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At least 469 records · Page 26Linked to original sources
PubMed1979

Sarcoidosis presenting with diabetes insipidus followed by acute cranial nerve syndrome. A case report.

Diabetes insipidus in a previously healthy 16-year-old girl led to surgical exploration of a pituitary stalk intumescence detected by oxygen cisternography with the use of tomography. Biopsy of the pituitary stalk contained chronically inflamed brain tissue. Subsequent liver and bone biopsies showed characteristic granulomata, confirming the diagnosis of sarcoidosis. Subfrontal craniotomy was followed by a rapidly progressive basal meningoencephalitis with multiple cranial nerve involvement. The need to establish a causal diagnosis in diabetes insipidus is stressed. The rarity of the disorder and the presumed role of subfrontal craniotomy with regard to the flare-up of the sarcoidosis of the brain are discussed.

Adolescent↗
PubMed1991

Rhabdomyolysis associated with cranial diabetes insipidus.

Rhabdomyolysis has been reported to be associated with hyperosmolality in diabetic ketoacidosis and non-ketotic hyperosmolal state. Whether the rhabdomyolysis was due to hyperosmolality per se or whether hyperglycaemia also played a role is not clear. We hereby report a case of cranial diabetes insipidus with hypernatraemia and hyperosmolality complicated by rhabdomyolysis. None of the known risk factors, such as coma, hypokalaemia, hypophosphataemia, diabetic ketoacidosis or non-ketotic hyperosmolality, were present in this patient. We believe that severe hyperosmolality per se is an important predisposing factor for non-traumatic rhabdomyolysis, and serum muscle enzymes should be closely monitored in the management of patients with diabetes insipidus.

Adult↗
PubMed1994

Effect of hydrochlorothiazide and indomethacin treatment on renal function in nephrogenic diabetes insipidus.

The purpose of this study was to investigate the effects of treatment with hydrochlorothiazide and hydrochlorothiazide and indomethacin combined on renal function in four boys, two with nephrogenic diabetes insipidus and two with partial nephrogenic diabetes insipidus using the clearances of inulin and para-aminohippuric acid under water diuresis and lithium clearance. Hydrochlorothiazide reduced urine flow and lithium clearance. These effects were further potentiated by addition of indomethacin. No consistent effects on renal plasma flow or glomerular filtration rate were found. It is concluded that treatment with hydrochlorothiazide alone and hydrochlorothiazide and indomethacin combined reduces urine flow in nephrogenic diabetes insipidus by increasing proximal tubular reabsorption of sodium.

Child↗
PubMed1996

[Pleiotropic physiological effects of mutation di, which determines diabetes insipidus in rats].

The main phenotypic expression of mutation di is diabetes insipidus, which is pronounced in didi homozygotes. Additional physiological traits have been revealed that are associated with diabetes insipidus and are accounted for by the pleiotropic effect of gene di on the function of the reproductive system, metabolism of neurotransmitters in brain, and central regulation of the stress response. In didi mutants, the age-related decrease in fertility is retarded, the increase in B monoamine oxidase activity associated with aging is shifted to an older age, and the level of corticosteroid-binding globulin is decreased in young animals.

Aging↗
PubMed2005

Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients.

OBJECT: Diabetes insipidus (DI) is a common complication of transsphenoidal surgery. The purpose of this study was to elucidate patient- and surgery-specific risk factors for DI. METHODS: The perioperative records of 881 patients who had undergone transsphenoidal microsurgery at the authors' institution between January 1995 and June 2001 were reviewed. Among 857 patients without preoperative DI, the overall incidence of immediate postoperative DI was 18.3%, with 12.4% of patients requiring treatment with desmopressin at some point during their hospitalization. Persistent DI requiring long-term treatment with desmopressin was noted in 2% of all patients. An observable intraoperative cerebrospinal fluid (CSF) leak was strongly associated with an increased incidence of both transient (33.3%) and persistent (4.4%) DI. Craniopharyngioma and Rathke cleft cyst (RCC) were also associated with an increased incidence of transient and persistent DI, whereas repeated operation was not. Among patients with pituitary adenomas, those with Cushing's disease had an increased risk of transient (22.2%), but not persistent, DI. Patients with a microadenoma were more likely to suffer transient DI than those harboring a macroadenoma (21.6 compared with 14.3%) but were not more likely to experience persistent DI. CONCLUSIONS: Diabetes insipidus remains a common complication of transsphenoidal surgery; however, it is most frequently transient in nature. Patients with an intraoperative CSF leak, a microadenoma, a craniopharyngioma, or an RCC appear to have an increased risk of transient DI. Risk factors for persistent DI include an intraoperative CSF leak, a craniopharyngioma, or an RCC.

Adenoma↗
PubMed1978

Malignant pituitary chromophobe adenoma in an infant accompanying diabetes insipidus.

This report deals with a 1.5-year-old male infant terminating in viral pneumonia and "diabetes insipidus". The autopsy revealed malignant pituitary chromophobe adenoma, invading the wall of the third ventricle, extending to the periventricular-, dorsomedial- and ventromedial area, skipping to the lateral area adjacent to the optic nerve, and permeating into the subarachnoid space of the cerebrum. At the onset of disease polydypsia and polyuria were marked followed by interstitial pneumonia with high fever, and later generalized tonic convulsion terminated in death. This case is peculiar in at least two respects. Firstly, this is the youngest reported case of malignant chromophobe adenoma. Secondly, the manifestation of diabetes insipidus is rare in chromophobe adenoma. The malignant adenoma probably occurred from the primitive gland rest of chromophobe cells in the posterior lobe becoming malignant during the course of growth development and destroyed the cells of the posterior lobe, resulting in diabetes insipidus.

Adenoma, Chromophobe↗
PubMed1978

Neurogenic diabetes insipidus: management with dDAVP (1-desamino-8-D arginine vasopressin).

We used dDAVP, the 1-desamino-8-D arginine analogue of arginine vasopressin with high antidiuretic and low vasopressor potency, to treat 29 patients with neurogenic diabetes insipidus for up to 22 months. Intranasal dDAVP, 2.5 to 15 microgram twice daily, provided excellent control in most patients. Individual responses were independent of age, weight, and severity of diabetes insipidus. Resistance to dDAVP may be a rare complication of prolonged therapy. Two patients with acute postoperative diabetes insipidus were effectively treated with 5 microgram of dDAVP every 14 to 18 h. Compared to previous therapy, side effects of dDAVP were minimal (headaches in two patients), and control of symptoms and urine volume was as good as with vasopressin tannate in oil or better than chlorpropamide and lysine vasopressin nasal spray. We conclude that intranasal dDAVP, because of efficacy, long duration of action, and infrequent side effects, is the preferred treatment of neurogenic diabetes insipidus in children and adults.

Adolescent↗
PubMed2001

Familial neurohypophysial diabetes insipidus in a large Dutch kindred: effect of the onset of diabetes on growth in children and cell biological defects of the mutant vasopressin prohormone.

Familial neurohypophysial diabetes insipidus (FNDI) is an autosomal dominant trait in which expression of a mutant vasopressin prohormone reduces vasopressin production. We investigated the NP85 Cys-->Gly mutant vasopressin prohormone in a large kindred in The Netherlands. We demonstrate that growth retardation is an important early sign in two children from this kindred, which recuperates by substitution therapy with 1-desamino-8-D-arginine vasopressin. To obtain clues about the basis for the dominant inheritance of FNDI, we analyzed the trafficking and processing of the mutant vasopressin prohormone in cell lines by metabolic labeling and immunoprecipitation. The mutant vasopressin prohormone was retained in the endoplasmic reticulum and thus was not processed to vasopressin. This defect was not caused by dimerization of the vasopressin prohormone via its unpaired cysteine residue. High level expression of the mutant vasopressin prohormone in cell lines resulted in strong accumulation in the endoplasmic reticulum and an altered morphology of this organelle. We hypothesize that disturbance of the endoplasmic reticulum results in dysfunction and ultimately cell death of the cells expressing the mutant prohormone. Our data support the hypothesis that FNDI is a progressive neurodegenerative disease with delayed onset of symptoms. Its treatment requires early detection of symptoms for which growth parameters are useful.

Adult↗
PubMed2000

Acute myeloid leukaemia with trilineage myelodysplasia complicated by masked diabetes insipidus.

We describe a rare case of acute myeloid leukaemia with trilineage myelodysplasia complicated by central diabetes insipidus. In the present case, diabetes insipidus was masked by corticosteroid deficiency due to hypopituitarism and clinical symptoms presented after administering methylprednisolone. Although the remission of leukaemia was not achieved by chemotherapy, excessive urinary output was well-controlled by nasal administration of 1-desamino-8-D-arginine vasopressin (DDAVP) during the course.

Acute Disease↗
PubMed1993

[Anesthetic management for cesarean section of a patient with transient diabetes insipidus and acute severe liver dysfunction].

A 26-year old woman presented with acute hepato-renal dysfunction, coagulation abnormalities and diabetes insipidus associated with hypernatremia in the latter term of pregnancy (39 weeks). Such transient diabetes insipidus during pregnancy as in this case has been reported to be resistant to AVP, but to respond to DDAVP. Because of fetal compromise, an urgent cesarean section was performed. Spinal anesthesia was chosen because of the possible deleterious effects of general anesthesia on liver function. After delivery of twin babies, her symptoms recovered gradually. In conclusion, diabetes insipidus during pregnancy as in this case is transient and disappear after delivery. However, multiple organ dysfunction may become worse and cause fetal death, unless surgical procedure with appropriate anesthetic management is performed.

Acute Disease↗
PubMedDate not supplied

Congenital toxoplasmosis complicated by central diabetes insipidus in an infant with Down syndrome.

We describe an infant with the unusual combination of Down syndrome, congenital toxoplasmosis, and central diabetes insipidus. Hydrocephalus was documented by fetal ultrasonography at 36 weeks' gestation. He developed central diabetes insipidus as a neonate, followed by interstitial pneumonia, anemia, and hepatosplenomegaly. The patient's serum titer for Toxoplasma-specific IgM (ELISA) at 37 days after delivery was negative, but the Toxoplasma SAG1 gene was detected from the cells of the cerebrospinal fluid on the same day using the polymerase chain reaction (PCR) method. Congenital toxoplasmosis can contribute to the development of central diabetes insipidus in infants. PCR was useful in diagnosing congenital toxoplasmosis rapidly and accurately.

Animals↗
PubMed1999

Effect of DDAVP on nocturnal enuresis in a patient with nephrogenic diabetes insipidus.

The case of an 8 year old boy with both nocturnal enuresis and nephrogenic diabetes insipidus is presented. Diagnosis of nephrogenic diabetes insipidus was based on a typical medical history, the characteristic result of a fluid restriction test, the lack of an effect of 1-desamino-8-D-arginine (DDAVP) on both urine osmolality and plasma coagulation factors and, finally, the detection of a hemizygous missense mutation within the arginine vasopressin (AVP) receptor gene. Hydrochlorothiazide treatment and dietary measures reduced the patient's urine volume to one third of its original volume. However, this had no effect on enuresis. The daily intranasal application of DDAVP did not further reduce urine output but dramatically decreased the frequency of bed wetting. This observation contradicts the common notion that the therapeutic effect of DDAVP in nocturnal enuresis is the result of compensation for a nocturnal AVP deficit. Rather, it points to a different mode of action of DDAVP in patients with enuresis. It is hypothesised that central AVP receptors are a target of DDAVP and that they might play an important role in the pathogenesis of nocturnal enuresis.

Child↗
PubMed1997

Emergency treatment of lithium-induced diabetes insipidus with nonsteroidal anti-inflammatory drugs.

Thiazides and amiloride are the most often suggested treatment for nephrogenic diabetic insipidus. We found this ineffectual in a patient with acute problems and reviewed the literature to see if there were other more efficient approaches. A 47-year-old woman on lithium had polyuria. When inadvertently fasted for 48 h she became confused, had a seizure, and her sodium was 170 mmol/L. Urinary output was 24 L/day. Large volumes of intravenous fluids were given but sodium remained > 170 mmol/L. Treatment with DDAVP, thiazides, and amiloride did not decrease urinary output. Indomethacin 150 mg was started and urine volume immediately fell to one-half. However, because of persistent high urine output the patient was then fluid depleted, with further reduction to normal in urine volume, and Na decreased to 140 mmol/L. Creatinine rose from 135 mumol/L to 173 mumol/L, but decreased to 152 mumol/L when indomethacin was decreased to 75 mg q.d.; urinary output remained stable around 2 L/day. The literature described 22 patients with nephrogenic diabetes insipidus (16 congenital, 6 lithium) treated with nonsteroidal anti-inflammatory drugs. Urine flow was reduced to 1/3, within hours. Rarely, mild renal failure ensued, improving in all but one case when nonsteroidal anti-inflammatory drugs were reduced. Indomethacin (and controlled volume reduction if continued high urine output), while observing renal function, appears the emergency treatment of choice for serious complications of nephrogenic diabetes insipidus.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

[Diabetes insipidus in chronic myeloid leukemia. Remission of hypophyseal infiltration during busulfan treatment].

In a 53-year-old male who presented with diabetes insipidus as the first symptom of chronic myelocytic leukemia, computed tomography of the sella showed infiltration of the posterior pituitary gland. Busulfan treatment was given for one month and the infiltration had disappeared ten weeks after initiation of therapy. At the same time the severity of the diabetes insipidus diminished for a period of three months. Diabetes insipidus is a rare complication of chronic myelocytic leukemia: only 8 similar cases have been reported in the last 75 years.

Busulfan↗