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psychogenic polydipsia). DI can be divided in central DI, caused by impaired secretion of the antidiuretic hormone arginine vasopressin (AVP) from the posterior pituitary and nephrogenic DI, which is due to decreased sensitivity of the kidney to AVP. In DI
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Introduction Patients with metabolic syndrome are at significant risk for developing type 2 diabetes mellitus and cardiovascular diseases ( 1 ). Arginine vasopressin (AVP) was suggested to play a causal role in the development of type 2
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antidiuretic actions of posterior pituitary extracts were discovered in the late 19th and early 20th centuries, including the use of posterior pituitary extracts to treat diabetes insipidus. In the mid-20th century, arginine vasopressin (AVP) was synthesized
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). The polyuria of PPS is characterized by a high output of hypotonic urine ( 2 ) and includes four conditions: arginine vasopressin (AVP) deficiency, nephrogenic diabetes insipidus, primary polydipsia, and gestational diabetes insipidus. The water
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arginine vasopressin (AVP) is produced paraneoplastically ( 6 , 7 , 8 ). Differentiation between these etiologies is important, especially in order to exclude or detect an underlying malignancy which is present in approximately one-third of patients with
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the central nervous system. (B) Relative expression of different genes in the hypothalamus. AVP, arginine vasopressin; CRH, corticotropin-releasing hormone; GR, glucocorticoid receptor; MR, mineralocorticoid receptor. (C) Relative expression of
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) ( 18 , 20 , 21 , 22 ) being characterized by an imbalanced arginine vasopressin (AVP) secretion ( 23 ). The exact pathophysiological mechanism leading to SIAD in these patients remains elusive, although the contribution of interleukin-6 (IL-6) is
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The pathomechanism of primary polydipsia is poorly understood. Recent animal data reported a connection between fibroblast growth factor 21 (FGF-21) and elevated fluid intake independently of hormonal control by the hormone arginine-vasopressin (AVP) and osmotic stimulation. We therefore compared circulating FGF-21 levels in patients with primary polydipsia to patients with AVP deficiency (central diabetes insipidus) and healthy volunteers. In this prospective cohort study, we analyzed FGF-21 levels of 20 patients with primary polydipsia, 20 patients with central diabetes insipidus and 20 healthy volunteers before and after stimulation with hypertonic saline infusion targeting a plasma sodium level ≥150 mmol/L. The primary outcome was the difference in FGF-21 levels between the three groups. Baseline characteristics were similar between the groups except for patients with central diabetes insipidus being heavier. There was no difference in baseline FGF-21 levels between patients with primary polydipsia and healthy volunteers (122 pg/mL (52,277) vs 193 pg/mL (48,301), but higher levels in patients with central diabetes insipidus were observed (306 pg/mL (114,484); P = 0.037). However, this was not confirmed in a multivariate linear regression analysis after adjusting for age, sex, BMI and smoking status. Osmotic stimulation did not affect FGF-21 levels in either group (difference to baseline: primary polydipsia −23 pg/mL (−43, 22); central diabetes insipidus 17 pg/mL (−76, 88); healthy volunteers −6 pg/mL (−68, 22); P = 0.45). To conclude, FGF-21 levels are not increased in patients with primary polydipsia as compared to central diabetes insipidus or healthy volunteers. FGF-21 therefore does not seem to be causal of elevated fluid intake in these patients.
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approach). However, most patients have a risk of developing arginine vasopressin deficiency after surgery ( 1 , 2 ). Therefore, sufficient hydration is needed to maintain fluid balance. In some cases, however, negative fluid balances still occur. The most
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. ( https://doi.org/10.1038/ni.3659 ) 19 Palin K Moreau ML Sauvant J Orcel H Nadjar A Duvoid-Guillou A Dudit J Rabié A Moos F . Interleukin-6 activates arginine vasopressin neurons in the supraoptic nucleus during immune challenge in