Diabetes Insipidus

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Related to nephrogenic diabetes insipidus: dipsogenic diabetes insipidus, Central diabetes insipidus

diabetes insipidus

[‚dī·ə′bēd·ēz in′sip·ə·dəs]
(medicine)
A form of diabetes due to a disfunction of the hypothalamus.

Diabetes Insipidus

 

an endocrine disease caused by a low content of the hormone vasopressin in the blood. It is characterized by constant intense thirst and excessive excretion of urine. Diabetes insipidus patients excrete 5 to 50 liters a day of transparent urine with a very low specific gravity (1.005-1.001); the urine is odorless and contains no pathological components, including sugar (unlike the urine of diabetes mellitus patients). As a result of dehydration, diabetes insipidus patients suffer from dryness of the skin and mucous membranes, marked emaciation, general weakness, depression, vertigo and headaches, nausea, and sometimes even vomiting. Diabetes insipidus is caused by injury (owing to infection, tumor, or trauma) to the hypothalamus and pituitary, which form a unified functional system that regulates the excretion of salts and water by the kidneys. A hereditary predisposition to the disease is sometimes noted, and the trait is dominant. Treatment consists of hormonal preparations; chemotherapy is prescribed if the disease is of infectious or inflammatory origin.

REFERENCES

Atabek, A. A. Nesakharnyi diabet. Moscow, 1951. (Bibliography.)
Ginetsinskii, A. G. Fiziologicheskie mekhanizmy vodno-solevogo ravnovesiia. Moscow-Leningrad, 1963.
Leaf, A. “Diabetes Insipidus.” In Clinical Endocrinology, vol. 1. New York-London, 1960. Page 73. (Bibliography.)

L. M. GOL’BER

References in periodicals archive ?
Nephrogenic diabetes insipidus, in contradistinction, is characterised by urine osmolality that increases by less than 50%.
Identification and characterization of aquaporin2 water channel mutations causing nephrogenic diabetes insipidus with partial vasopressin response.
Educate patients about signs and symptoms of nephrogenic diabetes insipidus (NDI), such as polyuria and polydipsia.
We seek to explain this delayed onset by a discussion of the molecular and genetic changes underlying the pathogenesis of lithium-induced nephrogenic diabetes insipidus
For example, nephrogenic diabetes insipidus can be caused by either deficient or defective AQP2 or a malfunction in response to ADH-mediated control of AQP2 activity.