Maternal hypothyroidism can cause adverse outcomes for both the pregnancy and fetus, and may affect intelligence quotient of the offspring. This article reviews mainly the diagnosis and treatment of maternal hypothyroidism.

Studies from clinical observation and animal experiments have indicated that maternal subclinical hypothyroidism during the first gestational term may lead to impairment of brain development of offspring, and early diagnosis and effective treatment may prevent the damage. Therefore, we suggest that it is pertinent to screen thyroid function before gestational 8 weeks in pregnant women, especially for those who have risk factors of thyroid diseases. We also suggest that maternal subclinical hypothyroidism should be treated with levo-thyroxine ( L-T4 ) before 12 gestational weeks. Thyroid function should be measured regularly in order to adjust the dosage of L-T4 and reach the goal of treatment on time, so as to protect the brain development of fetus and offspring.

Thyroid autoantibodies (TAA) in euthyroid women were associated with several adverse pregnancy outcomes,such as miscarriage,preterm birth.Maternal TAA frequently results in transient mild elevation of serum TSH above the normal reference value in women during pregnancy and in infants born in the first month of life,and may affect neuropsychological development of their offspring.The cause is still unclear.Medical interventions on TAA involve levothyroxine or selenium supplementation. The article reviews the effects of maternal thyroid autoantibodies on pregnancy outcomes,as well as on neonatal thyroid status,and neuropsychological development of the fetus and neonate,and summarizes therapeutic strategies used to intervene maternal thyroid autoimmunity.

Iodine is an essential micronutrient for pregnant women,which affects thyroid function of pregnant women and fetus,and thus influences the intellectual development of offspring.Severe iodine deficiency could lead to overt hypothyroidism and fetal cretinism.In the areas implemented the universal salt iodization (USI) program,mild to moderate iodine deficiency and iodine excess may coexist during pregnancy.Iodine deficiency could lead to hypothyroxinemia in pregnant women.Iodine more than adequate and iodine excess could increase the prevalence of subclinical hypothyroidism.The effect of iodine supplementation on thyroid function in pregnant women with mild to moderate iodine deficiency may result in different conclusion.Therefore,it is important to maintain optimal urinary iodine concentration to prevent thyroid dysfunction.

Overt hyperthyroidism and hypothyroidism can induce hypertension.Recent studies found that mild thyroid dysfunction including subclinical thyroid diseases and increased TSH during normal reference range also had effect on blood pressure which had not been agreed with others.The mechanism is complex and not yet very clear.The basic treatment for the patients with thyroid diseases and hypertension is to treat thyroid diseases.Beta-receptor blocking agents and diuretics are preferable drugs for hyperthyroidism.

Surgery is now still the first choice for treatment of thyroid cancer.Long-term post-operative follow-up and thyroid hormone treatment are of great importance in reducing recurrence,early detection of metastases or recurrence,and improving patients' quality of life.This article reviews the recent advancement in post-operative follow-up and hormone treatment in thyroid cancer patients.

In view of the possibility for serious adverse outcomes for mother and fetus associated with maternal thyroid dysfunctions during pregnancy,many experts have recommended conducting routine thyroid function screening in pregnancy,but guidelines from different academic communities have given varied recommendations.The aim of this review is to discuss the significance of thyroid function screening in pregnancy and evaluate efficiency of the case-finding strategy vs.the universal screening strategy.

Based on laboratory tests,subclinical hypothyroidism is diagnosed and defined as an elevated serum TSH concentration with FT4 within reference range.Alterations in thyroid function are associated with aging.All available studies show that prevalence of subclinical hypothyroidism increases with aging,especially in women.However,some studies advise that serum TSH reference range for older people should be modified,because serum TSH elevates with aging.Therefore,when to and how to treat subclinical hypothyroidism in the elderly has been debating fiercely.At present,levothyroxine sodium treatment is generally recommended when TSH is raised more than 10 mIU/L.When TSH level is between the upper limit of the reference range and 10 mIU/L,treatment should depend on symptoms,history and risk factors of cardiovascular disease.Therapeutic objective should be individualized,depending on age,cardiac function,and other conditions.

Objective　To study the effects of prolactin on interactions between Graves′ disease (GD) thyrocytes and autologous peripheral blood mononuclear cells (PBMC) in coculture. Methods　Primary thyrocytes and autologous PBMC were cocultured at various levels of ovine prolactin (oPRL) in vitro. The activation and proliferation of PBMC as well as HLA-DR and CD40 expressions on thyrocytes were determined by immunofluorescent staining and flow cytometry. Results　 With PBMC in GD cocultures, oPRL caused significant increase in the percentage of CD4+CD25+ cells at 200 μg/L ［(13.08±2.54)%, P＜0.01］ and in the proliferative index at 200 μg/L ［(17.82±3.02)%, P＜0.01］ and 1 000 μg/L ［(16.57±2.56)%, P＜0.05］, but not at 12.5 μg/L ［(10.43±2.38)% and (14.08±2.67)%, respectively］ or 50 μg/L ［(9.94±2.54)% and (14.56±2.80)%, respectively)］. The values at 200 or 1 000 μg/L as above were also significantly different from those at 12.5 or 50 μg/L. The percentage of CD40+ cells ［(48.25± 6.63)%，(52.28±6.94)%］ and delta mean fluorescence intensity (dMF; 42.94±10.24，49.51±12.34) were significantly lower in thyrocytes in GD cocultures treated with 200 or 1 000 μg/L oPRL than those untreated ［(58.38±6.62)% and 67.30±20.20］ or treated with two other concentrations of oPRL. The percentage of HLA-DR+ cells ［(46.79±7.51)%, P＜0.01］ and dMF (21.02±5.43, P＜0.01) were significantly higher in the thyrocytes treated with 50 μg/L oPRL than those untreated ［(33.51±8.58)% and 13.91±3.88］ or treated with three other concentrations. There were no significant differences between the dose groups of oPRL but those mentioned above. Conclusions　Prolactin could affect interactions between GD PBMC and autologous thyrocytes and might eventually influence the shift of helper T cells. High prolactin levels might aggravate GD.

Objective To explore the influencing factors of glycemic variability in 217 cases of hospitalized patients with type 2 diabetes. Meth-ods A total of 217 cases of hospitalized patients with type 2 diabetes,whom received continuous glucose monitoring from January 2013 to Janu-ary 2016,were enrolled for the study. The evaluation variables of glycemic variability included mean amplitude of glycemic excursion(MAGE) and standard deviation of blood glucose(SDBG). Results The difference of glycemic variability was compared by gender,age,diabetic duration, HbA1c,BMI. The values of MAGE and SDBG in females were higher than those in males(P<0.05). There was no significant difference between various age groups and various diabetic duration. The level of glycemic variability increased gradually with the extension of HbA 1c(P<0.05). The level of glycemic variability increased gradually with the extension of body mass index(BMI)(P<0.05). Logistic regression analysis showed that gender(OR=0.67,P=0.02),HbA1c(OR=0.8,P=0.02),diastolic blood pressure(OR=0.9,P=0.03),triglycerides(OR=4.6,P=0.007),cholesterol(OR=0.6,P=0.007). HDL-C(OR=0.09,P=0.006)were significant influencing factors of glycemic variability in hospital-ized patients with type 2 diabetes. Conclusion Gender,HbA1c,BMI,and blood fat are significant influencing factors of glycemic variability while age and duration are not related to the glycemic variability in hospitalized patients with type 2 diabetes.