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At least 667 records · Page 37Linked to original sources
PubMed1988

Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog.

Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.

Adrenocortical Hyperfunction↗
PubMed1976

Diabetes insipidus treated by DDAVP.

The symptomatic treatment of diabetes insipidus with pitressin is well known and very effective. The only problem concerns the type of pitressin to be used. In the past, pitressin snuff and various other intranasal instillations have been used, but these either have not been very effective, or have resulted in unpleasant side effects such as rhinitis. Until recently, the only effective form of the drug available in Australia has been pitressin tannate in oil. This often has to be given as a daily injection, which, like all intramuscular injections, is painful and, being in an oily base, is particularly likely to result in abscess formation. The recent introduction of 1-deamino-8-D-arginine-vasopressin (DDAVP), which can be simply instilled into the nostril, appears to present an advance in therapy.

Child, Preschool↗
PubMed1989

Three-point linkage analysis using multiple DNA polymorphic markers in families with X-linked nephrogenic diabetes insipidus.

The gene for X-linked nephrogenic diabetes insipidus (NDI), a disorder which, if untreated, causes severe dehydration, mental retardation, and possibly death in affected males, has been mapped recently to the Xq28 band through demonstration of linkage to the DX552 locus and other DNA markers (N. Knoers et al., 1987, Cytogenet. Cell Genet. 46:640; M. Kambouris et al., 1987, Cytogenet. Cell Genet. 46:636). Linkage studies in 11 families with NDI have enabled us to map the NDI gene between closely linked flanking markers in the Xq28 region and to obtain the following gene order: centromere-F9-DXS98-F8/CBD,CBP-DXS52/NDI-DXS134- telomere. These results have implications for presymptomatic and prenatal diagnosis of NDI and should also improve the prospects for identifying the fundamental gene defect underlying this disorder.

Chromosome Deletion↗
PubMed1985

Water-electrolyte balance and hypothalamo-pituitary-adrenocortical function in rats with inherited diabetes insipidus (Brattleboro strain).

Brattleboro rats, homozygous for hypothalamic diabetes insipidus (DI), compared to their Long Evans (LE) controls, revealed typical changes in water-sodium-potassium balance: hypernatremia and hyperosmolality and hypokalemia. Plasma renin activity was significantly increased (79%) and plasma concentration of aldosterone was significantly lower (--36%) in DI rats than in LE rats. Concomitantly aldosterone excretion in DI rats was increased sevenfold. Adrenal blood flow rates were not statistically different in both groups of rats but the aldosterone concentrations in the adrenal venous effluent were significantly lower (--66%) in DI rats than in LE rats, suggesting that the in vivo production rate of aldosterone was reduced in DI rats. Plasma concentration of ACTH was significantly decreased (by 25%) in DI rats. The reasons for the dissociation between the changes of aldosterone production and the variations of renin-angiotensin system activity were discussed.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Etiology of cranial diabetes insipidus in 164 adults.

The etiology of cranial diabetes insipidus (CDI) in adult patients has been studied in 164 cases hospitalized in the "G. I. Parhon" Institute of Endocrinology, over the last 10 years. Of those, 109 cases (66,9%) had the idiopathic form whereas 55 had secondary CDI. In the latter group, the most frequently encountered etiologies were traumatic (surgical and accidental head trauma) and tumoral (the primary hypothalamo-pituitary tumors and the metastatic ones had the same incidence). Sex distribution shows males and females to be equally affected. Fifteen cases (9,2%) showed associated allergic syndromes due to the wide use of posterior pituitary powder in Romania. The association of pregnancy with CDI was observed in 13 patients, and a normal evolution of gestation and delivery in 9 patients under therapy with desmopressin (DDAVP). The authors suggest that, at present, there is an increasing incidence both of posttraumatic CDI in adults and of well borne pregnancies.

Adolescent↗
PubMed1993

Nephrogenic diabetes insipidus: identification of the genetic defect.

Congenital nephrogenic diabetes insipidus (NDI) is an X-linked inherited disorder characterized by renal resistance to the antidiuretic hormonal action of arginine vasopressin. The disease gene has been assigned to the subtelomeric region of the X chromosome long arm by demonstrating close linkage between NDI and several X-chromosomal DNA markers. The finding of closely linked genetic markers is useful in the diagnosis of NDI. Receptor studies in patients have indicated that NDI might be due to the absence or an abnormality of the adenylate cyclase-bound vasopressin type 2 receptor. This assumption was supported by the discovery of functional vasopressin V2 receptor activity in somatic cell hybrid cell lines that carried at least the distal part of the human X chromosome long arm. Definite evidence for a V2 receptor defect being the cause of NDI was found in a recent study demonstrating point mutations in the V2 receptor gene from affected individuals. Direct mutation analysis is now applicable for accurate carrier detection and early (prenatal) diagnosis.

Diabetes Insipidus↗
PubMed1968

Impaired urinary concentration after vasopressin and its gradual correction in hypothalamic diabetes insipidus.

This study utilized rates with hereditary hypothalamic diabetes insipidus (D.I.) in order to explore possible mechanisms which prevent full urinary concentration after acute administration of vasopressin in hypothalamic D.I. and which correct this concentrating defect with prolonged therapy.IT WAS FOUND: (a) that the concentrating defect persisted even when the urinary osmolal excretion of D. I. rats was reduced to that of normal animals; (b) that the defect was not corrected more rapidly if larger doses of vasopressin were given; (c) that it persisted even when the D.I. rats were deprived of drinking water after vasopressin was given; (d) that there was osmotic equilibration between urine and renal papilla at a time when the concentrating defect was still evident; and (e) that the correction of the defect was associated with progressive and significant rise of the papillary osmolality. These studies appear to rule out osmotic diuresis, accumulation of exogenous vasopressin, persistent primary polydipsia, or delay in the induction of membrane permeability as causes for the concentrating defect. Rather, subnormal osmolality of the renal papilla, which can be corrected only gradually, accounts for the initial concentrating defect and the long time required for its correction. Reduction of water content and increase of urea content are primarily responsible for restoration of papillary osmolality to normal.

Animals↗
PubMed1994

A de novo mutation in the coding sequence for neurophysin-II (Pro24-->Leu) is associated with onset and transmission of autosomal dominant neurohypophyseal diabetes insipidus.

The molecular basis of autosomal dominant neurohypophyseal diabetes insipidus, a hereditary deficiency of vasopressin, was determined by nucleotide sequence analysis of the arginine vasopressin-neurophysin-II gene. A C-->T mutation at nucleotide 1761 was detected in one allele of this gene in each affected individual in three generations of one family. This mutant gene encodes a normal arginine vasopressin peptide, but predicts a substitution of leucine for proline at amino acid 24 of neurophysin-II, the arginine vasopressin carrier protein. This mutation was not detected 50 control individuals, thus demonstrating that it is not a common silent genetic polymorphism. The disease arose in the second generation of the studied family, and the chromosome 20 carrying this new mutation was identified by polymorphic CA microsatellite haplotype analysis. The first affected individual inherited this chromosome segment from her mother, who had neither the disease nor this mutation in her somatic cell DNA. Third generation individuals who subsequently inherited this mutation were affected. These data demonstrate that this amino acid substitution in neurophysin-II causes the disease. Two possibilities to explain the mechanism by which clinical deficiency of arginine vasopressin develops even in the presence of one normal arginine vasopressin-neurophysin-II allele are discussed.

Amino Acid Sequence↗
PubMed2000

Functional characterization of the molecular defects causing nephrogenic diabetes insipidus in eight families.

X-Linked nephrogenic diabetes insipidus (NDI) is a rare inherited disorder characterized by the excretion of abnormal large volumes of diluted urine mainly caused by mutations in the V2 vasopressin receptor (AVPR2) gene. By screening NDI patients for mutations within the AVPR2 gene we have identified three novel (I46K, F105V, I130F) and four recurrent (D85N, R106C, R113W, Q225X) mutations. In addition, a recurrent missense mutation (A147T) within the aquaporin-2 gene was identified in a female patient with autosomal recessive NDI associated with sensorineural deafness. Selected clinical data of the NDI patients were compared with the results from the in vitro studies. Functional analysis of I46K and I130F revealed reduced maximum agonist-induced cAMP responses as a result of an improper cell surface targeting. In contrast, the F105V mutation is delivered to the cell surface and displayed an unchanged maximum cAMP response, but impaired ligand binding abilities of F105V were reflected in a shifted concentration-response curve toward higher vasopressin concentrations. As the extracellularly located F105 is highly conserved among the vasopressin/oxytocin receptor family, functional analysis of this residue implicates an important role in high affinity agonist binding.

Amino Acid Sequence↗
PubMed1988

Management of early postoperative diabetes insipidus with parenteral desmopressin.

Management of early postneurosurgical diabetes insipidus (DI) requires parenteral vasopressin before intranasal administration of desmopressin-1 desamino-8 D arginine vasopressin (dDAVP) can be initiated. We have evaluated in 15 neurosurgical patients the effect and the tolerance of a 3-day regimen of dDAVP administered im every 12 h. Patients were randomly ascribed to one of 3 treatment groups: 1 microgram (N = 6), 2 micrograms (N = 5) or 4 micrograms (N = 4) were administered twice daily. dDAVP was effective whatever the dose, and DI was corrected by the 6th h of treatment. Effects were maximal on diuresis and urinary osmolality from the 18th h onwards. The effects were sustained throughout the treatment period. Reversal to pretreatment status occurred 24 h after the last injection. Moreover, 72 h after the last injection, natremia and osmolality reached values significantly below pretherapeutic values. The tolerance was excellent: hyponatremia which occurred in 11 patients, either occasionally or throughout the treatment period, remained mild and never had clinical consequences. In conclusion, before initiation of intranasal dDAVP, a 3-day treatment by 1, 2 or 4 micrograms of dDAVP injected im twice daily in neurosurgical patients corrected DI. Mild overhydration owing to a positive fluid balance was a side-effect which is also encountered in other therapeutic methods necessitating meticulous control of water intake.

Adolescent↗
PubMed1988

Salt preference in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain).

Brattleboro rats are homozygous for diabetes insipidus (HO-DI), lacking the ability to synthesize vasopressin. Besides increasing water consumption, HO-DI rats may compensate for their excessive renal water loss by reducing their intake of and preference for substances that elevate plasma osmolarity. In two experiments we assessed this possibility. In Experiment 1, salt preference of HO-DI and control Long-Evans (LE) rats was measured by presenting the rats with two tubes: one filled with water and the other with NaCl. In the first part of the experiment, 18 NaCl concentrations were presented in increasing order (from 6 to 300 mM). In the second part, other groups of HO-DI and LE rats were presented with 6 concentrations of NaCl, ranging from 6 to 450 mM in either increasing or decreasing order of concentrations. In Experiment 2, preference for 6 concentrations of citric acid ranging from 0.1 to 6 mM was assessed. With NaCl concentrations greater than 100 mM, intake and preference declined rapidly for the HO-DI group but very gradually for the LE group. In contrast, the HO-DI rats preferred all citric acid solutions more than LE rats. The results suggest that HO-DI rats compensate for their inability to concentrate urine not only by increasing water consumption, but also by decreasing consumption of and preference for salty solutions.

Animals↗
PubMed2005

Autophagy is a prosurvival mechanism in cells expressing an autosomal dominant familial neurohypophyseal diabetes insipidus mutant vasopressin transgene.

Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a progressive, inherited neurodegenerative disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of the antidiuretic hormone vasopressin (VP) from posterior pituitary nerve terminals. VP gene mutations cause adFNDI. Rats expressing an adFNDI VP transgene (Cys67stop) show a neuronal pathology characterized by autophagic structures in the cell body. adFNDI has thus been added to the list of protein aggregation diseases, along with Alzheimer's, Parkinson's and Huntington's, which are associated with autophagy, a bulk process that delivers regions of cytosol to lysosomes for degradation. However, the role of autophagy in these diseases is unclear. To address the relationships between mutant protein accumulation, autophagy, cell survival, and cell death, we have developed a novel and tractable in vitro system. We have constructed adenoviral vectors (Ads) that express structural genes encoding either the Cys67stop mutant protein (Ad-VCAT-Cys67stop) or an epitope-tagged wild-type VP precursor (Ad-VCAT). After infection of mouse neuroblastoma Neuro2a cells, Ad-VCAT encoded material enters neurite processes and accumulates in terminals, while the Cys67stop protein is confined to enlarged vesicles in the cell body. Similar to the intracellular derangements seen in the Cys67stop rats, these structures are of ER origin, and colocalize with markers of autophagy. Neither Ad-VCAT-Cys67stop nor Ad-VCAT expression affected cell viability. However, inhibition of autophagy or lysosomal protein degradation, while having no effect on Ad-VCAT-expressing cells, significantly increased apoptotic cell death following Ad-VCAT-Cys67stop expression. These data suggest that activation of autophagy by the stress of the expression of an adFNDI mutant protein is a prosurvival mechanism.

Acridine Orange↗
PubMed2003

Possible liposomal amphotericin B-induced nephrogenic diabetes insipidus.

OBJECTIVE: To report the development of nephrogenic diabetes insipidus (NDI) associated with the use of high-dose liposomal amphotericin B. CASE SUMMARY: A 38-year-old white man with relapsed acute myelogenous leukemia underwent a matched unrelated donor allogeneic bone marrow transplant with adequate engraftment and mild graft-versus-host disease responding to corticosteroids. Approximately 11 months after transplant, the patient was admitted to the hospital with suspected fungal pneumonia and started on liposomal amphotericin B (baseline serum creatinine 1.4-1.5 mg/dL). The dose was increased due to his immunosuppression and poor response, as the fungal etiology was identified as Torulopsis glabrata. The patient required mechanical ventilation due to biopsy-proven bronchiolitis olbiterans organizing pneumonia. Additionally, he developed diffuse alveolar hemorrhage and received intravenous desmopressin, with a reduction in bloody secretions. He also developed hypernatremia (serum sodium 155 mEq/L) on day 3 of the desmopressin and had an inappropriately increased urine output consistent with NDI. The most likely etiology for the NDI was liposomal amphotericin B and its associated hypokalemia. DISCUSSION: The observation of worsening hypernatremia (serum sodium increased from 135 to 164 mEq/L) with polyuria was associated with an increasing cumulative dosage of liposomal amphotericin B for fungal pneumonia despite the concurrent use of intravenous desmopressin. Aggressive water replacement was an effective treatment option in this patient. The Naranjo probability scale classified this as a possible adverse reaction because of the temporal sequence of NDI after high-dose liposomal amphotericin B and previously reported cases of NDI associated with amphotericin B desoxycholate. CONCLUSIONS: Amphotericin B desoxycholate has been implicated as an etiology for NDI, and the use of the newer liposomal amphotericin B reportedly avoids this rare complication. We observed the development of NDI despite the use of liposomal amphotericin B in a critically ill patient with bone marrow transplant.

Adult↗
PubMed1994

Bronchocentric granulomatosis and central diabetes insipidus successfully treated with corticosteroids.

Bronchocentric granulomatosis (BCG) is a rare chronic granulomatous lung disease that leads to destruction of the airway walls. It has been observed in association with various conditions, but never, so far, been reported to involve the central nervous system. We report a case of histologically confirmed pulmonary bronchocentric granulomatosis temporally associated with a partial central diabetes insipidus (CDI). Although the pathological basis of the posterior pituitary gland involvement was not ascertained, the temporal association of bronchocentric granulomatosis and central diabetes insipidus, as well as the fact that corticosteroid treatment provided stable remission of both conditions after a 10 month follow-up, strongly suggest that central diabetes insipidus was aetiologically related to bronchocentric granulomatosis in this patient.

Diabetes Insipidus↗
PubMed2001

A case of Rathke's Cleft Cyst inflammation presenting with diabetes insipidus.

Rathke's Cleft Cyst (RCC), which is located at the intrasellar region, is considered to be the distended remnants of Rathke's pouch, an invagination of the stomodeum. Lined with columnar or cuboidal epithelium of ectodermal origin, RCC usually contains mucoid material and it is found in 13-22% of normal pituitary glands. The cyst rarely leads to the development of symptoms but, when it does, the most common presenting symptoms are headache, visual impairment, hypopituitarism and hypothalamic dysfunction. However, in some cases it presents symptoms of diabetes insipidus, decreased libido and impotence. Recently we experienced a case of RCC inflammation presenting with diabetes insipidus and treated with transsphenoidal surgery. To our knowledge, this is the first report of RCC presenting with symptoms of diabetes insipidus in Korea.

Aged↗