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At least 289 records · Page 16Linked to original sources
PubMed1975

Diabetes insipidus secondary to penetrating thoracic trauma.

Three cases of diabetes insipidus following non-cranial trauma are presented. They are believed to be the first of their kind reported. The etiology, pathogenesis and differential diagnosis of diabetes insipidus are discussed. The literature if briefly reviewed and similarities between patients with DI due to long bone trauma with fat embolism, post open heart surgery hypotension, Sheehan's syndrome following postpartum hemorrhage, DI and our own patients are discussed. It is concluded that the diabetes insipidus is caused by selective disruption of posterior pituitary circulation due to fat globules, thrombi and hypovolemia resulting in hypoxia and tissue necrosis.

Adolescent↗
PubMed1989

[Etiopathogenetic aspects of central diabetes insipidus. Report of a clinical case].

The manifold etiopathogenetic conditions responsible for central diabetes insipidus are minutely examined. On the ground of these introductory remarks, the Authors report a case of diabetes insipidus following from pituitary metastasis in a patient with cancer of the lung. Some relations between diabetes insipidus and cancer are discussed. The uncommon remark of a metastatic lesion in the etiopathogenesis of the central diabetes insipidus and its early display in the patient at issue support this description.

Carcinoma↗
PubMed1980

The association of diabetes insipidus with hypoparathyroidism. Addison's disease and mucocutaneous candidiasis.

A case of central diabetes insipidus is reported in association with idiopathic hypoparathyroidism, adrenal failure and mucocutaneous candidiasis. The diabetes insipidus was recognised at the same time as the discovery of aldosterone and cortisol deficiency, and occurred several years after the initial onset of mucocutaneous candidiasis and hypocalcaemia. Control of the diabetes insipidus was achieved initially with nasal aqueous lysine vasopressin and later with desmopressin. The development of diabetes insipidus may be a further aspect of endocrine secretory failure associated with idiopathic hypoparathyroidism.

Addison Disease↗
PubMed1985

Ultrastructural markers of tubular transport in experimental diabetes insipidus.

Stereological analysis of changes in tubular transport markers in diabetes insipidus has been undertaken. Intracellular spaces and basal infolded channels were considered as the markers of water transport, while mitochondrial metabolic steady states were considered as the active transport markers. Transmission electron microscopic observations revealed morphometric differences in the surface area and volume of intercellular space and basal infolded channels in the distal tubules. Stereological markers of mitochondrial metabolic states demonstrated significant differences in the distal tubules between diabetes insipidus and control groups. In diabetes insipidus the volume and surface area of intercellular spaces and basal infolded channels in the distal tubules were decreased and the mitochondrial energy state was lowered.

Animals↗
PubMed1989

Recurrent diabetes insipidus associated with pregnancy: pathophysiology and therapy.

Diabetes insipidus during pregnancy is an uncommon medical problem. We present a woman who developed transient central diabetes insipidus during two successive pregnancies. A water deprivation study with plasma arginine vasopressin concentrations confirmed the diagnosis and established the efficacy of 1-desamino-8-d-arginine-vasopressin (dDAVP). The patient was then successfully and safely treated through the second pregnancy with dDAVP.

Adult↗
PubMed1984

Diabetes insipidus: occurrence after minor head trauma.

Post-traumatic diabetes insipidus is a rare entity, usually associated with severe head trauma, often with skull fracture and cranial nerve dysfunction. A 24-year-old male presented to a medical clinic 2 weeks after a minor head injury with presenting symptoms of polyuria with nocturia and intense polydipsia. A diagnosis of post-traumatic diabetes insipidus was made. Although other causes of polyuria syndromes must be ruled out, plotting urine versus plasma osmolalities can provide rapid preliminary diagnostic help when considering diabetes insipidus. First-line treatment should include a trial of chlorpropamide and hydrochlorothiazide. Caution should be exercised in not overlooking associated anterior pituitary damage, which may develop several years post-trauma.

Adult↗
PubMed1987

Thirst in diabetes insipidus: clinical relevance of quantitative assessment.

Patients with cranial diabetes insipidus are unable to concentrate urine, and depend on thirst and water intake to prevent hypertonic dehydration. Using a visual analogue scale (0-10 cm) we studied osmotically stimulated thirst induced by hypertonic saline infusion in 15 patients with diabetes insipidus and 15 healthy controls. Plasma osmolality in the patients rose from 292 +/- 1 to 316 +/- 1 mOsm/kg (p less than 0.001), and 13 patients showed a progressive rise in thirst ratings (1.4 +/- 0.4 to 8.1 +/- 0.3 cm, p less than 0.001) with abolition of thirst by drinking, in a similar fashion to controls. Water intake following infusion was greater in patients than controls (p less than 0.001). Linear regression analysis of thirst and plasma osmolality showed no difference in the osmotic threshold for thirst onset, or the sensitivity of thirst osmoreceptors, between 13 of the patients and the control group. One patient was shown to be hypodipsic and compulsive water drinking was demonstrated in another: abnormal thirst perception caused abnormalities of salt and water balance in these two patients. Most patients with cranial diabetes insipidus have normal thirst mechanisms, though clinically significant hypodipsia or hyperdipsia may co-exist with vasopressin deficiency.

Adult↗
PubMed2005

Diabetes insipidus in the third trimester of pregnancy.

BACKGROUND: Transient diabetes insipidus may rarely present during late pregnancy and/or the immediate puerperium, and if unrecognized, may cause neurologic injury and threaten the lives of mother and fetus. However, when recognized early and treatment is initiated with desmopressin acetate, an analog of vasopressin that is resistant to vasopressinase, water loss in the urine is eliminated and complications may be abrogated. This report aims to increase the awareness of this disorder and describes appropriate treatment. CASES: Two cases of diabetes insipidus, believed to be due to excess vasopressinase, are presented to demonstrate the clinical features, pathogenesis, and treatment of this syndrome. CONCLUSION: Awareness of the syndrome of transient diabetes insipidus may lead to early diagnosis and appropriate treatment that will reduce the risks of maternal and fetal morbidity.

Adult↗
PubMed1994

Etiologies of central diabetes insipidus in children.

The last major review of the etiologies of central diabetes insipidus in children was performed a quarter century ago, prior to the development of modern neuroimaging techniques. We retrospectively reviewed the records of children with central diabetes insipidus identified at Children's Hospital of Buffalo from 1979 to 1992. Of the 35 patients identified, 27 were males and 8 were females. Their ages ranged from 3 weeks to 20 years. Nineteen children had brain tumors, 7 had cerebral malformations, 3 had central nervous system infections, 1 had traumatic brain injury, and 5 were considered idiopathic. Patients with brain death were excluded from the review. Thirty-one of 35 patients developed diabetes insipidus in conjunction with other endocrinopathies. Brain tumor and its treatment account for the most common cause. Cranial magnetic resonance imaging has improved the identification of structural lesions and the understanding of the pathophysiology of central diabetes insipidus.

Adolescent↗
PubMed1978

Inhibition of the renin-angiotensin-system in Brattleboro rats with hereditary hypothalamic diabetes insipidus.

Brattleboro rats homozygous for hypothalamic hereditary diabetes insipidus (DI rats) were used to investigate the following questions: a) Do exogenous and endogenous angiotensin II (AII) have an antidiuretic effect in diabetes insipidus? b) Does AII mediate the antidiuresis induced by furosemide? The following results were obtained: 1. AII (5 mg/kg s.c. in oil) and furosemide (50 mg/kg i.p.) decreased urine flow and increased urinary sodium excretion. Furosemide led to a two-fold increase of AII plasma concentrations and a decrease of plasma sodium levels. 2. SQ 14 225 (2 x 2.5 mg/kg p.o.), an angiotensin I-converting enzyme inhibitor, led to an increase of urine flow and to a slightly elevated urinary sodium excretion. 3. When the formation of AII was blocked by SQ 14 225 (2 x 2.5 mg/kg p.o.), AII plasma concentrations were 2.5-fold decreased, but furosemide still reduced urine flow. We conclude that plasma AII might have an antidiuretic action in DI rats. However, AII does not mediate the antidiuresis induced by furosemide.

Angiotensin II↗
PubMed1993

Control of sodium excretion in patients with cranial diabetes insipidus maintained on desamino-[8-D-arginine]vasopressin.

1. We have studied the response of six patients with cranial diabetes insipidus and six age-matched control subjects to dietary sodium restriction during constant administration of the synthetic vasopressin analogue desamino-[8-D-arginine]vasopressin. 2. Urine flow increased on the first low salt day in the normal control subjects but not in the patients with cranial diabetes insipidus. Body weight fell 1.35 kg in the control subjects but was constant in the patients with cranial diabetes insipidus. 3. Urinary sodium excretion fell at the same rate in both groups. Diurnal variation of urinary sodium excretion and creatinine clearance was present in the control subjects but not in the patients with cranial diabetes insipidus. 4. Changes in plasma sodium concentration and osmolality were similar. Plasma protein concentration increased more in the control subjects (from 69.1 +/- 1.5 to 73 +/- 1.2 versus from 71.7 +/- 1 to 73.2 +/- 1.1 milligrams). The responses of plasma atrial natriuretic peptide, plasma renin activity and salivary aldosterone concentration were similar between the two groups. Salivary aldosterone concentration levels were consistently higher in the patients with cranial diabetes insipidus. 5. We confirm that the low salt diuresis is triggered by release from the antidiuretic activity of arginine vasopressin. In the patients with cranial diabetes insipidus extracellular fluid osmoregulation appeared to be achieved by the movement of water out of and sodium into the extracellular fluid. 6. Absent posterior pituitary function and hypothalamic disturbances did not alter renal sodium conservation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Central diabetes insipidus. 22 years' experience.

The etiology of diabetes insipidus (DI) was determined in 73 children evaluated from 1962 through 1983. Intracranial tumors produced DI in 34 children, but 27 of these 34 children developed DI only after excision of the tumor. Diabetes insipidus occurred in ten children with intracranial birth defects, eight with severe central nervous system infections, and six with histiocytosis. Six had other causes. No etiology was detected in nine. Division of the cases into two time periods (1962 through 1972 and 1973 through 1983) revealed a decrease in the frequency of idiopathic DI (26.7% to 8.6%), an increase in the frequency of intracranial birth defects (0% to 17.3%), and an increase in the frequency of severe central nervous system infections (0% to 13.8%). Significant changes in therapy for DI have occurred during these 22 years. Use of desmopressin acetate has facilitated treatment of this complex management problem.

Brain Neoplasms↗
PubMed1977

DDAVP in the treatment of diabetes insipidus: a clinical study.

In three cases of established cranial diabetes insipidus, the effectiveness of the new vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) in controlling diabetes insipidus is demonstrated. A single dose of 20 micrograms of DDAVP given intranasally had an antidiuretic action from 16 to 24 hours in the three cases, and 10 micrograms given twice daily intranasally was effective in controlling the diabetes insipidus with no side effects. All the patients preferred this form of therapy to their previous treatment.

Adult↗
PubMedDate not supplied

Embolization of the meningohypophyseal trunk as a cause of diabetes insipidus.

We present an unusual case of diabetes insipidus occurring after selective embolization of 50% dextrose and pure ethanol into an enlarged left meningohypophyseal trunk (MHT) supplying a dural carotid cavernous fistula. The inferior hypophyseal artery was not opacified during the selective preembolization MHT injection; however, diabetes insipidus developed abruptly a few hours after the procedure. The patient required intranasal 1-deamino-(8-D-arginine)-vasopressin for approximately 3 months, after which his symptoms resolved. The hazards of using liquid embolic agents, especially ethanol, in the cavernous branches of the internal carotid artery should always be borne in mind.

Angiography, Digital Subtraction↗
PubMed1995

Diabetes insipidus as an early sign of pineal tumor.

A 13-year-old boy's acute onset of diabetes insipidus was the first manifestation of a pineal tumor. One year after the physical symptoms of diabetes insipidus occurred, neurological examinations, tumor markers, and computed tomography brain scan were all normal. Three years later, rapid development of neurological changes was observed with the prevailing symptoms of increased intracranial pressure. The changes were related to a pineal germ cell tumor identified by a high level of beta-human chorionic gonadotropin in plasma and neuroradiological investigations, including computed tomography and magnetic resonance imaging. The clinical course of this case is unusual and we advocate the following: (1) the follow-up of children with diabetes insipidus is important for determining whether or not it is an idiopathic type and (2) elevation of plasma beta-human chorionic gonadotropin and development of neurological signs in patients with so-called idiopathic diabetes insipidus should arouse clinical suspicion of an intracranial germ cell tumor. It should be noted that the brain tumor is significant as the underlying pathology of childhood diabetes insipidus.

Administration, Intranasal↗