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Results for “DIABETES INSIPIDUS”

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At least 937 records · Page 52Linked to original sources
PubMed1975

Elevated serum dopamine-beta-hydroxylase activity in rats with inherited diabetes insipidus.

The activity of dopamine-beta-hydroxylase, the enzyme that catalyzes the conversion of dopamine to norepinephrine, was measured in the serum of a strain of Wistar rats homozygous and heterozygous for a genetic form of hypothalamic diabetes insipidus and in Wistar control rats. Serum dopamine-beta-hydroxylase activity and water intake was highest in the homozygous affected rats and lowest in normal controls. Treatment with pitressin tannate reduced serum enzyme activity and water intake in rats with diabetes insipidus to levels which did not differ from controls. Thus serum dopamine-beta-hydroxylase activity appeared to vary directly with changes in sympathetic nerve activity in response to intravascular volume depletion and repletion.

Animals↗
PubMed1992

The primary empty-sella syndrome and diabetes insipidus in a child.

The empty-sella syndrome is uncommon in pediatric patients. Hypothalamic-pituitary dysfunction is common in these patients but involvement of the posterior pituitary gland is very rare. We report a seven-year-old girl with empty-sella syndrome who first developed arginine-vasopressin deficient diabetes insipidus and then anterior pituitary gland deficiency. The empty-sella syndrome should be included among the causes of arginine-vasopressin deficient diabetes insipidus in pediatric patients.

Child↗
PubMed1976

Monamines in brain and urine of rats with hereditary hypothalamic diabetes insipidus.

Monoamine levels in brain and urine of homozygous and heterozygous diabetes insipidus (DI) rats (Brattleboro strain) were assessed. Homozygous DI rats had a higher whole brain content of serotonin than their heterozygous littermates. However, when corrected for differences in brain weight, homozygous DI also appeared to have higher brain concentrations of noradrenaline, tyrosine and GABA. The total 24 h excretion of all amines and their precursors was greater in the homozygous than in the heterozygous rats.

Animals↗
PubMed2006

[Cranial diabetes insipidus in Wegener's granulomatosis].

We describe three cases of cranial diabetes insipidus (CDI) caused by Wegener's granulomatosis (WG). Panhypopituitarism was the presenting symptom in one patient. Magnetic resonance imaging (MRI) showed enlargement of the pituitary gland with an intrasellar mass lesion and absence of posterior pituitary lobe hyperintensity. Follow-up MRI disclosed reduction of the intrasellar lesion but sustained loss of posterior lobe hyperintensity. The patients still have CDI despite a marked clinical response to the treatment of WG. Pituitary dysfunction may be the presenting symptom as well as a complication of WG.

Diabetes Insipidus, Neurogenic↗
PubMed1991

Nephrogenic diabetes insipidus. An unusual presentation of recurrent rectal cancer.

The occurrence of diabetes insipidus (DI) in patients with systemic cancer is caused usually by tumor metastasis to the hypothalamus or posterior pituitary. A 43-year-old man with DI 8 months after radical surgery for a poorly differentiated adenocarcinoma of the distal rectum is reported. A therapeutic trial of intranasal desmopressin acetate did not correct the hyposthenuria, thus localizing the defect to the kidneys. A large tumor recurrence in the pelvis caused bilateral hydroureteronephrosis, resulting in nephrogenic DI. This report shows that not all cases of DI in cancer patients are of central origin.

Adenocarcinoma↗
PubMed1991

A variant of nephrogenic diabetes insipidus: V2 receptor abnormality restricted to the kidney.

In congenital nephrogenic diabetes insipidus (NDI) blunted responses of plasma factor VIII, von Willebrand factor, and plasminogen activator to the synthetic V2 analogue 1-desamino-8-D-arginine vasopressin (DDAVP) have been reported. In addition, vasodilatory responses to DDAVP appear to be absent in NDI. We describe a boy, who presented shortly after birth with the typical features of NDI, but who showed normal coagulation, fibrinolytic and vasodilatory responses to DDAVP. We conclude that in this patient the defect is confined to the kidney, while in other NDI patients there may be a general V2 receptor abnormality. These findings point to heterogeneity in NDI.

Diabetes Insipidus↗
PubMed1999

A novel mutation in the vasopressin V2 receptor gene in a woman with congenital nephrogenic diabetes insipidus.

A 56-year-old Japanese woman with congenital nephrogenic diabetes insipidus (CNDI) is reported. She was diagnosed with CNDI accompanied by advanced gastric cancer. After total gastrectomy, approximately 500 ml fluid per hour was necessary to prevent dehydration. Urinary volume was decreased by administration of hydrochlorothiazide. We detected a novel mutation in the vasopressin V2 receptor gene of her chromosomal DNA. A substitution from G to A was found at the 631 nucleotide position, altering codon 12 from glycine (GGG) to glutamic acid (GAG) in the first extracellular domain. This missense mutation appeared to be the cause of her resistance to arginine vasopressin.

Amino Acid Sequence↗
PubMed1994

[Clinical trial of indapamide in the management of central diabetes insipidus].

To investigate antidiuretic effect of indapamide, ten patients with central diabetes insipidus (CDI) were observed with the treatment of 2.5-7.5 mg of indapamide per day. After the third day of therapy, their mean daily urine output reduced by about 50%, and urine osmolality increased 1.36 times. No further change was seen in urine volume and urine osmolality on the sixth day of treatment. This antidiuretic effect was similar to that of 50-75 mg dihydrochlorothiazide per day. No adverse reaction was observed in blood pressure and serum potassium concentration during indapamide therapy. These data suggest that indapamide may be a new drug in the management of CDI.

Adolescent↗
PubMed1988

[Central diabetes insipidus in the very young child. Treatment with oral desmopressin].

Neonatal diabetes insipidus (DI) is extremely rare. An efficacious substitutive treatment can be particularly difficult to ensure. We have treated two children with central DI, revealed during the neonatal period, successively with an intranasal preparation of desmopressin at one month of age and with an oral preparation at one and 3 years respectively. We conclude that oral treatment with desmopressin is possible, secure and effective in DI presenting in the first months of life. This new form of administration seems even better for younger children when the difficulties of intranasal administration can be responsible for severe complications. As with the intranasal form, the doses given orally are very variable and individual.

Administration, Intranasal↗
PubMed1992

Two families with hereditary diabetes insipidus not due to osmoreceptor failure.

Two families with hereditary central diabetes insipidus (CDI) are reported. The pedigree in both families shows an autosomal dominant trait. The plasma arginine-8-vasopressin (AVP) determined by radioimmunoassay was markedly lower in these CDI patients than in healthy controls; the difference being even more pronounced after a hyperosmotic challenge. Since in the present study histamine also failed to increase the plasma AVP concentration, the authors consider it unlikely that an osmoreceptor failure would be implicated in the pathogenesis of CDI in these cases. The AVP concentration of the lumbar cerebrospinal fluid was also measured in two members of one of the families: the level found at the lower normal range indicates that some AVP secretion has been maintained in the extrahypothalamic vasopressinergic system of these patients.

Adolescent↗
PubMed2002

Two novel aquaporin-2 mutations responsible for congenital nephrogenic diabetes insipidus in Chinese families.

Mutations in the aquaporin-2 gene (AQP2), encoding the vasopressin-regulated water channel of the renal collecting duct, are responsible for the autosomal recessive or dominant forms of congenital nephrogenic diabetes insipidus. We describe two new families with normal hypotensive and coagulation responses following the administration of desamino-8-D-arginine AVP, a clinical suggestion of normal vasopressin-2 receptors. The patients were compound heterozygotes for point mutations at nucleotide position 170 (CAG to CCG; Q57P) and at position 299 (GGA to GTA; G100V) in exon 1 of the AQP2 gene. Expression of the G57P and G100V AQP2 proteins in Xenopus oocytes showed only 1.3-fold and 1.2-fold increase, respectively, in the water permeability in contrast to 8.0-fold increase in oocytes injected with wild-type cRNA. Immunoblots of oocyte lysate revealed the intensities of the 29-kDa bands were comparable among oocytes injected with wild-type and mutant cRNAs. Immunocytochemistry showed the plasma membrane was not stained in oocytes injected with cRNA of Q57P and of G100V. These results provide evidence that the Q57P and G100V mutations in congenital nephrogenic diabetes insipidus are attributable to the misrouting of AQP2.

Adult↗
PubMed1984

Two cases of hereditary diabetes insipidus, with an autopsy finding in one.

Two cases of hereditary diabetes insipidus (DI) are described, with an autopsy finding in one. The patients were brothers and 7 other relatives had symptoms of DI. The transmission of the disease in this family seemed to be an autosomal dominant trait with incomplete penetration. Both patients had the incomplete type of DI, which is diagnosed by the response of plasma AVP and the change in Uosm/Posm to 14 h water deprivation. The post-mortem examination in Case 1 showed that there was no atrophy of the supraoptic nucleus and paraventricular nucleus, but immunohistochemical studies revealed, that the paraventricular nucleus scarcely had any vasopressin positive cells in contrast to an autopsy control. This finding suggests that there may be a congenital defect in AVP synthesis in some cases of hereditary DI.

Adult↗
PubMed1985

Lack of effect of Pitressin on the learning ability of Brattleboro rats with diabetes insipidus using positively reinforced operant conditioning.

Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) received daily subcutaneous injections of vasopressin in the form of Pitressin tannate (0.5 IU/24 hr). They were initially deprived of food and then trained to work for food reward in a Skinner box to a fixed ratio of ten presses for each pellet received. Once this schedule had been learned the rats were given a discrimination task daily for seven days. The performances of these BDI rats were compared with those of rats of the parent Long Evans (LE) strain receiving daily subcutaneous injections of vehicle (arachis oil). Comparisons were also made between these two groups of treated animals and untreated BDI and LE rats studied under similar conditions. In the initial learning trial, both control and Pitressin-treated BDI rats performed significantly better, and manifested less fear initially, than the control or vehicle-injected LE rats when first placed in the Skinner box. Once the initial task had been learned there was no marked difference in the discrimination learning between control or treated BDI and LE animals. These results support the view that vasopressin is not directly involved in all types of learning behaviour, particularly those involving positively reinforced operant conditioning.

Animals↗