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PubMed1980

Diabetes insipidus: a physiologic approach to diagnosis.

Diabetes insipidus can be delineated in the context of the normal physiology of water metabolism. This approach highlights the common pathway taken by the variety of diseases that can progress to an insufficiency of antidiuretic hormone (ADH) and to diabetes insipidus. A simple diagnostic approach uses homeostatic pathways to separate diabetes insipidus from the other polyuric states. New developments in the biochemical alteration of ADH have improved the ability to individualize hormonal replacement and promise better therapy in the near future.

Deamino Arginine Vasopressin↗

PubMed1987

[Diabetes insipidus after selective pituitary adenomectomy. A case with late appearance].

Diabetes insipidus is a well-known complication of hypophyseal surgery. The case is described of a women presenting with evident polyuropolydipsic syndrome arising 9 years after transphenoidal hypophyseal adenectomy. The diagnosis insipidus diabetes was secondary to intrasellar scars revealed by a hypophyseal CAT scan. The unusually long interval between surgery and the onset of the syndrome is emphasised.

Adult↗

PubMed1977

[Diabetes insipidus in infancy. II. Study of eleven cases (author's transl)].

Eleven cases of diabetes insipidus are revised and distributed in the following four groups: I. Idiopathic diabetes insipidus, three. II. Secondary diabetes insipidus, four. III. Nephrogenic diabetes insipidus, two. IV. Psychogenic diabetes insipidus, two. In all these cases, clinical parameters, general analysis, hydric metabolism (static and dinamic), are studied. The precocious beginning of psychogenic diabetes insipidus, and some conclusions, on a difficult case of hard diagnosis are emphasized.

Adolescent↗

PubMed2001

[A case of congenital nephrogenic diabetes insipidus accompanied by hypertension].

Congenital nephrogenic diabetes insipidus is a rare disorder in which the kidney is insensitive to the antidiuretic hormone, vasopressin. In most cases, a mutation in the vasopressin type 2(V2) receptor gene is the genetic cause of the disease. So far, few cases of congenital nephrogenic diabetes insipidus with hypertension have been reported. We report one male case of congenital nephrogenic diabetes insipidus accompanied by hypertension. The patient was a 24-year-old man who had suffered from polyuria and polydipsia since infancy and had been found to have hypertension at about 16 years. He was admitted to hospital in May 2000 for investigation of polyuria and hypertension with a high plasma level of renin activity of 10.4 ng/ml/hr. On physical examination, the blood pressure was 150/90 mmHg and the daily urinary output was 18.5 l. There was no change in urine volume and urine osmolality after an intramascular injection of vasopressin and water deprivation. The blood pressure and plasma renin activity were increased from 127/73 mmHg to 146/87 mmHg and from 4.9 ng/ml/hr to 6.1 ng/ml/hr, respectively, by a 4-hour dehydration test. He was found to have a C-to-T transition at nucleotide position 675 by sequencing analysis of the V2 receptor gene. After administration of hydrochlorothiazide, both the blood pressure and urine volume were reduced. Consequently, it was suggested that activation of the renin-angiotensin system by dehydration, at least in part, contributed to high blood pressure in this case.

Adult↗

PubMedDate not supplied

Continuous infusion of vasopressin in comatose children with neurogenic diabetes insipidus.

Three comatose children with neurogenic diabetes insipidus were treated with intravenous infusion of vasopressin. The infusion of vasopressin was started at a dose of 1.3 to 2.7 mU/kg/h as soon as diabetes insipidus was diagnosed. The effect (urine flow < 2 ml/kg/h with increased specific gravity) was noted in 1 to 6 hours. The infusion rate of vasopressin was adjusted according to urine flow rate which was usually kept around 65 ml/100 kcal metabolized/day. Hypernatremia was corrected 17 to 53 hours after the initiation of infusion of vasopressin. The levels of sodium stayed between 127 and 151 mmol/l during a period of 2.5 to 22 days until the patients' death due to the termination of respiratory support or cardiac decompensation. A continuous infusion of vasopressin offered the advantage of rapid onset and termination of effect and therefore could be easily titrated. It seems a rational therapy for comatose children with neurogenic diabetes insipidus.

Child↗

PubMed2006

Use of subcutaneous DDAVP in infants with central diabetes insipidus.

Traditional methods for treating central diabetes insipidus during infancy, such as fluid therapy or the use of intranasal hormone replacement, have significant potential limitations. In a retrospective study of infants with diabetes insipidus, we examined outcome using subcutaneous (sc) DDAVP, and compared this to infants treated with intranasal lysine vasopressin or DDAVP. After in-patient dosage titration, outpatients' serum sodium concentrations were maintained in a narrower range in the sc group compared with the intranasal group, and the percentage of serum sodium concentrations within the normal range was greater in the sc group. There were no significant complications in either group. We conclude that DDAVP administered subcutaneously can be a safe and effective alternative to traditionally recommended treatments of central diabetes insipidus during infancy.

Administration, Intranasal↗

PubMed1992

Klinefelter's syndrome accompanied by diabetes mellitus and diabetes insipidus.

The first case of Klinefelter's syndrome accompanied by diabetes insipidus and diabetes mellitus is reported. A 41-year-old man admitted for hyperosmolar diabetic coma with a past history of diabetes insipidus was diagnosed as having Klinefelter's syndrome by endocrinological examination and sex chromosome analysis. In this case, glucose tolerance test was normalized half a year later and blood glucose was well controlled with diet therapy alone.

Adult↗

PubMed2000

Central diabetes insipidus in children and young adults.

BACKGROUND: Central diabetes insipidus is rare in children and young adults, and up to 50 percent of cases are idiopathic. The clinical presentation and the long-term course of this disorder are largely undefined. METHODS: We studied all 79 patients with central diabetes insipidus who were seen at four pediatric endocrinology units between 1970 and 1996. There were 37 male and 42 female patients whose median age at diagnosis was 7.0 years (range, 0.1 to 24.8). All patients underwent magnetic resonance imaging (MRI) and periodic studies of anterior pituitary function. The median duration of follow-up was 7.6 years (range, 1.6 to 26.2). RESULTS: The causes of the central diabetes insipidus were Langerhans-cell histiocytosis in 12 patients, an intracranial tumor in 18 patients, a skull fracture in 2 patients, and autoimmune polyendocrinopathy in 1 patient; 5 patients had familial disease. The cause was considered to be idiopathic in 41 patients (52 percent). In 74 patients (94 percent) the posterior pituitary was not hyperintense on the first MRI scan obtained, and 29 patients (37 percent) had thickening of the pituitary stalk. Eighteen patients had changes in the thickness of the pituitary stalk over time, ranging from normalization (six patients) or a decrease in thickness (one patient) to further thickening (seven patients) or thickening of a previously normal stalk (four patients). Anterior pituitary hormone deficiencies, primarily growth hormone deficiency, were documented in 48 patients (61 percent) a median of 0.6 year (range, 0.1 to 18.0) after the onset of central diabetes insipidus. CONCLUSIONS: Most children and young adults with acquired central diabetes insipidus have abnormal findings on MRI scans of the head, which may change over time, and at least half have anterior pituitary hormone deficiencies during follow-up.

Adolescent↗

PubMed2006

Diabetes insipidus: diagnosis and treatment of a complex disease.

Diabetes insipidus, characterized by excretion of copious volumes of dilute urine, can be life-threatening if not properly diagnosed and managed. It can be caused by two fundamentally different defects: inadequate or impaired secretion of antidiuretic hormone (ADH) from the posterior pituitary gland (neurogenic or central diabetes insipidus) or impaired or insufficient renal response to ADH (nephrogenic diabetes insipidus). The distinction is essential for effective treatment.

Diabetes Insipidus↗

PubMed1984

[Neurohypophyseal diabetes insipidus. Anatomo-clinical correlations].

Eighteen patients aged between 14 and 60 years suffering from diabetes insipidus were studied. Diabetes insipidus was diagnosed by means of Robertson's test. All patients underwent C.T. scanning and evaluation of PRL basally and after TRH (200 mcg e.v.). Twelve patients (66%) showed neurological lesions (secondary central diabetes insipidus). Six of these patients had hyperprolactinaemia. Our data suggest that most of central diabetes insipidus are associated with central system nervous (S.N.C.) damage. In same cases the presence of hyperprolactinaemia suggests a brain damage. Therefore neuroradiological study is very important in all cases of neurohypophyseal diabetes insipidus.

Adolescent↗

PubMed1981

Vasopressin function in familial cranial diabetes insipidus.

A family suffering from cranial diabetes insipidus, that extends over 4 generations, is described. Inheritance of polyuria was autosomal dominant. Vasopressin function was studied in members of the last 2 generations, 4 of whom had polyuria. Osmoregulation of vasopressin secretion was assessed by infusion of hypertonic saline. Plasma vasopressin remained undetectable in one patient, while 2 others had very blunted vasopressin responses to osmotic stimulation. Three non-osmotic stimuli were applied. Controlled hypotension produced by trimetaphan infusion and insulin-induced hypoglycaemia did not increase plasma vasopressin but apomorphine-induced nausea caused a minimal rise in plasma vasopressin to 0.7 pg/ml. Polyuria and thirst resolved with antidiuretic therapy in all patients studied. Congenital absence of vasopressin as in Brattleboro rats is unlikely to account for diabetes insipidus in this disorder since small increases in vasopressin have been demonstrated in these patients. In view of previous post-mortem findings, familial cranial diabetes insipidus is most likely to be due to degeneration of vasopressin-synthesizing neurones.

Adult↗

PubMed1990

[Contribution of MRI in 5 cases of central diabetes insipidus].

Five cases of central diabetes insipidus demonstrate the potential of MRI to explore the hypothalamohypophysial axis. The diversity of the detected pathologies are illustrated: abnormal signal of the posterior pituitary in an idiopathic diabetes insipidus, lobar prosencephaly, malignant teratoma (embryonal carcinoma), histiocytosis X, craniopharyngioma.

Child↗

PubMed2006

Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review.

Dipsogenic diabetes insipidus is a syndrome of disordered thirst, in patients without psychiatric disease, which may be confused with partial central diabetes insipidus. Distinguishing these entities involves monitored water testing. Therapy with antidiuretic hormone in patients with dipsogenic diabetes insipidus is thought to be contraindicated for fear of inducing water intoxication. We report a case of a 26-year-old woman without psychiatric illness referred for longstanding polyuria and polydipsia. Otherwise healthy, she complained of near-constant thirst and frequent urination, causing severe disruption of her personal and professional life. She had been consistently eunatremic and polyuric, with low urine osmolality. Results of extensive water testing revealed intact urinary concentrating and diluting capacity, physiologic though blunted antidiuretic hormone (ADH) release, and an abnormally low thirst threshold, consistent with the diagnosis of dipsogenic diabetes insipidus. To control her polyuria we initiated treatment with intermittent, low-dose, intranasal desmopressin and strict water restriction during drug dosing. In follow-up she reported excellent control of polyuria and significant functional improvement. The reviewed literature demonstrates a limited number of reports about dipsogenic diabetes insipidus, and no prior report of a similar treatment strategy. Dipsogenic diabetes insipidus is an uncommonly (and not universally) recognized disorder, requiring monitored testing in order to distinguish it from incomplete forms of central diabetes insipidus. Though therapy with desmopressin cannot be recommended based on the results of a single case, the outcome presented here is intriguing and suggests that larger studies in such patients is warranted to assess the broader application of such an intervention.

Adult↗

PubMed1991

[The diagnosis of nephrogenic diabetes insipidus in the dog].

Nephrogenic diabetes insipidus is characterized by polyuria, hyposthenuria and compensatory polydipsia. With conventional clinical and laboratory examinations the diagnosis can be established and the differential diagnostic diseases excluded. In order to verify the diagnosis, differentiate the condition from central and nephrogenic diabetes insipidus and rule out psychogenic polydipsia, additional laboratory studies are required: of these, the concentration test, modified Carter-Robbins test and AVP stimulation test are described.

Animals↗

PubMed1977

Vasopressin administration in the first month of life: effects of growth and water metabolism in hypothalamic diabetes insipidus rats.

Rats homozygous for the mutant gene for diabetes insipidus (Brattleboro strain) are stunted in growth compared to rats heterozygous for the mutant gene and normal rats without the mutant gene. The hypothesis was tested that normal growth depends upon the presence of vasopressin. It was expected that replacement therapy of vasopressin rats homozygous for diabetes insipidus would make possible a normal growth rate similar to that of rats heterozygous for diabetes insipidus. Rats heterozygous and homozygous for diabetes insipidus were treated with 0.25 U (Days 0-9) and 0.5 U (Days 10-29) of vasopressin during the first month of life. During the treatment period, vasopressin significantly increased the urine osmolatities of the homozygous rats demonstrating the renal effectiveness of the vasopressin. The results showed that remedial vasopressin administration could not produce normal growth rates in homozygous rats and may be detrimental. Six weeks following vasopressin treatment, homozygous, diabetes insipidus rats which had received vasopressin had increased 24 hr water intakes and decreased urine osmolalities compared to control, homozygous rats, Heterozygous rats also had decreased urine osmolalities resulting from vasopressin six weeks after the cessation of vasopressin treatment.

Aging↗

PubMedDate not supplied

Nephrogenic diabetes insipidus in sibling colts.

Nephrogenic diabetes insipidus was diagnosed in two full sibling Thoroughbred colts. Each colt had a history of excessive urination. Extreme polydipsia (greater than 80 L per day) was documented in both colts. Inability to concentrate urine in response to water deprivation, infusion of hypertonic saline, or exogenous vasopressin administration indicated insensitivity of the collecting duct epithelial cells to vasopressin. A diagnosis of nephrogenic diabetes insipidus was further supported by a normal increase in plasma vasopressin concentration after water deprivation in the one colt in which such testing was pursued.

Animals↗

PubMed1997

Diabetes insipidus due to hypophysitis.

Central diabetes insipidus is a chronic disorder which in most patients occurs secondary to tumor, infection, trauma or other lesions. In about 20-30% of patients etiology is unclear, however a destructive autoimmune process in the hypophysis may play a role. We report the case of an 18-year-old girl with central diabetes insipidus. Vasopressin levels were typically decreased. Examinations performed 1.5 years after manifestation showed no pathologic changes on MRI and no additional endocrine disorder. MRI was repeated 1.5 years later whereon a thickening of the pituitary stalk as a typical sign of hypophysitis was apparent. No other reasons could be found for the vasopressin deficiency. The finding of hypophysitis in our patient 3 years after disease manifestation suggests that the characteristic MRI changes may take as long as 3 years to become apparent.

Adolescent↗

PubMed2001

Thickened pituitary stalk with central diabetes insipidus: report of three cases.

Diabetes insipidus of central origin usually results from lesions in the hypothalamic neurohypophyseal system. Lymphocytic infundibuloneurohypophysitis is an uncommon cause. Cases of lymphocytic infundibuloneurohypophysitis with thickening of the pituitary stalk and enlargement of the neurohypophysis with no hyperintense signal in the posterior pituitary have been reported. Reported cases presenting with isolated thickening of the pituitary stalk are very rare. We report three such cases, one in a nulliparous woman and the other two in men. Magnetic resonance (MR) imaging in these patients revealed isolated thickening of the pituitary stalk, loss of the hyperintense signal of the posterior pituitary, and an adenohypophysis of normal size. All cases had abnormal nodular infundibular enlargement. One male patient had hypogonadism; the other patients showed no sign of adenohypophyseal deficiency on stimulation test. Serial follow-up MR imaging revealed that all three patients had persistent thickening of the pituitary stalk. Diabetes insipidus was controlled by the administration of desmopressin acetate in all patients.

Adult↗