A novel c.64G > T (p.G22C) NR5A1 variant in a Chinese adolescent with 46,XY disorders of sex development: a case report.

BACKGROUND: Adolescents with 46,XY disorders of sex development (DSD) face additional medical and psychological challenges. To optimize management and minimize hazards, correct and early clinical and molecular diagnosis is necessary. CASE PRESENTATION: We report a 13-year-old Chinese adolescent with absent Müllerian derivatives and suspected testis in the inguinal area. History, examinations, and assistant examinations were available for clinical diagnosis of 46,XY DSD. The subsequent targeting specific disease-causing genes, comprising 360 endocrine disease-causing genes, was employed for molecular diagnosis. A novel variation in nuclear receptor subfamily 5 group A member 1 (NR5A1) [c.64G > T (p.G22C)] was identified in the patient. In vitro functional analyses of the novel variant suggested no impairment to NR5A1 mRNA or protein expression relative to wild-type, and immunofluorescence confirmed similar localization of NR5A1 mutant to the cell nucleus. However, we observed decreased DNA-binding affinity by the NR5A1 variant, while dual-luciferase reporter assays showed that the mutant effectively downregulated the transactivation capacity of anti-Müllerian hormone. We described a novel NR5A1 variant and demonstrated its adverse effects on the functional integrity of the NR5A1 protein resulting in serious impairment of its modulation of gonadal development. CONCLUSIONS: This study adds one novel NR5A1 variant to the pool of pathogenic variants and enriches the adolescents of information available about the mutation spectrum of this gene in Chinese population.

Circular RNAs in the Origin of Developmental Lung Disease: Promising Diagnostic and Therapeutic Biomarkers.

Circular RNA (circRNA) is a newly discovered noncoding RNA that regulates gene transcription, binds to RNA-related proteins, and encodes protein microRNAs (miRNAs). The development of molecular biomarkers such as circRNAs holds great promise in the diagnosis and prognosis of clinical disorders. Importantly, circRNA-mediated maternal-fetus risk factors including environmental (high altitude), maternal (preeclampsia, smoking, and chorioamnionitis), placental, and fetal (preterm birth and low birth weight) factors are the early origins and likely to contribute to the occurrence and progression of developmental and pediatric cardiopulmonary disorders. Although studies of circRNAs in normal cardiopulmonary development and developmental diseases have just begun, some studies have revealed their expression patterns. Here, we provide an overview of circRNAs' biogenesis and biological functions. Furthermore, this review aims to emphasize the importance of circRNAs in maternal-fetus risk factors. Likewise, the potential biomarker and therapeutic target of circRNAs in developmental and pediatric lung diseases are explored.

Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats.

Background: Bronchopulmonary dysplasia (BPD) is characterized by impaired alveolar and microvascular development. Claudin-18 is the only known lung-specific tight junction protein affecting the development and transdifferentiation of alveolar epithelium. Objective: We aimed to explore the changes in the expression of claudin-18, podoplanin, SFTPC, and the canonical WNT pathway, in a rat model of hyperoxia-induced BPD, and to verify the regulatory relationship between claudin-18 and the canonical WNT pathway by cell experiments. Methods: A neonatal rat and cell model of BPD was established by exposing to hyperoxia (85%). Hematoxylin and eosin (HE) staining was used to confirm the establishment of the BPD model. The mRNA levels were assessed using quantitative real-time polymerase chain reaction(qRT-PCR). Protein expression levels were determined using western blotting, immunohistochemical staining, and immunofluorescence. Results: As confirmed by HE staining, the neonatal rat model of BPD was successfully established. Compared to that in the control group, claudin-18 and claudin-4 expression decreased in the hyperoxia group. Expression of ß-catenin in the WNT signaling pathway decreased, whereas that of p-GSK-3ß increased. Expression of the AEC II marker SFTPC initially decreased and then increased, whereas that of the AEC I marker podoplanin increased on day 14 (P < 0.05). Similarly, claudin-18, claudin-4, SFTPC and ß-catenin were decreased but podoplanin was increased when AEC line RLE-6TN exposed to 85% hyperoxia. And the expression of SFTPC was increased, the podoplanin was decreased, and the WNT pathway was upregulated when claudin-18 was overexpressed. Conclusions: Claudin-18 downregulation during hyperoxia might affect lung development and maturation, thereby resulting in hyperoxia-induced BPD. Additionally, claudin-18 is associated with the canonical WNT pathway and AECs transdifferentiation.

GNAS mutation is an unusual cause of primary adrenal insufficiency: a case report.

BACKGROUND: Primary adrenal insufficiency in children has non-specific and extensive clinical features, so the diagnosis of its etiology is complex and challenging. Although congenital adrenal hyperplasia is the most common cause, more and more other genetic causes have been identified. GNAS mutation is easily overlooked as a rare cause of primary adrenal insufficiency. Here we firstly report a neonatal case of primary adrenal insufficiency caused by GNAS mutation. CASE PRESENTATION: A boy was diagnosed with congenital hypothyroidism 10 days post-partum and treated immediately. He also had persistent hyperkalaemia and hyponatraemia with elevated adrenocorticotropic hormone. At 70 days after birth, he was transferred to our hospital on suspicion of congenital adrenal hyperplasia. Physical examination found no other abnormalities except for growth retardation. Laboratory examination revealed increased aldosterone and normal cortisol, 17-hydroxyprogesterone, and androstenedione levels. Abnormally elevated parathyroid hormone was accompanied by normal blood calcium. Genetic assessment found a de novo, heterozygous c.432 + 1G > A variant in GNAS. CONCLUSIONS: We report this case to highlight that GNAS mutation is an unusual cause of primary adrenal insufficiency. The combination of primary hypothyroidism and /or pseudohypoparathyroidism will provide diagnostic clues to this condition.

Clinical Characteristics and Follow-Up of 19 Children With Hashimoto's Thyroiditis Aged Below 3 Years: A Single-Center Retrospective Analysis.

Aim: To analyze the clinical characteristics of Hashimoto's thyroiditis (HT) in children below 3 years of age in order to improve the understanding of the disease, avoid misdiagnosis, and achieve early diagnosis and treatment. Methods: The study retrospectively analyzed the clinical data of 19 patients diagnosed with HT in the first three years of life. Results: The patients (12 female, 7 male) had an average age of 26.1 ± 8.2 months (range 10-36 months). At presentation, one patient had euthyroidism, ten had hypothyroidism, seven had subclinical hypothyroidism, and one had hyperthyroidism. The most common reasons for doctor's visits were thyroid enlargement (21.1%), global developmental delay (21.1%), and routine thyroid function tests in patients with type 1 diabetes (26.3%). Sixteen patients provided follow-up data, and the mean follow-up time was 23.31 ± 16.44 months (range 1-48 months). In the hypothyroidism group, one patient stopped levothyroxine (LT4) treatment after 2 months; the remaining patients had been treated with LT4 since their diagnosis. In the subclinical hypothyroidism group, one patient whose thyroid function returned to normal after 1 month of being diagnosed was not treated. The remaining patients received LT4 treatment at their diagnosis or during follow-up. The patient with hyperthyroidism was treated with methimazole after diagnosis, but treatment was discontinued 11 months later and LT4 was initiated 26 months after diagnosis. One in four patients with global developmental delay approached normal mental development after LT4 treatment. Four in six patients with short stature achieved height catch-up. Conclusion: At their initial HT diagnosis, most of the children showed hypothyroidism or subclinical hypothyroidism. Children with global developmental delay require continual screening, even if the thyroid function is normal after birth, to determine whether they have HT-induced hypothyroidism. Thyroxine replacement could partially relieve the clinical manifestations of hypothyroidism and early diagnosis and treatment are essential for improving patient prognosis.

Intrauterine Hypoxia and Epigenetic Programming in Lung Development and Disease.

Clinically, intrauterine hypoxia is the foremost cause of perinatal morbidity and developmental plasticity in the fetus and newborn infant. Under hypoxia, deviations occur in the lung cell epigenome. Epigenetic mechanisms (e.g., DNA methylation, histone modification, and miRNA expression) control phenotypic programming and are associated with physiological responses and the risk of developmental disorders, such as bronchopulmonary dysplasia. This developmental disorder is the most frequent chronic pulmonary complication in preterm labor. The pathogenesis of this disease involves many factors, including aberrant oxygen conditions and mechanical ventilation-mediated lung injury, infection/inflammation, and epigenetic/genetic risk factors. This review is focused on various aspects related to intrauterine hypoxia and epigenetic programming in lung development and disease, summarizes our current knowledge of hypoxia-induced epigenetic programming and discusses potential therapeutic interventions for lung disease.

[A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants].

Bronchopulmonary dysplasia (BPD) has the main manifestations of pulmonary edema in the early stage and characteristic alveolar obstruction and microvascular dysplasia in the late stage, which may be caused by structural and functional destruction of the lung epithelial barrier. The Claudin family is the main component of tight junction and plays an important role in regulating the permeability of paracellular ions and solutes. Claudin-18 is the only known tight junction protein solely expressed in the lung. The lack of Claudin-18 can lead to barrier dysfunction and impaired alveolar development, and the knockout of Claudin-18 can cause characteristic histopathological changes of BPD. This article elaborates on the important role of Claudin-18 in the development and progression of BPD from the aspects of lung epithelial permeability, alveolar development, and progenitor cell homeostasis, so as to provide new ideas for the pathogenesis and clinical treatment of BPD.

Application Prospects of Mesenchymal Stem Cell Therapy for Bronchopulmonary Dysplasia and the Challenges Encountered.

Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in premature babies, especially affecting those with very low or extremely low birth weights. Survivors experience adverse lung and neurological defects including cognitive dysfunction. This impacts the prognosis of children with BPD and may result in developmental delays. The currently available options for the treatment of BPD are limited owing to low efficacy or several side effects; therefore, there is a lack of effective treatments for BPD. The treatment for BPD must help in the repair of damaged lung tissue and promote further growth of the lung tissue. In recent years, the emergence of stem cell therapy, especially mesenchymal stem cell (MSC) therapy, has improved the treatment of BPD to a great extent. This article briefly reviews the advantages, research progress, and challenges faced with the use of MSCs in the treatment of BPD. Stem cell therapy is beneficial as it repairs damaged tissues by reducing inflammation, fibrosis, and by acting against oxidative stress damage. Experimental trials have also proven that MSCs provide a promising avenue for BPD treatment. However, there are challenges such as the possibility of MSCs contributing to tumorous growths, the presence of heterogeneous cell populations resulting in variable efficacy, and the ethical considerations regarding the use of this treatment in humans. Therefore, more research must be conducted to determine whether MSC therapy can be approved as a treatment option for BPD.

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.

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 mug/l may reflect the safe range of iodine intake levels. Serum thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine status.

Influence of iodine on the reference interval of TSH and the optimal interval of TSH: results of a follow-up study in areas with different iodine intakes.

OBJECTIVE: The aim of the present study was to evaluate whether the status of iodine nutrition influences the TSH concentration in a selected Chinese reference population according to the criteria proposed by National Academy of Clinical Biochemistry (NACB) and regular thyroid ultrasonography, to establish a new reference interval of TSH based on the wide variation of iodine nutrition in populations, and to identify an optimal interval of TSH by following up the cohort with normal TSH concentrations at baseline. DESIGN: The study was conducted in Panshan, Zhangwu and Huanghua, the regions with mildly deficient, more than adequate and excessive iodine intake, respectively. Of the 3761 unselected subjects who were enrolled at baseline, 2237 met the criteria for a reference population. Of 3048 subjects with normal serum TSH at baseline, 2727 (80.0%) participated in the 5-year follow-up study. TSH and thyroid autoantibodies in serum and iodine in urine were measured, and B-mode ultrasonography of the thyroid was performed. RESULTS: In the reference population, there was a urinary iodine-related increment of serum TSH levels (r = 0.21, P = 0.000), and the mean levels of TSH in Panshan, Zhangwu and Huanghua were 1.15, 1.28 and 1.93 mIU/l, respectively (P = 0.000), corresponding to the rising regional iodine intake. Based on the overall data, we obtained a reference interval of 0.3-4.8 mIU/l. TSH concentrations obtained in the follow-up study correlated well with those at baseline (r = 0.58, P = 0.000). A baseline serum TSH > 1.9 mIU/l was associated with an increased incidence of development of supranormal TSH and a baseline serum TSH < 1.0 mIU/l was associated with an increased incidence of subnormal TSH development. CONCLUSIONS: Iodine nutrition is an important factor associated with TSH concentration even in the rigorously selected reference population. Baseline TSH of 1.0-1.9 mIU/l is an optimal interval with the lowest incidence of abnormal TSH in 5 years.

Effect of iodine intake on thyroid diseases in China.

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].

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.

[Long-term effects of high iodine intake: inhibition of thyroid iodine uptake and organification in Wistar rats].

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 spectrophotograph. 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 different iodine intake on schoolchildren's thyroid diseases and intelligence in rural areas.

BACKGROUND: Reports are increasingly appearing on the side effects caused by excessive iodine intake. Our objective was to find out whether iodine excess would impair the thyroid function and intelligence of schoolchildren in rural areas of China. METHODS: A comparative epidemiological study was made on thyroid function and intelligence of the schoolchildren in the areas of low, moderate or excessive intake of iodine. In the area of low intake of iodine (Panshan, Liaoning province, median urinary iodine (MUI) was 99 microg/L), of moderate intake of iodine (Zhangwu, Liaoning Province, MUI was 338 microg/L) and of excessive intake of iodine (Huanghua, Hebei Province, MUI was 631 microg/L). The numbers of schoolchildren from each area selected to take part in a Chinese version of Raven's Test were 190, 236 and 313, respectively, and then 116, 110 and 112 of them were tested for thyroid function, thyroid autoantibody (TAA) and urinary iodine (UI). RESULTS: There were no significant differences in the incidences of overt hyperthyroidism, subclinical hyperthyroidism and overt hypothyroidism in Panshan, Zhangwu and Huanghua. But significant differences were found in the incidences of subclinical hypothyroidism (P = 0.001) in these three areas. The incidences of subclinical hypothyroidism in Huanghua and Zhangwu were 4.76 and 3.37 times higher than that in Panshan. TAA were negative in all the schoolchildren with subclinical hypothyroidism except for one. No significant difference was found among the rates of thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in these three areas. Mean serum thyroglobulin (TG) value of Huanghua was markedly higher than those of the other two (P = 0.02). Mean serum TG value of Zhangwu was higher than that of Panshan but the difference was not significant. Mean IQ value of the schoolchildren in Huanghua was markedly higher than that for Zhangwu (P = 0.001). Mean IQ value of the schoolchildren in Panshan was lower than that of Huanghua and higher than that of Zhangwu but, again, the differences were not significant. CONCLUSIONS: The increase of iodine intake may increase the risk for schoolchildren of subclinical hypothyroidism. In the area of iodine excess, most of the subclinical hypothyroidism cases are not of autoimmune origin. No obvious effect of excess iodine was found on mental development of schoolchildren.

[Multifactor analysis of relationship between the biological exposure to iodine and hypothyroidism].

OBJECTIVE: To assess the relationship between the biological exposure to iodine and hypothyroidism. METHODS: Logistic regression model was used to analyze the risk factors of hypothyroidism, according to the epidemiologic data of 3761 adults in 3 kinds of rural communities: mild iodine deficiency area (4 natural villages in Panshan County, Liaoning Province), more than adequate iodine (7 natural villages of Zhangwu County, Liaoning Province), and excessive iodine area (2 natural villages of Huanghua City, Hebei Province). RESULTS: More than adequate iodine and excessive iodine were independent risk factors of subclinical hypothyroidism (OR = 3.172 and 6.391, P < 0.05) and overt hypothyroidism (OR = 3.696 and 9.213, P < 0.05). When interactions of iodine exposure and thyroid peroxidase antibody (TPOAb) or thyroglobulin antibody (TgAb) were included, more than adequate iodine was still a risk factor of subclinical hypothyroidism (OR = 2.788, P < 0.01), but had no such effect on overt hypothyroidism. Interaction of more than adequate iodine and positive TgAb significantly affected subclinical hypothyroidism and overt hypothyroidism (OR = 2.656 and 3.347, P < 0.05). CONCLUSION: More than adequate and excessive iodine exposure are independent risk factors of hypothyroidism. The risk of hypothyroidism grows up and thyroid dysfunction becomes more serious with the increasing of the biological exposure to iodine.

[An epidemiological study on factors affecting serum thyroglobulin levels].

OBJECTIVE: To investigate the effects of several factors affecting serum thyroglobulin (TG) levels among people aged 14 or more. METHODS: We selected Panshan with median urinary iodine (MUI) 83.45 micro g/L as a deficient iodine intake community, Zhangwu with MUI 242.85 micro g/L as a sufficient iodine intake community and Huanghua with MUI 650.87 micro g/L as an excessive iodine intake community. Serum TG and thyroid stimulating hormone (TSH) were measured in 3,335 subjects whose thyroglobulin antibody (TGAb) were negative and thyroid volume were examined using B-ultrasound. RESULTS: In the population with MUI of 80 - 650 micro g/L, serum TG levels presented a "V" curve. An elevated serum TG was found in both the communities with deficient iodine intake and excessive iodine intake. The same trend was shown in the groups with different levels of serum TSH. An elevated serum TG was found in both the groups of TSH < 0.3 mU/L and TSH > 4.8 mU/L. The serum TG levels was positively correlated with thyroid volume and was higher in female subjects than in male. An increased serum TG was found in subjects of aged 50 in the community with deficient iodine intake. CONCLUSION: Serum TG level is affected by gender, amount of iodine intake, serum TSH level and thyroid volume.