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PubMed1995

Molecular biology of diabetes insipidus.

The identification, characterization, and mutational analysis of three different genes, namely the prepro-arginine-vasopressin-neurophysin II gene (prepro-AVP-NPII), the arginine-vasopressin receptor 2 gene (AVPR2), and the vasopressin-sensitive water channel gene (aquaporin-2, AQP2), provide the basis for our understanding of three different hereditary forms of diabetes insipidus: autosomal dominant neurogenic diabetes insipidus, X-linked nephrogenic diabetes insipidus, and autosomal recessive nephrogenic diabetes insipidus, respectively. These advances provide diagnostic tools for physicians caring for these patients.

Amino Acid Sequence↗
PubMed1992

Familial nephrogenic diabetes insipidus: report of two families.

Familial nephrogenic diabetes insipidus is a hereditary disorder, generally transmitted by sex-linked recessive genes with varying degrees of penetrance in females. The onset of this disorder occurs in infancy, usually characterized by unexplained fever, recurrent dehydration and failure to thrive. If left unrecognized, recurrent hyperosmolality and hypernatremia will lead to retarded growth and neurologic sequelae. Intracranial hemorrhage, consciousness disturbance and even mortality may occur in cases of acute dehydration episodes. We report on two families with nephrogenic diabetes insipidus, whose various symptoms and signs were studied to establish an accurate diagnosis. In pediatric practices, it is very important to recognize early those infants with obscure symptoms in order to preserve their psychomotor development and growth potential.

Adolescent↗
PubMed2004

Diabetes insipidus in the head-injured patient.

Diabetes insipidus (DI) is an uncommon but important complication in the head-injured population. A retrospective review of all trauma patients admitted to the intensive care unit (ICU) during a 4-year period who developed DI was undertaken. The incidence of DI was 1.3 per cent in ICU trauma admissions and 2.9 per cent in traumatic head injuries admitted to the ICU. The overall mortality was 69 per cent (18/26). The mean onset time of DI in nonsurvivors (1.5 +/- 0.7 days) was shorter compared to survivors (8.9 +/- 10.2 days) (P < 0.001). All patients who died developed DI within the first 3 days of hospitalization. Patients who develop DI early in their course have a higher mortality than those who develop DI later in their hospital course. The development of diabetes insipidus after head injury carries a 69 per cent mortality rate, and if the onset is within the first 3 days after injury, mortality rate rises to 86 per cent.

Adolescent↗
PubMed1992

Radiation therapy for diabetes insipidus caused by Langerhans cell histiocytosis.

Hypothalamic-pituitary radiation therapy has been the standard treatment for the diabetes insipidus of Langerhans cell histiocytosis. The goal of this study was to assess the role of radiation therapy in Langerhans cell histiocytosis-associated diabetes insipidus and to compare the results with nonirradiated controls. Forty-seven patients with pathologically confirmed Langerhans cell histiocytosis were diagnosed with diabetes insipidus between 1950 and 1989 and were treated at the Mayo Clinic. These patients were divided into two groups on the basis of treatment for the diabetes insipidus: The first group (radiation group) included 30 patients (28 of whom were evaluable for response) who received hypothalamic-pituitary radiation therapy, and the second group (control group) included 17 patients who did not. A partial response to treatment was defined as a reduction in vasopressin dosage or improvement in computed tomography (CT) or magnetic resonance imaging (MRI). A complete response was defined as no further need for vasopressin therapy or normalization of CT or MRI. End points analyzed included treatment response, patient characteristics, morbidity, dose-response relationship, and survival. Patient characteristics of the two groups were similar except for age and lung involvement, both of which were significantly less in the radiation group. Thirty-six percent of patients (10 of 28) in the radiation group responded to hypothalamic-pituitary radiation therapy (22% complete response and 14% partial response), whereas none in the control group responded. Five of the six complete responders were irradiated within 14 days of the diagnosis of diabetes insipidus. The mean dose used in the responding and nonresponding patients was 11.2 and 10 Gy, respectively. Three of five patients (60%) treated with more than 15 Gy responded compared to seven of 23 (30%) treated with less than 15 Gy. Eight of the 10 responders (80%), compared to 16 of 35 nonresponders (46%), were female. Only one in 20 patients with concomitant lung histiocytosis responded. Complications of therapy may include insufficiency in other hypothalamic-pituitary axes in the treated patients. Actuarial survivals at 5, 10, 20, and 40 years for the entire group were 80%, 78%, 75%, and 65%, respectively, with a median follow-up in living patients of 14.7 years.

Adolescent↗
PubMed2004

Vasopressin and desmopressin in central diabetes insipidus: adverse effects and clinical considerations.

The management of central diabetes insipidus has been greatly simplified by the introduction of desmopressin (DDAVP). Its ease of administration, safety and tolerability make DDAVP the first line agent for outpatient treatment of central diabetes insipidus. The major complication of DDAVP therapy is water intoxication and hyponatremia. The risk of hyponatremia can be reduced by careful dose titration when initiating therapy and by close monitoring of serum osmolality when DDAVP is used with other medications affecting water balance. Herein we review the adverse effects of DDAVP and its predecessor, vasopressin, as well as discuss important clinical considerations when using these agents to treat central diabetes insipidus.

Antidiuretic Agents↗
PubMed1997

Normal MR appearances of the posterior pituitary in central diabetes insipidus associated with septo-optic dysplasia.

Magnetic resonance (MR) imaging of the pituitary in children with central diabetes insipidus usually shows absence of the normal high signal within the posterior gland. The high signal of the normal posterior pituitary is thought to be due to the presence of intra- cellular storage granules of vasopressin. MR imaging has been advocated as a useful investigation to aid in the distinction between central diabetes insipidus and other causes of thirst and polydipsia. We report the case of an infant with central diabetes insipidus in association with septo-optic dysplasia in whom MR imaging showed normal appearances of the posterior pituitary. The mechanism of central diabetes insipidus in this case may be related to a failure of hypothalamic function affecting osmoreception, rather than to a deficiency of vasopressin. Normal MR appearances of the pituitary do not exclude central diabetes insipidus in infants with midline cerebral malformations.

Abnormalities, Multiple↗
PubMedDate not supplied

Diabetes insipidus as a consequence of neurologic involvement in Behcet's syndrome.

OBJECTIVE: To describe a case of central diabetes insipidus that was associated with Behçet's syndrome. METHODS: We present a case report, including clinical, laboratory, and radiologic data. The pertinent literature is reviewed relative to diabetes insipidus and Behçet's syndrome, and a discussion about a possible association is presented. RESULTS: A 32-year-old man presented with diplopia and severe headaches and was found to have transverse sinus thrombosis. He reported having recurrent mouth and genital ulcers for 3 months before the current consultation. On the basis of the clinical picture, Behçet's syndrome was diagnosed. During hospitalization of the patient, polyuria and polydipsia developed, along with hypernatremia and hypotonic urine, indicative of diabetes insipidus. After desmopressin treatment was initiated, considerable improvement in clinical status and laboratory data was evident and persisted during follow-up. CONCLUSION: Behçet's syndrome, probably through vasculitic mechanisms, may result in central diabetes insipidus. This case report emphasizes that Behçet's syndrome should be considered in the differential diagnosis of diabetes insipidus.

Adult↗
PubMed1973

Vasopressin analogue DDAVP in diabetes insipidus: clinical and laboratory studies.

In seven patients with cranial diabetes insipidus an analogue of vasopressin, DDAVP, produced an antidiuresis lasting up to 20 hours after a single intranasal dose. Lysine vasopressin (LVP) in the same dose produced a less potent antidiuresis which lasted for only three to four hours. The plasma half life of DDAVP was 7.8 and 75.5 min for the fast and slow phases, compared with 2.5 and 14.5 min for LVP. Radioiodine-labelled DDAVP was not destroyed by incubation with late pregnancy plasma, which contains an enzyme that inactivates vasopressin. The slow metabolic clearance of DDAVP, its absorption through the nasal mucosa, and its lack of side effects make this the ideal drug for the treatment of vasopressin-sensitive diabetes insipidus. Patients usually require 10 to 20 mug DDAVP given intranasally twice daily for good clinical control of their diabetes insipidus.

Adolescent↗
PubMedDate not supplied

Central diabetes insipidus due to herpes simplex in a patient immunosuppressed by Cushing's syndrome.

OBJECTIVE: To describe a patient immunocompromised by Cushing's syndrome in whom central diabetes insipidus developed as a complication of herpes simplex involvement of the hypothalamus. METHODS: We present a case, including results of laboratory and histopathologic studies, in which herpes simplex was established as the causative agent for central diabetes insipidus. RESULTS: A woman with ectopic corticotropin-dependent Cushing's syndrome, diabetes mellitus, carcinoid tumor, and a history of thyroid cancer had the precipitous onset of seizure and fever, and hypotonic polyuria and progressive hypernatremia developed. Central diabetes insipidus was diagnosed and successfully treated with desmopressin. Nevertheless, the patient's condition deteriorated and she died. Autopsy revealed herpes simplex encephalitis involving the magnicellular neurons of the hypothalamus. CONCLUSION: Central diabetes insipidus caused by viral infections has been reported in immunosuppressed patients, such as those with acquired immunodeficiency syndrome (AIDS). To our knowledge, this is the first report of a herpes infection causing diabetes insipidus in a patient immunosuppressed by Cushing's syndrome. This case demonstrates that, in patients with Cushing's syndrome, diabetes insipidus may develop as a result of herpes simplex infection of the hypothalamus.

Cushing Syndrome↗
PubMed1987

Oral desmopressin in neonatal diabetes insipidus.

A neonate with cranial diabetes insipidus was successfully treated with oral desmopressin. The patient had a midline cleft lip and palate and we obtained a more consistent response using the oral route than using the usual nasal route.

Administration, Oral↗
PubMed1990

Continuous vasopressin replacement in diabetes insipidus.

Five children who developed diabetes insipidus as a manifestation of severe brain injury received continuous intravenous treatment with a solution containing both aqueous vasopressin and appropriate crystalloid replacement. Polyuria, hypernatraemia, and decreased urine osmolalities were safely corrected in all patients within eight to 28 hours.

Adolescent↗
PubMed2005

[Nephrogenic diabetes insipidus induced by colchicine--a case report].

In some cases diabetes insipidus may be induced by taking medications. In this article we report the case of a 58-year-old man with manifest polyuria induced by colchicine administered because of a gout attack. Interestingly, similar symptoms were observed 6 years earlier after treatment with gentamycin. In the described state of the examined patient early detection of the disease, colchicine withdrawal and temporary amiloride (and indometacin) administration led to a full normalisation of the patient's clinical status. A similar reaction to two different drugs responsible for only a small percentage of iatrogenic diabetes insipidus suggests that some patients may exhibit a general "hypersensitivity" to the development of a drug-induced vasopressin resistance and that patients with the history of iatrogenic diabetes insipidus should not be treated or should be treated cautiously with other drugs known to induce vasopressin-resistant polyuria.

Amiloride↗