碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

目的 观察碘过量对自身免疫性疾病敏感品系NOD鼠和非敏感品系Balb/c鼠甲状腺细胞凋亡相关基因肿瘤坏死因子的相关凋亡诱导配体(tumor necrosis factor-related apoptosis-inducing ligand, TRAIL)和其受体TRAIL刺激性受体1(TRAIL-sR1)表达的影响,了解碘过量诱导实验性自身免疫性甲状腺炎(EAT)发病过程中TRAIL和TRAIL-sR1的作用机制.方法 6～7周龄雌性NOD鼠和Balb/c鼠各16只,按体质量各随机分为对照组和碘过量(HI)组,每组8只.对照组饮高压灭菌水,HI组饮0.05%NaI添加水,饲养8周后处死.测量甲状腺相对质量,进行甲状腺组织形态学观察,测量血清甲状腺素(TT4)和甲状腺刺激激素(TSH),检测甲状腺滤泡上皮细胞凋亡情况,应用实时定量PcR(real time PCR)方法检测TRAIL和TRAIL-sR1 mRNA表达情况.结果 NOD鼠HI组甲状腺相对质量[(104.8±14.5)mg/kg]高于对照组[(71.8±20.4)mg/kg],血清TT4水平[(30.77±3.59)mmol/L]低于对照组[(36.43±2.66)mmol/L],TSH水平[(6.98±0.66)μg/L]高于对照组[(5.55±0.56)μg/L],组间比较差异均有统计学意义(t值分别为7.773、-9.526、-4.458,P均<0.05).HI组甲状腺出现滤泡扩张、胶质潴留及明显的淋巴细胞浸润伴灶性纤维化.Balb/c鼠川组甲状腺相对质量[(155.8±20.8)mg/kg]高于对照组[(105.1±22.0)mg/kg],血清TT4水平[(19.75±3.32)mmol/L]低于对照组[(23.46±6.21)mmol/L],TSH水平[(4.14±1.71)μg/L]高于对照组[(3.55±1.41)μg/L],组间比较差异均有统计学意义(t值分别为7.554、-7.239、3.140,P均<0.05);HI组甲状腺仅有甲状腺滤泡扩张,胶质潴留,而未见明显的淋巴细胞浸润.HI组NOD鼠和Balb/c鼠甲状腺滤泡上皮细胞的凋亡指数(3.97±0.91、1.05±0.45)分别高于对照组(0.21±0.15、0.10±0.03),组间比较差异均有统计学意义(t值分别为-7.167、-17.772,P均<0.05),Balb/c鼠HI组的甲状腺滤泡上皮细胞的凋亡指数低于NOD鼠HI组,组间比较差异有统计学意义(t=-7.625,P<0.05).NOD鼠HI组TRAIL mRNA表达水平(0.018 88±0.005 77)高于对照组(0.00961±0.005 91),组间比较差异有统计学意义(t=-2.710,P<0.05);Balb/c鼠HI组TRAIL表达水平(0.001 24±0.000 46)与对照组(0.000 59±0.000 39)比较,差异无统计学意义(t=-1.940,P>0.05);NOD鼠和Balb/c鼠HI组的TRAIL-sR1 mRNA表达水平(0.000 53±0.000 15、0.000 42±0.000 09)均高于对照组(0.000 28±0.000 05、0.000 17±0.000 06),组间比较差异有统计学意义(t值分别为3.050,3.990,P均<0.05),Balb/c鼠HI组的TRAIL和TRAIL-sR1的mRNA表达水平均低于NOD鼠HI组,组间比较差异均有统计学意义(t值分别为-3.370、-4.760,P均<0.05).结论 碘过量可使NOD和Balb/c鼠发生胶质潴留性甲状腺肿,并可造成NOD鼠甲状腺发生明显的炎症反应.TRAIL和TRAIL-sR1表达水平升高是碘过量导致甲状腺滤泡上皮凋亡和炎症发生的分子基础之一.遗传在甲状腺炎的发病过程中起到至关重要的作用.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.     

甲状腺自身抗体阳性妇女孕期干预对婴儿甲状腺功能的影响

目的 探讨甲状腺自身抗体阳性妇女孕期甲状腺功能干预对婴儿甲状腺功能的影响.方法选择产前检查发现的甲状腺过氧化物酶抗体(TPOAb)和(或)甲状腺球蛋白抗体(TgAb)阳性妊娠妇女55例.随机分为干预组(子代为A)36例和非干预组(子代为B)19例,设同期自身抗体阴性对照组(子代为N)30例.选择左旋甲状腺素片作为干预制剂.采用化学发光酶免疫分析法测定3组入选后和分娩前空腹血清TPOAb、TgAb、TSH、TT3、TT4、FT3、FT4水平,同时测定母体尿碘含量.新生儿出生后测定脐血、出生后3～4周及8～10周静脉血TSH、TT3、TT4、FT3、FT4水平.结果干预组、非干预组母体基线血清TSH水平显著高于对照组(P＜0.05).分娩前非干预组与另两组比较,血清TSH增高和TT3、TT4、FT4降低具有统计学差异(P＜0.05或P＜0.01).胎儿出生后脐血TSH水平在B组(7.06±1.31)mIU/L和A组(6.23±1.26)mIU/L均显著高于N组(5.48±1.17)mIU/L(P＜0.01或P＜0.05).出生3～4周新生儿B组血清TSH(3.21±0.70)mIU/L高于N组[(2.72±0.51)mIU/L]和A组[(2.78±0.42)mIU/L,均P＜0.05].出生8～10周婴儿B组血清TSH[(2.99±0.57)mIU/L]高于N组[(2.48±0.68)mIU/L,P＜0.05].多元逐步回归分析,母体TSH、TPOAb及尿碘含量与婴儿TSH独立相关.结论不同甲状腺功能状态的妊娠妇女,其子代出生后的甲状腺功能存在差异.胎儿出生后甲状腺功能与母亲甲状腺自身抗体及孕期甲状腺功能状态有关.     

碘过量和甲状腺球蛋白免疫诱发NOD小鼠甲状腺炎的病变特征

目的 观察碘过量和甲状腺球蛋白(Tg)免疫诱发甲状腺炎的病变特点,进一步了解碘过量在自身免疫性甲状腺炎发病中的作用机制.方法 选用NOD小鼠,饮0.05%碘化钠(NaI)水和(或)Tg皮下免疫.观察甲状腺形态学改变和细胞凋亡情况;检测血清中TT4、TSH、甲状腺球蛋白抗体(TgAb)和甲状腺过氧化物酶抗体(TPOAb)水平;检测颈部淋巴结和脾脏淋巴细胞对Tg刺激的增殖反应和脾脏细胞培养上清中白细胞介素4(IL-4)和1γ-干扰素(IFN-γ)水平;实时荧光定量PCR法检测甲状腺绀织内IL-4、IFN-γ、趋化冈子配体10(CXCL10)、细胞间黏附因子1(ICAM-1)mRNA的表达.结果 碘过量组甲状腺滤泡扩张、胶质潴留;大昔淋巴细胞浸润和结构破坏;滤泡上皮细胞凋亡数量增加(34.66±2.78//vs 5.1 1±0.62,P<0.01);总T4下降、TSH升高,无自身抗体产生;淋巴结和脾脏细胞对Tg刺激增殖实验呈阳性反应.脾脏细胞上清中IL-4水平无升高,而IFN-升γ高[(1.272±0.049 vs 1.139±0.025)ng/L,P<0.01];甲状腺组织中除了IL4外,IFN-γ、CXCL10、ICAM-1 mRNA表达升高(均P<0.01).而Tg组甲状腺内有少量散在淋巴细胞浸润,产生了甲状腺自身抗体,脾脏细胞上清中IL-4水平升高[(18.508±0.113绑13.368±0.016)ng/L,P<0.01].碘和Tg联合作用炎症反应加重.结论 碘过量所致的NOD小鼠甲状腺炎主要是以Th1反应为主的器官特异性自身免疫性疾病.碘过量联合Tg免疫对诱发实验性自身免疫性甲状腺炎具有协同作用.     

碘缺乏和碘过量对实验性甲状腺功能减退小鼠血脂代谢的影响

目的 观察碘缺乏和碘过量对实验性甲状腺功能减退(简称甲减)小鼠血脂代谢的影响,探讨碘不依赖于甲状腺激素的独立作用机制.方法 将雌性Balb/c小鼠按体质量随机分为6组:对照、重度低碘(SID)、轻度低碘(MID)、适碘(NI)、10倍碘过量(10HI)和50倍碘过量(50HI)组,每组10只.对照组饲以低碘饲料,其他各组饲以含0.2%甲基硫氧嘧啶的低碘饲料,同时饮用碘化钾(KI)配制的含碘量分别为326.79、0、196.08、326.79、3856.21、19 542.50 μg/L的去离子水.喂养3个月后,处死并收集小鼠外周血,分离血清.放射免疫分析法测定甲状腺激素水平,酶法检测血清中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)及低密度脂蛋白胆固醇(LDL-C)水平.结果 ①SID[(21.27±9.63)μg/L]、MID[(23.41±3.93)μg/L]、NI[(22.57±4.66)μg/L]、10HI[(21.07±5.03)μg/L]和50HI组[(21.46±5.90)μg/L]血清TT4水平明显低于对照组[(42.15±8.26)μg/L,P均＜0.01],而各组间血清TT3水平比较,差异无统计学意义(F=0.99,P＞0.05).②10HI组TG水平[(1.17±0.16)mmol/L]与对照组[(1.39±0.22)mmol/L]和NI组[(1.51±0.22)mmol/L]比较,明显降低(P均＜0.05).50HI组TG和TC水平[(1.18±0.22)、(1.78±0.15)mmol/L]与对照组[(1.39±0.22)、(2.14±0.37)mmol/L]和NI组[(1.51±0.22)、(2.00±0.15)mmol/L]比较,明显降低(P均＜0.05).各组HDL-C、LDL-C水平比较,差异无统计学意义(F值分别为0.55、0.54,P均＞0.05).结论 碘可不依赖于甲状腺激素独立发挥调节甲减小鼠血脂的作用;监控碘的摄入量,对有效防治心血管疾病亦有重要作用.

Abstract：

Objective To observe the effects of iodine deficiency and iodine excess on the lipid metabolism in an experimental hypothyroid model of mice and to explore the roles of iodine independent of its role in thyroid hormones. Methods Female Balb/c mice were randomly divided into 6 groups: control, severe iodine deficiency (SID), mild iodine deficiency(MID), normal iodine (NI), 10-fold high iodine (10HI) and 50-fold high iodine(50HI), 10 in each group. The mice in control group were fed with low iodine forage, other mice were fed with low iodine forage containing 0.2% methylthiouracilum. All mice drank deionic water containing different concentrations of potassium iodide(KI). The iodine content in water was 326.79, 0, 196.08,326.79, 385621, 19 542.50 μg/L, respectively. After three months, thyroid hormones in the serum were determined by radioimmunoassay.Also, the blood samples were analyzed for total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesteiol (HDL-C) and low density lipoprotein cholesterol (LDL-C) and measured enzymatically by automatic analyzer. Results ①The levels of Tr4 in SID[(21.27 ± 9.63)μg/L], MID[(23.41 ± 3.93)μg/L], NI[(22.57 ±4.66)μg/L], 10HI [(21.07 ± 5.03) μg/L] and 50HI groups [(21.46 ± 5.90) μg/L] were distinctively decreased compared with control group[(42.15 ± 8.26)μg/L, all P ＜ 0.01]. There were no statistical significant differences of TT3 between different groups (F = 0.99, P > 0.05 ). ②The level of TG in 10HI group [ ( 1.17 ± 0.16)mmol/L ] was obviously decreased compared with control [(1.39 ± 0.22 )mmol/L] and NI groups[(151 ± 0.22)mmol/L, all P＜ 0.05].Both TG and TC in 50HI group[(1.18 ± 0.22), (1.78 ± 0.15)mmol/L] were significantly decreased compared with control [( 1.39 ± 0.22), (2.14 ± 0.37)mmol/L] and NI groups [(1.51 ± 0.22), (2.00 ± 0.15)mmol/L, all P ＜ 0.05].The difference of serum HDL-C and LDL-C between the groups was not significant(F = 0.55,0.54, all P ＞ 0.05 ).Conclusions Dietary iodine plays a role in the metabolism of serum lipids independent of thyroid hormones.Thus, monitoring the amount of iodine intake during sodium restriction should also be taken extremely important for effectively prevention and cure of cardiovascular disease.     

原发性胆汁性胆管炎患者血清甲状腺激素水平和抗甲状腺抗体阳性率变化*

目的 探讨原发性胆汁性胆管炎(PBC)患者血清甲状腺激素水平和抗甲状腺抗体阳性率变化。方法 2018年1月～2020年1月我院收治的PBC患者94例,其中肝硬化50例(Child-Pugh A级29例,B级15例,C级6例)和胆管炎44例,另选择同期于我院健康体检者60名,采用化学发光免疫法测定血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)和促甲状腺激素(TSH)水平及血清甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TGAb)。结果 胆管炎患者血清FT3、FT4和TSH水平分别为(2.4±0.5)ng/L、(1.4±0.2)ng/L和(8.9±2.3)ng/L,血清TPOAb和TGAb阳性率分别为77.3%和81.8%,肝硬化患者血清FT3、FT4和TSH水平分别为(1.9±0.3)ng/L、(1.0±0.1)ng/L和(19.7±4.9)ng/L,血清和TPOAb和TGAb阳性率分别为70.0%和64.0%,而健康人血清FT3、FT4和TSH水平分别为(2.8±0.8)ng/L、(1.8±0.3)ng/L和(3.4±1.2)ng/L,血清TPOAb和TGAb阳性率均为0.0%,肝硬化和胆管炎患者血清FT3和FT4水平显著低于,血清TSH水平显著高于健康人(P＜0.05),而肝硬化患者血清FT3和FT4水平显著低于,血清TSH水平显著高于胆管炎患者(P＜0.05),肝硬化和胆管炎患者血清TPOAb和TGAb阳性率比较,无统计学差异(P＞0.05);在肝硬化患者中,Child-Pugh A级患者血清FT3和FT4水平显著高于,血清TSH水平显著低于Child-Pugh B级或C级患者(P＜0.05),而Child-Pugh B级患者血清FT3和FT4水平显著高于,血清TSH水平显著低于Child-Pugh C级患者(P＜0.05),不同肝功能分级的肝硬化患者血清TPOAb和TGAb阳性率比较,无统计学差异(P＞0.05)。结论 原发性胆汁性肝硬化和胆管炎患者血清FT3、FT4和TSH水平显著不同于健康人,血清TPOAb和TGAb阳性率较高,其临床意义值得进一步观察和研究。     

克山病患者抗氧化能力测定

目的 探讨克山病患者体内抗氧化水平与克山病心肌损伤的关系,分析其可能的发病机制.方法 2005和2006年期间,在黑龙江省克山病重病区富裕县永进村和新发村、尚志市扶安村、五大连池市星火村选择慢型、潜在型克山病患者41名作为病例组,61名健康人作为病区对照组;在非病区望奎县厢兰三村选取48名健康人作为非病区对照组,分别采集清晨空腹外周静脉血检测全血硒水平、全血谷胱甘肽过氧化物酶(GSH-Px)活力、血浆总超氧化物歧化酶(T-SOD)活力及血浆丙二醛(MDA)水平.结果 病例组血硒水平[(34.80±13.30)μg/L]、GSH-Px活力[(104.10±34.19)U/L]、T-SOD活力[(92.16±17.98)×103 U/L]显著低于病区对照组[(41.24±13.57)μg/L、(118.57±25.49)U/L、(104.82±13.56)×103 U/L]和非病区对照组[(48.33±16.51)μg/L、(155.00±24.01)U/L、(108.48±12.73)×103 U/L],组间比较差异有统计学意义(P均<0.05);病例组MDA水平[(7.12±1.37)μmol/L]高于病区对照组[(5.36±1.18)μmol/L]和非病区对照组[(5.22±0.83)μmol/L],组间比较差异有统计学意义(P均<0.05);病区对照组血硒水平、GSH-Px活力低于非病区对照组(P<0.05),组间比较差异均有统计学意义(P<0.05).结论 克山病病人体内存在硒缺乏所致的抗氧化能力降低,氧化损伤增强.氧化应激障碍可能与克山病的心肌损伤有一定的关系.     

短期铁缺乏对大鼠甲状腺功能的影响

目的 研究短期铁缺乏对大鼠甲状腺功能的影响,并探讨其机制,为碘缺乏病的防治工作提供新的线索和思路.方法 选择健康SPF/VAF级初断乳SD雄性大鼠22只,按体质量随机分为对照组(饲料含铁量为65 mg/kg)和铁缺乏组(饲料含铁量为15 mg/kg),每组11只.喂养4周后,测定大鼠体质量和甲状腺质量,并计算甲状腺相对质量.取大鼠全血并分离血清,采用生化法检测血红蛋白、血清铁水平和总铁结合力;化学发光法检测血清游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)和促甲状腺激素(TSH)水平.甲状腺常规固定包埋切片后,免疫组化染色观察甲状腺过氧化物酶(TPO)蛋白表达情况.结果 铁缺乏组大鼠体质量[(214.3±18.1)g]比对照组[(243.8±16.4)g]减轻(t=4.002,P＜0.01),甲状腺绝对质量[(11.9±1.6)mg]比对照组[(13.4±1.3)mg]降低(t=2.369,P＜0.01),但甲状腺相对质量[(0.055±0.004)g/kg]与对照组[(0.055±0.006)g/kg]比较未见明显变化(t=0.162,P＞0.05).铁缺乏组大鼠血红蛋白水平[(100.4±8.9)g/L]和血清铁水平[(7.0±0.8)μmol/L]比对照组[(146.5±16.3)g/L、(26.1±5.1)μmol/L]降低(t值分别为8.233、12.277,P均＜0.01),总铁结合力[(124.8±6.3)μmol/L]比对照组[(74.0±4.6)μmol/L]升高(t=21.531,P＜0.01).铁缺乏组大鼠血清FT3、FT4和FT3/FT4[(4.71±0.53)、(29.69±2.63)pmol/L、0.16±0.02]均较对照组[(5.69±0.61)、(31.98±2.49)pmol/L、0.18±0.01]降低(t值分别为4.044、2.096、3.255,P＜0.01或＜0.05).铁缺乏组大鼠TPO蛋白表达强度较对照组减弱.结论 铁缺乏可导致甲状腺功能低下,可能与铁缺乏状态下TPO活性降低有关,碘铁联合补充可能会改善铁缺乏地区碘缺乏病防治的效果.

Abstract：

Objective To explore the effect of short-term iron deficiency on thyroid function of rat and its mechanism, and to provide new clues and ideas for prevention and control of iodine deficiency disorders. Methods Twenty-two healthy SPF/VAF level weaning male SD rats were randomly divided into control group(iron content in diet was 65 mg/kg) and iron deficiency group(iron content in diet was 15 mg/kg) by body weight, and 11 in each group respectively. After 4 weeks feeding, body weight and thyroid glands weight were measured, and the relative weight of thyroid gland was calculated. Rat whole blood was collected and serum was separated. Hemoglobin, serum iron levels and total iron binding capacity were tested using biochemical assay;serum free iodine thyroid three original acid (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) levels were detected by chemiluminescence;after thyroid were fixed in formalin, embedded with paraffin and sectioned regularly, and immunohistochemical stained, the protein expression of thyroid peroxidase(TPO) was observed. Results Compared with control group [(243.8 ± 16.4)g], iron deficiency group of animals had less body weight[(214.3 ± 18.1 )g, t = 4.002, P ＜ 0.01];there was a lower absolute thyroid weight in iron deficiency group[(11.9 ± 1.6)mg]than in control group[(13.4 ±1.3)mg, t = 2.369, P ＜ 0.01], but no significant changes of the relative weight of thyroid gland between the two groups[(0.055 ± 0.004),(0.055 ± 0.006)g/kg, t = 0.162, P ＞ 0.05]. Hemoglobin and serum iron in iron deficiency group were ( 100.4 ± 8.9)g/L and (7.0 ± 0.8)μmol/L, which were less than that in control group[( 146.5 ±16.3)g/L, (26.1 ± 5.1 )μmol/L, t = 8.233,12.277, all P ＜ 0.01]. Total iron binding capacity in control group was (74.0 ± 4.6)μ mol/L and that in iron deficiency group[(124.8 ± 6.3)μmol/L], and the difference was significant (t = 21.531, P＜ 0.01). At the same time, their serum hormones FT3, FT4 and FT3/FT4[(4.71 ± 0.53), (29.69 ±2.63)pmol/L, 0.16 ± 0.02]were lower than that in control group[(5.69 ± 0.61),(31.98 ± 2.49)pmol/L, 0.18 ±0.01, t = 4.044,2.096,3.255, P ＜ 0.01 or ＜ 0.05]. The expression of TPO protein decreased in iron deficiency group than in control group. Conclusions Iron deficiency reduces thyroid function, which perhaps is due to the reduction of TPO activity. Combined supplementation of iodine and iron will possibly improve the prevention effect on iodine deficiency disorder in iron deficiency areas.     

碘充足地区血清TSH正常值范围及其影响因素的流行病学研究

目的 分析血清TSH测定的影响因素,参考美国国家临床生化协会(NACB)指南,建立中国辽宁碘充足地区血清TSH的正常参考范围.方法 2007年,来自辽宁省3个碘充足地区的5 348人参加了甲状腺疾病的社区调查,进行了TSH、甲状腺自身抗体[甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TgAb)]的测定,并作了甲状腺超声检查和问卷调查.结果 正常人群的TSH分布向右偏斜,接近于对数正态分布.年龄在12～19岁血清TSH水平明显高于其他年龄段(P＜0.01),而其他年龄段之间无统计学差异.血清TSH水平女性[(1.68±1.90)mIU/L]明显高于男性[(1.45±1.92)mIU/L,P＜0.01].因此,年龄大于20岁的健康男性TSH的分布范围是0.43～4.74 mIU/L,健康女性TSH的分布范围是0.48～5.39 mIU/L.甲状腺疾病家族史、甲状腺超声异常、甲状腺抗体阳性均影响TSH的测定水平,非甲状腺疾病对TSH参考范围没有显著影响.结论建立了碘充足地区血清TSH参考范围.

Abstract：

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.     

氟中毒大鼠骨组织中内质网应激实验研究

目的 观察内质网应激在氟中毒大鼠骨组织中的变化,探索内质网应激在氟骨症发病机制中的可能作用.方法 48只Wistar大鼠,按体质量分成4组,每组12只.对照组和低钙组分别饲以常食饲料(含钙量为0.790%)和自制低钙饲料(含钙量为0.063%),饮用自来水(含NaF＜1 mg/L);高氟组和低钙高氟组分别饲以常食饲料和自制低钙饲料,饮用加氟(NaF,221 mg/L)自来水.实验期间动物自由进食、进水,每周测体质量1次.实验期3个月.生化方法检测大鼠血清氧化应激酶、尿酸(URIC)和碱性磷酸酶(ALP)活性.抽提大鼠一侧股骨骨干的总RNA,利用RT-PCR技术分析内质网应激相关基因BIP、Xbp1、CHOP和PDI的表达水平.结果 低钙高氟组血清丙二醛(MDA)水平高于对照组[(14.74±3.11)μmol/L比(10.15±1.96)μmol/L,P＜0.05];高氟组血清谷胱甘肽过氧化物酶(GPx)的活性高于对照组[(3.87±0.41)×103 U/L比(2.85±0.55)×103U/L,P＜0.05];高氟组和低钙高氟组的尿酸(URIC)分别低于对照组和低钙组[(73.95±9.52)μmol/L比(110.43±25.48)μmol/L,(54.32±22.09)μmol/L比(101.71±17.01)μmol/L/L,P＜0.05].低钙高氟组大鼠的ALP活性高于对照组[(24.77±4.57)×103 U/L比(12.91±3.97)×103 U/L,P＜0.01)].低钙组和低钙高氟组BIP/GAPDH的表达高于对照组(1.38±0.24、1.35±0.12比1.14±0.06,P＜0.05).低钙高氟组的Xbp1/GAPDH的表达高于对照组和低钙组(1.48±0.20比1.02±0.25、1.07±0.25,P＜0.01);低钙高氟组的CHOP/GAPDH的表达高于对照组(0.84±0.18比0.52±0.07,P＜0.05).结论 氟中毒大鼠机体内氧化应激态和骨形成有明显的增强,并伴有骨组织细胞的内质网应激.说明内质网应激与氧化应激很可能都参与了氟骨症的发病机制.     

结节性甲状腺肿患者血清胰岛素样生长因子-1水平与摄131碘率相关性研究

目的 研究结节性甲状腺肿患者血清胰岛素样生长因子-1(IGF-1)水平与甲状腺摄131碘(131Ⅰ)率的相关性,为临床鉴别甲状腺结节的性质寻找更简捷,安全的方法 .方法 运用放射核素扫描技术检测甲状腺摄131Ⅰ率,据此将患者分为热结节组,冷结节组,并设对照组,放射免疫分析法检测各组血清IGF-1,FT3,FT4,sTSH水平,分析其与摄131Ⅰ率的相关性.结果 热结节组患者血清IGF-1,FT3,FT4水平[(315.86±22.74)μg/L,(9.95±5.62),(67.27±27.31)ng/L]明显高于对照组[(256.13±39.85)μg/L,(2.80±1.30),(13.5l±5.50)ng/L],摄131Ⅰ率(0.64±0.17)明显高于对照组(0.35±0.15),血清sTSH水平[(0.35±0.03)mU/L]明显低于对照组[(2.71±1.17)mU/L].差异均有统计学意义(P＜0.01).而冷结节组患者血清IGF-1,FT3,FT4,sTSH水平[(263.17±30.23)μg/L,(2.89±0.98),(14.23±2.84)ng/L,(2.81±0.42)mU/L]与对照组比较差异无统计学意义(P＞0.05).热结节组IGF-1水平与甲状腺摄131Ⅰ率呈正相关(r＝0.835,P＜0.01),与sTSH水平呈轻度负相关(r＝-0.326,P＜0.05).结论 结节性甲状腺肿患者血清IGF-1水平与甲状腺摄131Ⅰ率可能有一定的相天性.