Abstract：
Diabetes insipidus is a disorder characterized by hypo-osmotic polyuria secondary to abnormal synthesis, regulation, or renal action of antidiuretic hormone. Recently, an expert group, with the support of patient associations, proposed that diabetes insipidus be renamed to avoid confusion with diabetes mellitus. The most common form of diabetes insipidus is secondary to a dysfunction of the neurohypophysis (central diabetes insipidus) and would be therefore named \'vasopressin deficiency\'. The rarer form, which is linked to renal vasopressin resistance (nephrogenic diabetes insipidus), would then be named \'vasopressin resistance\'. The etiology of diabetes insipidus is sometimes clear, in the case of a neurohypophyseal cause (tumoral or infiltrative damage) or a renal origin, but in some cases diabetes insipidus can be difficult to distinguish from primary polydipsia, which is characterized by consumption of excessive quantities of water without any abnormality in regulation or action of antidiuretic hormone. Apart from patients\' medical history, physical examination, and imaging of the hypothalamic-pituitary region, functional tests such as water deprivation or stimulation of copeptin by hyperosmolarity (induced by infusion of hypertonic saline) can be proposed in order to distinguish between these different etiologies. The treatment of diabetes insipidus depends on the underlying etiology, and in the case of a central etiology, is based on the administration of desmopressin which improves patient symptoms but does not always result in an optimal quality of life. The cause of this altered quality of life may be oxytocin deficiency, oxytocin being also secreted from the neurohypophysis, though this has not been fully established. The possibility of a new test using stimulation of oxytocin to identify alterations in oxytocin synthesis is of interest and would allow confirmation of a deficiency in those patients presenting with diabetes insipidus linked to neurohypophyseal dysfunction.
摘要：
尿崩症是一种以低渗多尿为特征的疾病，继发于合成异常，regulation,或抗利尿激素的肾脏作用。最近,一个专家组,在患者协会的支持下，建议重新命名尿崩症以避免与糖尿病混淆。尿崩症最常见的形式是继发于神经垂体功能障碍（中枢尿崩症），因此称为“加压素缺乏症”。更罕见的形式，这与肾加压素抵抗（肾性尿崩症）有关，然后被命名为“抗血管加压素”。尿崩症的病因有时是明确的，在神经垂体原因（肿瘤或浸润性损伤）或肾脏起源的情况下，但在某些情况下，尿崩症可能很难与原发性多饮区分开来，其特征在于消耗过量的水而没有抗利尿激素的调节或作用的任何异常。除了患者的病史，体检,和下丘脑-垂体区的成像，为了区分这些不同的病因，可以提出功能测试，例如缺水或通过高渗透压（由输注高渗盐水引起）刺激和肽素。尿崩症的治疗取决于潜在的病因，在中央病因的情况下，是基于去氨加压素的给药，它可以改善患者的症状，但并不总是导致最佳的生活质量。这种生活质量改变的原因可能是催产素缺乏，催产素也从神经垂体分泌，虽然这还没有完全确立。使用催产素刺激来识别催产素合成变化的新测试的可能性是令人感兴趣的，并且可以确认那些患有与神经垂体功能障碍有关的尿崩症的患者的缺陷。
