Central diabetes insipidus (CDI) is the result of a deficiency of arginine vasopressin, and its major causes are idiopathic, primary or secondary tumors, neurosurgery and trauma.
Central diabetes insipidus (DI) is a rare disease characterized by the excretion of excessive volumes of dilute urine due to reduced levels of the antidiuretic hormonearginine vasopressin (AVP), caused by an acquired or genetic defect in the neurohypophysis.
CDI in inflammatory bowel disease is significantly associated with markers of disease severity, increased health care utilization and poor quality of life during the year of infection, and a 5-fold increase in health care charges in the year after infection (see Video Abstract, Supplemental Digital Content, http://links.lww.com/IBD/B658).
CDI was associated with ever use of TNF therapy (multivariate OR 6.09, 95% CI 2.07-17.93) but not vedolizumab (multivariate OR 0.76, 95% CI 0.08-7.36).
CDI was independently associated with calcineurin inhibitor use at time of C. difficile testing (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.08, 5.24, P = 0.03) and systemic antibiotic exposure within 30 days of C. difficile testing (OR 1.74, 95% CI 1.08, 2.79, P = 0.02).
Rabphilin-3A has been suggested as a novel autoantigen in infundibulo-neurohypophysitis (LINH), which leads to central diabetes insipidus through insufficient secretion of AVP.
Copeptin identified CDI with an AUC of 0.99 (95% CI 0.97-1.00), and a cut-off value ≤ 4.4pmol/L showed a sensitivity of 100% and a specificity of 99% to predict CDI.