scholarly journals Oxcarbazepine Therapy for Complete Central Diabetes Insipidus

2018 ◽  
Vol 8 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Basmah Abdallah ◽  
Spencer Hodgins ◽  
Daniel Landry ◽  
Michael O’Shea ◽  
Gregory Braden

Oxcarbazepine and carbamazepine cause hyponatremia by unknown mechanisms. We describe a patient with complete central diabetes insipidus and seizures who developed worsening hyponatremia when her dose of oxcarbazepine was increased. The patient maintained a normal serum sodium level and has had appropriately concentrated urine for 5 years on just oxcarbazepine, despite undetectable antidiuretic hormone (ADH) levels. This suggests that oxcarbazepine (or one of its metabolites) may stimulate collecting tubule V2 receptor-G protein complex independent of ADH, resulting in increased renal tubular water reabsorption. Oxcarbazepine may be useful as an alternative therapy for patients with central diabetes insipidus.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoo Hyung Kim ◽  
Yong Hwy Kim ◽  
Young Soo Je ◽  
Kyoung Ryul Lee ◽  
Hwan Sub Lim ◽  
...  

AbstractCopeptin levels reflect arginine vasopressin (AVP) release from the hypothalamus. Pituitary surgery often impairs AVP release and results in central diabetes insipidus (CDI). Here, we aimed to investigate how serum copeptin level changes 3 months after pituitary surgery and whether it has a diagnostic value for postoperative permanent CDI. Consecutive patients who underwent endoscopic transsphenoidal surgery at a single tertiary hospital were recruited. Serum copeptin levels were measured preoperatively and 3 months postoperatively. Among 88 patients, transient and permanent CDI occurred in 17 (19.3%) and 23 (26.1%), respectively. Three-month postoperative copeptin levels significantly declined from preoperative levels in permanent CDI group (P < 0.001, percentage difference =  − 42.2%) and also in the transient CDI group (P = 0.002, − 27.2%). Three months postoperative copeptin level < 1.9 pmol/L under normal serum sodium levels was the optimal cutoff value for diagnosing permanent CDI with an accuracy of 81.8%, while 3-month postoperative copeptin level ≥ 3.5 pmol/L excluded the CDI with a negative predictive value of 100%. Conclusively, 3 months postoperative copeptin levels significantly decreased from preoperative levels in the transient CDI group as well as the permanent CDI group. Three-month postoperative copeptin levels ≥ 3.5 pmol/L under normal serum sodium levels may be diagnostic for excluding postoperative CDI.


1986 ◽  
Vol 20 (10) ◽  
pp. 787-789 ◽  
Author(s):  
Rita A. Mitsch ◽  
Albert K. Lee

Among the various medications that have been associated with the development of syndrome of inappropriate antidiuretic hormone secretion (SIADH) are the tricyclic antidepressants. A 69-year-old man admitted for treatment of a depressive disorder that had not responded to trazodone was prescribed imipramine. Twenty-two days after initiation of therapy, the patient developed hyponatremia. The patient also had depressed serum osmolality and elevated urine sodium concentrations consistent with SIADH. With the discontinuation of imipramine, fluid restriction, and several doses of furosemide, normal serum sodium concentrations were attained. As antidepressant therapy was indicated, doxepin was selected. The patient maintained normal electrolyte values and water balance over the next two months of follow-up. No reports of doxepin-related SIADH were found in the literature; therefore, this agent may be considered as an alternative therapy in patients developing SIADH during antidepressant drug therapy.


2006 ◽  
Vol 291 (2) ◽  
pp. F257-F270 ◽  
Author(s):  
Joris H. Robben ◽  
Nine V. A. M. Knoers ◽  
Peter M. T. Deen

In the renal collecting duct, water reabsorption is regulated by the antidiuretic hormone vasopressin (AVP). Binding of this hormone to the vasopressin V2 receptor (V2R) leads to insertion of aquaporin-2 (AQP2) water channels in the apical membrane, thereby allowing water reabsorption from the pro-urine to the interstitium. The disorder nephrogenic diabetes insipidus (NDI) is characterized by the kidney's inability to concentrate pro-urine in response to AVP, which is mostly acquired due to electrolyte disturbances or lithium therapy. Alternatively, NDI is inherited in an X-linked or autosomal fashion due to mutations in the genes encoding V2R or AQP2, respectively. This review describes the current knowledge of the cell biological causes of NDI and how these defects may explain the patients' phenotypes. Also, the increased understanding of these cellular defects in NDI has opened exciting initiatives in the development of novel therapies for NDI, which are extensively discussed in this review.


Author(s):  
C. N. Sun ◽  
H. J. White ◽  
E. J. Towbin

Diabetes insipidus and compulsive water drinking are representative of two categories of antidiuretic hormone (ADH) lack. We studied a strain of rats with congenital diabetes insipidus homozygote (DI) and normal rats on an isocaloric fortified dilute milk diet. In both cases, the collecting tubules could not concentrate urine. Special staining techniques, Alcian Blue-PAS for light microscopy and lanthanum nitrate for electron microscopy were used to demonstrate the changes in interstitial mucopolysaccharides (MPS). The lanthanum staining was done according to the method of Khan and Overton.Electron microscopy shows cytoplasmic lesions, vacules, swelling and degenerating mitochondria and intercellular spaces (IS) in the collecting tubule cells in DI and rats on milk diet.


2018 ◽  
Author(s):  
Ana Ferreira ◽  
Tiago Silva ◽  
Filipa Bastos ◽  
Isabel Manita ◽  
Maria Carlos Cordeiro ◽  
...  

2019 ◽  
Author(s):  
Najoua Lassoued ◽  
Salmane Wannes ◽  
Asma Wardani ◽  
Abir Omrane ◽  
Raoudha Boussofara ◽  
...  

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