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作 者:赵红莉[1] 翁育[1] 刘桂治[2] 陈昕 傅晓英[1] ZHAO Hongli;WENG Yu;LIU Guizhi;CHEN Xin;FU Xiaoying(Department of Endocrinology,the Second People's Hospital of Guangdong Province,Guangzhou510317,China;Laboratory Center,the Second People's Hospital of Guangdong Province,Guangzhou510317,China)
机构地区:[1]广东省第二人民医院内分泌科,广东广州510317 [2]广东省第二人民医院检验中心,广东广州510317
出 处:《中国现代医生》2019年第9期5-7,12,共4页China Modern Doctor
基 金:广东省医学科学技术研究基金项目(B2016013)
摘 要:目的探讨自身免疫性甲状腺病与多囊卵巢综合征之间的相关性。方法选取2016年5月~2017年5月我院收治的多囊卵巢综合征伴糖脂代谢紊乱患者45例为研究组,选取同期我院收治的多囊卵巢综合征未伴糖脂代谢紊乱患者45例为对照组。结果研究组FSH低于对照组,差异有统计学意义(P<0.05),研究组LH、雌二醇、催乳素以及睾酮高于对照组,差异有统计学意义(P<0.05);研究组FT3、FT4、TSH以及TSH>2.5μIU/mL例数与对照组比较,差异无统计学意义(P>0.05);研究组TGAb、TPOAb高于对照组,差异有统计学意义(P<0.05),研究组TGAb>60 U/mL例数、TPOAb>60 U/mL例数高于对照组,差异有统计学意义(P<0.05)。结论自身免疫性甲状腺病可能会参与患者多囊卵巢综合征的发病并使其代谢表型恶化。Objective To investigate the relationship between autoimmune thyroid disease and polycystic ovary syndrome.Methods 45 patients with polycystic ovary syndrome combined with glucose and lipid metabolism disorders in our hospital from May 2016 to May 2017 were enrolled as the study group.45 patients with polycystic ovary syndrome without glucose and lipid metabolism disorders who were admitted in our hospital in the same period were enrolled as the control group.Results The FSH of the study group was lower than that of the control group,with statistically significant difference(P<0.05).The LH,estradiol,prolactin and testosterone in the study group were higher than those of the control group,and the difference was statistically significant(P<0.05).There were no significant differences in the number of FT3,FT4,TSH and TSH>2.5μIU/mL between the study group and the control group(P>0.05).The TGAb and TPOAb in the study group were higher than those of the control group,and the difference was statistically significant(P<0.05).The number of TGAb>60 U/mL and TPOAb>60 U/mL in the study group was higher than that in the control group,and the difference was statistically significant(P<0.05).Conclusion Autoimmune thyroid disease may be involved in the pathogenesis of polycystic ovary syndrome and worsen its metabolic phenotype.
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