objective To investigate the effect of treatment with levothyroxine in early maternal subclinical hypothyroidism (SCH) on the neural development of the progeny. Methods 75 thyroidectomized female Wistar rats were divided randomly into groups of hypothyroidism (CH), SCH, SCH treated with levothyroxine at embryonic day 10 (E10), E13, and E17. There were 15 sham operated controls. Body weight,thyroid function, and the development of progeny by morris water maze, immunohistochemistry, and Nissl's staining of progeny were made. Results Pups from SCH or CH group had significantly lower body weight than euthyroid group ( P<0. 05 ). Pups from E10, E13 or E17 groups had normal body weight compared to pups of control (P>0.05). The levels of TSH and total T4( TT4 ) of all pups were normal. The mean latencies were longer in pups from CH, SCH, and E17 group than the control (P<0.05). The mean escape latencies did not differ between the control and E10 group pups and between the control and E13 pups (P>0.05). There were changes in the cytoarchitecture of the barrel cortex and of the hippocampus ( toluidine blue-stained sections) in CH, SCH, and E17 pups. The barrel cortex of E10 or E13 pups was similar to that of control pups. The distribution of BrdUlabeled cells was more widespread in CH, SCH, and E17 pups than in control, E10, and E13 progeny.Conclusion Maternal SCH disturbs learning and memory performances, cytoarchitecture and cell migration of the pups. Treatment with levothyroxine in early maternal SCH before E13 improves the cell migration in the developing brain of the progeny.
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Objective To explore whether maternal subclinical hypothyroidism gives rise to poor performance in the offspring and whether this is associated with the expression of several genes that are under the control of thyroid hormones. Methods Sixty female rats were divided into three groups ( each group n = 20): ( 1 )maternal subclinical hypothyroidism ( total thyroidectomy with T4 infusion), (2) maternal hypothyroidism ( total thyroidectomy without T4 infusion), and (3) control (sham operated). All rats were mated 10 days after the start of infusion. The infusion continued until 10 days postpartum. Pups were sacrificed at postnatal day 3, 7, and 21. The hippocampus was collected and tested for brain-derived neurotrophic factor (BDNF) and Rap1 protein expression by Western blotting and for BDNF and neural cell adhesion molecule ( NCAM ) mRNA expression by real-time polymerase chain reaction. On day 41-49, rat pups explored the Morris water maze. Time spent in the quadrant previously containing the plat form was recorded. Results The present study found decreases in BDNF mRNA (on day 3 ) and protein levels (on day 3 and 7 ) in hippocampi of pups from subclinical hypothyroidism dams (P<0.05). No change was observed in the levels of NCAM mRNA, whereas at day 21, expression of Rap1 protein was higher than that of control offspring. In addition, pups of subclinical hypothyroidism dams showed a trend toward depression in short-term memory (P>0.05), and long-term memory testing revealed a trend toward subclinical hypothyroidism group pups being less able to remember a fixed platform position than controls, spending less time in the proper quadrant ( P<0. 05 ). Conclusion The long-term memory deficits of pups born to maternal subclinical hypothyroidism dams are likely related with decrease in BDNF expression as well as increase in Rap1 expression in hippocampi.
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Objective To assess the effects of maternal subclinical hypothyroidism (SCH) during the first trimester on neuropsychological development of the offspring by 20-30 months. Methods In this study, 1 761 pregnant women from 10 hospitals with about 8 weeks of gestation were enrolled. Urinary iodine excretion and serum thyrotropin ( TSH ), free thyroxine ( FT4 ), and thyroid peroxidase antibody ( TPOAb ) levels were determined in all subjects. Pregnant women with SCH (TSH≥2.5 mIU/L) were divided into two subgroups using trimester-specific thyroid function reference: group A (2.5 mIU/L≤TSH<3.93 mIU/L, 18 cases), and group B (TSH ≥3.93 mIU/L, 20 eases). Thirty euthyroid and TPOAb-negative women from the same cohort were selected as controls. Intellectual and motor development score evaluations were performed in the children by 20-30 months of age. Results Children of women with SCH and subgroups A and B had lower mean intelligence scores 6.55,3.39, and 9.40 points compared with those of the control group (P=0. 001, P=0. 125, and P<0. 001 ); the respective mean motor scores were 6.31,4.35, and 8.07 points being lower than that of the control ( P=0. 003,P=0. 070, and P=0. 001 ). Intelligence scores and motor scores were negatively correlated with TSH levels (r=-0.425, P<0. 001 and r=-0. 394, P=0. 001 ). Multiple group comparisons revealed that differences of TSH affected intelligence and motor scores (F=9. 277, P<0. 001 and F=5. 909, P=0. 004). Ordinal logistic regression analysis showed that possibilities for the reduction of filial mental development index ( MDI ) and psychomotor development index ( PDI ) scores in SCH with maternal TSH levels≥3.93 mIU/L were 8.66 and 6.27 times that of controls ( OR = 8.66,95% CI 2.72-27.57, OR =6.27,95% CI 2.03-19.34 ). Conclusion Maternal elevated TSH levels diagnosed by trimester-specific reference during early gestation are independently associated with lowered filial neurodevelopment scores by 20-30 months.
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Objective To prospectively observe the effect of levothyroxine treatment on neuropsychological development in offspring of pregnant women with subclinical hypothyroidism. Methods Twenty-three pregnant women with subclinical hypothyroidism received levothyroxine therapy (SCH+LT4 group) and 17 who did not receive levothyroxine ( SCH group) were enrolled; 24 pregnant women with normal thyroid function were referred as controls (C group). All the subjects underwent the planned thyroid tests regularly. Serum TSH, TT4, FT4, TT3,FT3, TPOAb, and TgAb levels were determined. Their 14-30 month-old children underwent the tests relating to intelligence and motor activity with the Bayley scale. Results In SCH group, SCH+LT4 group, and C group, the MDI were 115. 12, 118.56, and 117.63, respectively. And the PDI were 115.47, 120.65, and 117.50,respectively. The MDI and PDI were the highest in SCH+LT4 group and were the lowest in SCH group. Serum TSH levels remained above 2.0 mIU/L during the whole course of pregnancy in SCH group and higher than that in C group at all time points ( P<0.05 ). Serum TT4 and FT4 levels were lower in SCH group than in C group at all time points except G28 and G32. The baseline TSH level in SCH+LT4 group was the highest ( P<0.01 ), their TT4 and FT4 levels were the lowest among the three groups. In SCH + LT4 group, serum TSH, TT4, and FT4 levels were similar to C group after L-T4 treatment. Conclusion The prompt L-T4 treatment can maintain normal TSH levels in pregnant women with subclinical hypothyroidism during the whole course of pregnancy, and impairment of neuropsychological development in infants may be avoided.
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Objective To investigate the epidemiological characteristics of non-toxic goiter and non-toxic thyroid nodules in the regions with different iodine intakes and the factors influencing the occurrence, development and outcome of goiter and thyroid nodules. Methods 3 385 subjects, who had taken part in the previous survey in 1999 with the ultrasonic examination of thyroid, were composed of individuals in Panshan with chronic mild iodine deficiency,in Zhangwu with more than adequate iodine "after iodine supplementation and in Huanghua with excessive iodine. These 3 groups of subjects were followed up in 2004. Results (1) The cumulative incidences of diffuse goiter in Panshan ,Zhangwu and Huanghua were 7.1% ,4.4% and 6.9% ,respectively ,being the lowest in Zhangwu (P<0.01) and those of nodular goiter were 5.0% ,2. 4% and 0.8%, respectively, being the highest in Panshan (P<0.01). (2) The incidences of single nodule were 4.0% ,5.7% and 5.6%, respectively, and those of multiple nodules 0.4%, 1.2% and 1.0%, respectively. (3)The result of logistic analysis showed that iodine deficiency,iodine excess and positive thyroid autoantibodies (TAA) were the independent risk factors for the occurrence of goiter. (4)In Zhangwu ,the incidence of non-toxic goiter in the group with positive TAA was higher than that in the group with negative TAA(P<0.01) ,while there were no such differences in Panshan and Huanghua. (5)In these three regions, the rates of positive TAA in the individuals with diffuse non-toxic goiter were higher than those in the healthy subjects (P<0.05). And in Huanghua,the rate of positive TAA in subjects with non-toxic nodular goiter was also higher than that in the healthy individuals (P<0.05). Conclusion Iodine deficiency and iodine excess may both induce the raising incidence of goiter. Nodular goiter is prevalent in iodine deficient district and diffuse goiter is the predominant form in places with iodine excess. Thyroid autoimmunity is associated with occurrence and maintenance of goiter, and this phenomenon is more obvious in the community with previous iodine deficiency followed then by treatment with more than adequate iodine.
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Thyrocytes expressing MHC class Ⅱ molecules were separated from transgenic mice and were co-cultured with autologous spleen T lymphocytes. T cells did not proliferate and were not activated, but CD4+ T cells were promoted into apoptosis.
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Objective To clarify the effect of iodine intake on serum thyroglobulin (Tg). Methods A 5-year prospective study was conducted in the 3 different iodine intake areas in China [Panshan (miht deficiency) ,Zhangwu (more than adequate) and Huanghua (excess)]. A total of 3 099 people with normal serum levels of Tg in 1999 were followed and 2 448 of these participants were feasible to be observed in 2004 and included in the present study. The serum levels of Tg, thyraglobulin antibody(TgAb), thyroid peroxidase antibody(TPOAb) and TSH, thyroid volume, family and personal histories of thyroid diseases were measured and inquried. The general linear model (GLM) was used to explore the determinants of Tg. Results Among the study population at baseline, serum Tg were significantly different in three areas [7.5 (4.4-13. 1) μg/L at Panshan, 6.8 (3.6-11.2)μg/L at Huanghua, 5.9 (3.2-10.7) μg/L at Zhangwu, P<0.01]. They were associated with age, sex and the rate of positive TgAb, abnormal thyroid volume, abnormal TSH and positive personal history of thyroid diseases, in order to control the effects of confounding factors, the data from 1856 subjects with thyroid-related indexes all in normal range and without personal history of thyroid diseases were analyzed to clarify the effect of iodine intake on Tg. The serum Tg among three areas were significantly different in both 1999 and 2004, they were all increased in 5 years with significant augment (△ Tg) among the three areas[3.1 (-0.2-8.0) μg/L at Panshan, 3.5 (0.5-9.0)μg/L at Huanghua vs 2. 5(0.3-6.1) μg/L at Zhangwu,P<0.01]. The GLM analysis revealed that age, Tg and TSH levels at baseline were the determinants of △Tg in addition to iodine intake. Conclusion Iodine intake is a dominant determinant of serum Tg. Age and TSH should also be considered while indicating iodine intake by serum Tg.
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Objective To explore the correlation between anti-thyroid autoantibodies and hepatitis C virus (HCV) infection. Methods Four hundred and sixty-two samples with positive thyroid peroxidase antibody (TPOAb) and (or) thyroglobulin antibody (TgAb) were collected. Three hundred and eighty age and gender matched subjects with negative TPOAb and TgAb were selected as controls. The anti-HCV antibody was examined in all the cases using the third-generation enzyme-linked immunosorbent assay (ELISA), HCV RNA qualitative examination was examined further in those who had positive anti-HCV antibody. Meanwhile, 195 subjects with hepatitis C, 150 healthy subjects and 150 subjects with hepatitis B were tested for thyroid-related markers. The data were analyzed by independent-sample t test and chi square test. Results The HCV infection rate in 462 thyroid autoantibodies positive subjects was 1.30% and 0.53% in 380 thyroid autoantibodies negative subjects. There was no significant difference of the HCV infection rate between two groups (X2=1.322, P>0.05). In the subjects with hepatitis C, 30.8% were TPOAb positive, 30.8% were TgAb positive, which were significantly different from those of healthy subjects and subjects with hepatitis B (X2=21.496,X2=30.454;P<0.01). Conclusions HCV infection rate does not increase in subjects with abnormal thyroid autoimmunity. However, positive rate of thyroid autoantibodies increases in subjects with hepatitis C, which suggests that thyroid-related markers should be examined in hepatitis C patients.
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Objective To determine the factors that influence the development of abnormal thyrotropin (TSH) level in an euthyroid population.Methods We conducted a follow-up study in 3 communities with different iodine status.Of the 3403 euthyroid subjects at baseline screened in 1999,80.1% ( n = 2727 ) was visited and sampled in 2004 for measuring TSH,thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb).Results Iodine status in the 3 communities were stable.Decreased TSH level( <0.3 mU/L) developed in 2.5% (n =68) of sampled subjects,while raised TSH level( > 4.8 mU/L) in 2.4% (n = 64).A logistic analysis showed that risk factors for developing decreased TSH level included positive conversion of TPOAb (OR = 5.5 ),positive TPOAb both in 1999 and in 2004 ( OR = 4.0),positive TgAb in 2004 ( OR = 3.7) and TSH < 1.0 mU/L in 1999 ( OR = 2.6).Risk factors involved in developing raised TSH level included iodine status of Zhangwu community ( OR = 4.1 ),iodine status of Huanghua community ( OR = 3.9),positive TgAb in 2004 ( OR = 3.7 ),positive TPOAb both in 1999 and 2004 (OR =3.6),positive conversion of TPOAb (OR =2.7) and TSH > 1.9 mU/L in 1999 (OR = 2.6 ).Conclusions Exposure to long-term iodine excess imposes danger of developing hypothyroidism.The risk will be even higher when exposing to iodine adequacy after correction of iodine deficiency.An interval between 1.0 and 1.9 mU/L of TSH level was optimul with the least probability of developing abnormal TSH level.