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首页> 外文期刊>BMC Endocrine Disorders >The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report
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The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report

机译:青少年妊娠尿崩症的临床过程和病理生理学调查:一例报告

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Gestational diabetes insipidus (GDI) is a rare endocrine complication during pregnancy that is associated with vasopressinase overproduction from the placenta. Although increased vasopressinase is associated with placental volume, the regulation of placental growth in the later stage of pregnancy is not well known. A 16-year-old pregnant woman was urgently transferred to our hospital because of threatened premature labor when the Kumamoto earthquakes hit the area where she lived. During her hospitalization, she complained of gradually increasing symptoms of polyuria and polydipsia. The serum level of arginine vasopressin (AVP) was 1.7?pg/mL, which is inconsistent with central DI. The challenge of diagnostic treatment using oral 1-deamino-8-D-AVP (DDAVP) successfully controlled her urine and allowed for normal delivery. DDAVP tablets were not necessary to control her polyuria thereafter. Based on these observations, clinical diagnosis of GDI was confirmed. Pathophysiological analyses revealed that vasopressinase expression was more abundant in the GDI patient’s syncytiotrophoblast in placenta compared with that in a control subject. Serum vasopressinase was also observed during gestation and disappeared soon after delivery. Vasopressinase is reportedly identical to oxytocinase or insulin regulated aminopeptidase (IRAP), which is an abundant cargo protein associated with the glucose transporter 4 (GLUT4) storage vesicle. Interestingly, the expression and subcellular localization of GLUT4 appeared to occur in a vasopressinase (IRAP)-dependent manner. Because placental volume may be associated with vasopressinase overproduction in GDI, vasopressinase (IRAP)/GLUT4 association appears to contribute to the growth of placenta in this case.
机译:妊娠期尿崩症(GDI)是妊娠期间罕见的内分泌并发症,与胎盘中血管加压素酶的过量产生有关。尽管增加的血管加压素酶与胎盘体积有关,但妊娠后期胎盘生长的调节尚不清楚。当熊本地震袭击她居住的地区时,一名16岁的孕妇因早产受到威胁而紧急转移到我们医院。在住院期间,她抱怨多尿和多饮的症状逐渐加重。精氨酸加压素(AVP)的血清水平为1.7?pg / mL,与中枢DI不一致。使用口服1-deamino-8-D-AVP(DDAVP)进行诊断治疗的挑战成功地控制了她的尿液并允许正常分娩。此后,不必使用DDAVP片剂来控制她的多尿症。基于这些观察,证实了GDI的临床诊断。病理生理学分析显示,与对照组相比,GDI患者胎盘合体滋养层中的血管加压素表达更为丰富。妊娠期也观察到了血清加压素酶,分娩后不久消失。据报道,血管加压素酶与催产素酶或胰岛素调节的氨肽酶(IRAP)相同,后者是与葡萄糖转运蛋白4(GLUT4)储存囊泡相关的丰富货物蛋白。有趣的是,GLUT4的表达和亚细胞定位似乎以血管加压素(IRAP)依赖性方式发生。由于胎盘体积可能与GDI中血管加压素酶的过量产生有关,因此在这种情况下,血管加压素(IRAP)/ GLUT4的结合似乎有助于胎盘的生长。

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