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Tytuł pozycji:

Acquired forms of central diabetes insipidus: Mechanisms of disease.

Tytuł:
Acquired forms of central diabetes insipidus: Mechanisms of disease.
Autorzy:
Verbalis JG; Georgetown University, Washington, DC, 20007 USA. Electronic address: .
Źródło:
Best practice & research. Clinical endocrinology & metabolism [Best Pract Res Clin Endocrinol Metab] 2020 Sep; Vol. 34 (5), pp. 101449. Date of Electronic Publication: 2020 Jul 10.
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Publication: 2002- : Amsterdam : Elsevier
Original Publication: Amsterdam : Harcourt Publishers, c2001-
MeSH Terms:
Diabetes Insipidus, Neurogenic/*etiology
Pituitary Diseases/*complications
Pituitary Gland, Posterior/*pathology
Aquaporin 2/metabolism ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/diagnosis ; Brain Injuries, Traumatic/epidemiology ; Brain Injuries, Traumatic/therapy ; Diabetes Insipidus, Nephrogenic/etiology ; Diabetes Insipidus, Nephrogenic/metabolism ; Diabetes Insipidus, Neurogenic/diagnosis ; Diabetes Insipidus, Neurogenic/epidemiology ; Diabetes Insipidus, Neurogenic/therapy ; Homeostasis/physiology ; Humans ; Neurophysins/physiology ; Pituitary Diseases/diagnosis ; Pituitary Diseases/epidemiology ; Pituitary Diseases/therapy ; Polydipsia/diagnosis ; Polydipsia/epidemiology ; Polydipsia/etiology ; Polydipsia/therapy ; Polyuria/diagnosis ; Polyuria/epidemiology ; Polyuria/etiology ; Polyuria/therapy ; Protein Precursors/physiology ; Vasopressins/physiology ; Water-Electrolyte Balance/physiology
Contributed Indexing:
Keywords: adipsic diabetes insipidus; central diabetes insipidus; neurohypophysis; neuroinfundibulohypophysitis; osmoreceptors; vasopressin
Substance Nomenclature:
0 (AVP protein, human)
0 (Aquaporin 2)
0 (Neurophysins)
0 (Protein Precursors)
11000-17-2 (Vasopressins)
Entry Date(s):
Date Created: 20200815 Date Completed: 20210315 Latest Revision: 20210315
Update Code:
20240105
DOI:
10.1016/j.beem.2020.101449
PMID:
32792133
Czasopismo naukowe
Most cases of acquired central diabetes insipidus are caused by destruction of the neurohypophysis by: 1) anatomic lesions that destroy the vasopressin neurons by pressure or infiltration, 2) damage to the vasopressin neurons by surgery or head trauma, and 3) autoimmune destruction of the vasopressin neurons. Because the vasopressin neurons are located in the hypothalamus, lesions confined to the sella turcica generally do not cause diabetes insipidus because the posterior pituitary is simply the site of the axon terminals that secrete vasopressin into the bloodstream. In addition, the capacity of the neurohypophysis to synthesize vasopressin is greatly in excess of the body's needs, and destruction of 80-90% of the hypothalamic vasopressin neurons is required to produce diabetes insipidus. As a result, even large lesions in the sellar and suprasellar area generally are not associated with impaired water homeostasis until they are surgically resected. Regardless of the etiology of central diabetes insipidus, deficient or absent vasopressin secretion causes impaired urine concentration with resultant polyuria. In most cases, secondary polydipsia is able to maintain water homeostasis at the expense of frequent thirst and drinking. However, destruction of the osmoreceptors in the anterior hypothalamus that regulate vasopressin neuronal activity causes a loss of thirst as well as vasopressin section, leading to severe chronic dehydration and hyperosmolality. Vasopressin deficiency also leads to down-regulation of the synthesis of aquaporin-2 water channels in the kidney collecting duct principal cells, causing a secondary nephrogenic diabetes insipidus. As a result, several days of vasopressin administration are required to achieve maximal urine concentration in patients with CDI. Consequently, the presentation of patients with central diabetes insipidus can vary greatly, depending on the size and location of the lesion, the magnitude of trauma to the neurohypophysis, the degree of destruction of the vasopressin neurons, and the presence of other hormonal deficits from damage to the anterior pituitary.
(Copyright © 2020. Published by Elsevier Ltd.)

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