ديابت بي‌مزه پس از زايمان واژينال: گزارش موردي

Diabetes Insipidus after normal vaginal delivery: a case report

زمينه و هدف: ديابت بی‌مزه در حاملگی بيماری نادری است كه در نتيجه ترشح ميزان ناكافی هورمون آنتی‌ديورتيك (وازوپرسين) اتفاق می‌افتد. به‌دليل افزايش فيلتراسيون گلومرولی در حاملگی، نياز به هورمون آنتی‌ديورتيك بيشتر می‌شود. معرفی بيمار: خانم 39 ساله شش روز بعد از زايمان طبيعی به‌علت تشنگی، پرنوشی، تب، پلی‌اوری و ضعف در مهر ماه 1392 به بيمارستان اكبرآبادی مراجعه كرد. افزايش قابل توجه حجم ادرار با كاهش وزن مخصوص ادرار همراه بود. اسمولاريته ادرار كمتر از اسمولاريته سرم بود. در آزمايش خون هيپرناترمی ديده شد. درمان با تجويز دسموپرسين استات كه آنالوگ آنتی‌ديورتيك هورمون است صورت گرفت نتيجه‌گيری: انواع اختلالات غدد درون ريز ممكن است بارداری را دچار مشكل نمايند. ديابت بی‌مزه چندان شايع نيست، در صورت عدم تشخيص و درمان به‌موقع می‌تواند اثرات نامطلوبی بر روند بارداری داشته باشد. بيشتر افراد مبتلا، در زمان بارداری نياز به‌مقادير بيشتر دسموپرسين استات دارند، شايد به‌دليل افزايش كليرانس متابوليك ناشی از وازوپرسيناز جفتی باشد. با همين مكانيسم، مواردی از انواع تحت بالينی ديابت بی‌مزه ممكن است در حاملگی علامت‌دار شوند.

Background: A variety of endocrine disorders can complicate pregnancy. Diabetes insipidus although uncommon, may have devastating effect on pregnancy outcome, if unrecognized and untreated. The etiology of diabetes insipidus is often unknown, many cases are likely autoimmune, with lymphocytic infiltration of the posterior pituitary gland. Massive polyuria, caused by failure of the renal tubular concentrating mechanism, and dilute urine, with a specific gravity 1.005, are characteristic of diabetes insipidus. The diagnosis of diabetes insipidus relies on the finding of continued polyuria and relative urinary hyposmolarity when water is restricted. Most women require increased doses Desmopressin Acetate during pregnancy because of an increased metabolic clearance rate stimulated by placental Vasopressinase. By this same mechanism, subclinical diabetes insipidus may become symptomatic during pregnancy. Transient diabetes insipidus is associated with acute fatty liver and HELLP syndrome as well as twin gestation. Increased placental Vasopressinase activity, along with insufficient liver degradation in HELLP syndrome and acute fatty liver, may unmask this condition. Diabetes insipidus in pregnancy is rare. The disease results from inadequate or absent antidiuretic hormone (vasopressin) production by the posterior pituitary gland. The increased glomerular filtration rate seen in pregnancy may increase the requirement for antidiuretic hormone. Case presentation: We present a 39 years old woman, gravida3 para3, was admitted to Akbarabadi Teaching Hospital in september 2013. She was admitted due to polyuria, malaise, thirst with slight fever, six days after normal vaginal delivery. The urine volume was 8 lit/day and the specific gravity (S.G.) of the urine was 1.010. The urine osmolarity was lower than the plasma osmolarity. Electrolyte serum examination showed hypernatremia. The patient received 5 µg/day of synthetic vasopressin, in the form of l- deamino-8-Darginine vasopressin (DDAVP). This drug was given as intranasal spray in doses 0.25 mg twice daily. Plasma electrolytes and fluid status monitored carefully with initiation of therapy. DDAVP was used because it was not degraded by vasopressinase. Treatment was continuing, when the symptoms of central diabetes insipidus resolve and urinary concentrating ability was preferred. Maximum urinary osmolality over the next 11 hours was assessed, 730 mosm/kg was considered normal. Conclusion: Close attention to electrolyte and fluid balance is important in the postpartum period. The symptoms of transient vasopressin-resistant diabetes insipidus resolve in few days to a few weeks after vaginal delivery or when hepatic function returns to normal.