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.

[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.

Clinical features at the onset of childhood type 1 diabetes mellitus in Shenyang, China.

AIM: To describe the clinical picture and laboratory features of Chinese children with newly diagnosed type 1 diabetes mellitus. METHODS: The clinical and laboratory data of a total of 203 children who presented with newly diagnosed type 1 diabetes mellitus during a 5-year period (2004-2008) were retrospectively analysed based on hospital records. RESULTS: There were 88 boys (43.3%) and 115 girls (56.7%) with a median age of 8.3 years. The age distribution was categorised as 0-4 years: 52 (25.6%), 5-9 years: 57 (28.1%) and 10-14 years: 94 (46.3%). We found a peak incidence rate in the older age group. No significant seasonality was observed. The most common symptoms were polydipsia, polyuria and weight loss. Eighty-five (41.9%) of all patients presented with diabetic ketoacidosis (DKA). The average duration of presenting symptoms before the hospital encounter was 24.5 days. Young age group children had shorter duration (17.1 days, P = 0.03) and significantly lower levels of C-peptide (P = 0.003) and haemoglobin A1c (P = 0.049) than the other groups. Children with DKA had a higher incidence of preceding infections (P = 0.032), lower free triiodothyronine and free thyroxine levels (P= 0.035, 0.046), and higher white blood cell counts (P = 0.000) than the non-DKA group. CONCLUSION: The duration between the onset of the symptoms and diagnosis was long, and the proportion of DKA in children with newly diagnosed diabetes mellitus was high. These findings call for a collaborative effort for the early recognition of symptoms by patients and physicians in order to avoid more severe types of presentation.

[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.

[An epidemiological study on the relationship between selenium and thyroid function in areas with different iodine intake].

OBJECTIVE: To investigate the relationship between selenium status and thyroid dysfunction in 3 areas with different iodine intake. METHODS: An epidemiological research was performed in the rural communities of Panshan County (iodine-deficient area) and Zhangwu County (iodine-sufficient area), Liaoning Province, and Huanghua County, Hebei Province (iodine-excessive area). Serum selenium, TSH, FT3 and FT4 levels were examined in 329 patients with thyroid dysfunction (including clinical hypothyroidism, subclinical hypothyroidism, clinical hyperthyroidism and subclinical hyperthyroidism) and 183 normal inhabitants. RESULTS: The median serum selenium concentrations in Panshan, Zhangwu and Huanghua were 91.4, 89.1, and 83.2 microg/L respectively. There was no difference in serum selenium levels between the patients with subclinical hypothyroidism, clinical hypothyroidism, and clinical hyperthyroidism and their normal controls. The median serum selenium concentration of the subclinical hyperthyroidism patients was 82.6 microg/L, significantly lower than that of the normal controls (87.3 microg/L). The FT3/FT4 ratio was decreased, the FT4 level was increased in the subclinical hyperthyroidism patients in comparison with the normal controls, and no significant difference in FT3 level was found between them. No significant effect of sex and age was found on serum selenium level of normal inhabitants. In normal controls serum selenium was inversely correlated with serum TSH level, and the subjects with serum selenium < or = 80 microg/L had the median TSH level of 2.10 mU/L, markedly higher than that of the subjects with the serum selenium of 80-100 microg/L (1.29 mU/L) and that of the subjects with the serum selenium of 100 approximately 120 micro g/L (1.28 mU/L). For the thyroid dysfunction patients with positive thyroid auto-antibody (TPOAb) in Zhangwu County, the serum selenium was negatively associated with TPOAb level. The serum selenium level of the TPOAb highly positive group (TPOAb > 600 IU/ml) was 83.6 IU/ml, significantly lower than those of the TPOAb lowly positive group and TPOAb moderately positive group (83.6, 92.9 and 95.6 microg/L respectively). CONCLUSION: No obvious effect of selenium status is found on the development of thyroid dysfunction in these three areas. But selenium deficiency can impair thyroid function by means of disturbing thyroid hormone metabolism and decreasing antioxidant ability of the thyroid.