Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIABETES INSIPIDUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1995

Central diabetes insipidus caused by pituitary metastasis of lung cancer.

Tumor metastasis to the hypophyseal system has rarely been reported with either clinical or radiographic evidence. A 52-year-old woman presented with polydipsia, polyuria, and loss of appetite. She was diagnosed as having diabetes insipidus caused by pituitary micrometatasis of lung adenocarcinoma. After she had been treated with radiation therapy to the pituitary gland, the gland size was reduced as confirmed by magnetic resonance imaging, and her urine volume decreased. However, meningitis carcinomatosa appeared later. This was a rare case of secondary diabetes insipidus due to pituitary metastasis of lung cancer.

Adenocarcinoma↗
PubMed1985

Urinary adenosine 3',5'-monophosphate (cAMP) response to antidiuretic hormone in diabetes insipidus (DI): comparison between congenital nephrogenic DI type 1 and 2, and vasopressin sensitive DI.

Urinary adenosine 3',5'-monophosphate (cAMP) excretion before and after administration of aqueous vasopressin (pitressin) and 1-deamino-8-D-arginine vasopressin (DDAVP) was measured in congenital nephrogenic and in vasopressin sensitive diabetes insipidus (VS-DI). Excretion of cAMP into the urine increased markedly in response to pitressin (676%) and to DDAVP (252%) in VS-DI. Nephrogenic diabetes insipidus (N-DI) could be divided into two categories (type 1 and type 2) in respect to urinary cAMP responsiveness. In type 1, cAMP excretion showed no definite change after stimulation with pitressin (102%) or DDAVP (127%). On the other hand, urinary excretion of cAMP was significantly elevated in response to DDAVP in familial cases of N-DI type 2 (1269%) without producing any concentrating effect on the urine. Two different defects are considered to be involved in the pathogenesis of N-DI.

Adolescent↗
PubMed1992

Reversal of diabetes insipidus in Brattleboro rats: intrahypothalamic injection of vasopressin mRNA.

Messenger RNAs occur within the axons of magnocellular hypothalamic neurons known to secrete oxytocin and vasopressin. In Brattleboro rats, which have a genetic mutation that renders them incapable of vasopressin expression and secretion and thus causes diabetes insipidus, injection into the hypothalamus of purified mRNAs from normal rat hypothalami or of synthetic copies of the vasopressin mRNA leads to selective uptake, retrograde transport, and expression of vasopressin exclusively in the magnocellular neurons. Temporary reversal of their diabetes insipidus (for up to 5 days) can be observed within hours of the injection. Intra-axonal mRNAs may represent an additional category of chemical signals for neurons.

Animals↗
PubMed1987

Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy.

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.

Adult↗
PubMed2003

Transient lymphocytic panhypophysitis associated with SIADH leading to diabetes insipidus after glucocorticoid replacement.

A 52-year-old man presented with vomiting, general fatigue and hyponatremia. His symptoms and signs were consistent with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Endocrine studies revealed hypopituitarism and administration of hydrocortisone resulted in a marked polyuria. The patient was diagnosed as masked diabetes insipidus. The lymphocytic hypophysitis was also diagnosed on the basis of MRI findings and anti-pituitary antibody. Six months later, these abnormalities disappeared. Diabetes insipidus may exist in a case of hyponatremia due to contrastive SIADH. Such patients may recover spontaneously and careful follow-up is required, avoiding a long-term treatment by monotonous continuation of hormonal replacement.

Autoimmune Diseases↗
PubMed2006

[A case of sarcoidosis with diabetes insipidus].

A 23-year-old man was admitted because of polydipsia and polyuria. As chest radiographs and computed tomography showed mediastinal and bilateral hilary lymph node swelling, and diffuse small nodules in bilateral lung fields, we suspected sarcoidosis. Sarcoidosis was diagnosed by biopsy of a cervical lymph node, and central diabetes insipidus was diagnosed by fluid restriction test and vasopressin load test. A pituitary mass was also revealed by magnetic resonance imaging. Prednisolone therapy improved all of his clinical findings except diabetes insipidus. He had to continue intranasal 1-desamino-8-D-arginine vasopressin (DDAVP) therapy.

Adult↗
PubMed1988

Cranial diabetes insipidus secondary to arrested hydrocephalus.

An unusual case is described linking cranial diabetes insipidus with longstanding arrested hydrocephalus. The latter was demonstrated by computed tomographic (CT) and nuclear magnetic resonance (NMR) scans and cerebrospinal fluid pressure measurements. The increasing use of CT and NMR scans may result in this association of cranial diabetes and hydrocephalus being better defined.

Diabetes Insipidus↗
PubMed1995

Diabetes insipidus.

The advances in our understanding of the pathophysiology of defects in the antidiuretic hormone, the V2 receptor and the water channel, owing to mutations in the prepro-AVP-NPII, AVPR2 and AQP2 genes respectively, is providing insight into inherited diabetes insipidus as well as the more numerous sporadic cases. Further structure-function analyses of these mutated genes will increase our understanding of normal vasopressin-regulated water transport across the kidney epithelium at the molecular level.

Animals↗
PubMedDate not supplied

[Diabetes insipidus in infancy. I. Review (author's transl)].

Diabetes insipidus and its' treatment, are revised. New pathogenic concepts stressing the roll of osmoreceptors in its' etiological causes are explained. In the diagnosis, great importance is given to recently sistematized proof by Miller-Moses. This allows, to evaluate the grade of deficiency in vasopressin as well as new therapeutic possibilities, using differents drugs other from the classical "oily" solution of vasopressin.

Diabetes Mellitus, Type 1↗