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PubMedDate not supplied

Occurrence of diabetes mellitus in neurogenic diabetes insipidus.

The occurrence of a family history of diabetes mellitus, of overt diabetes mellitus and of impaired glucose tolerance was investigated in a group of 43 patients with neurogenic diabetes insipidus. Family history was positive in 16.2% of these, similar to that in control subjects; manifest diabetes mellitus was present in 9.3%, impaired glucose tolerance in 20%. This prevalence appears to be even more significant, considering the patients' mean age, 26.9 +/- 2.3 years.

Diabetes Complications↗
PubMedDate not supplied

[Long-term course of 6 boys with congenital nephrogenic diabetes insipidus].

From 1975-1986 6 boys with congenital nephrogenic diabetes insipidus were diagnosed at the age of 3 months to 10 years. Symptoms appeared within the first few weeks of life. The diagnosis was confirmed by polyuria, low urinary osmolality (97-225 mosm/kg H20), hypernatraemia (max. 171 mmol/l) and the missing response to vasopressin. The treatment was variable; 4 boys received only hydrochlorothiazide (2-2.5 mg/kg/d) which lead to a reduction of the daily urinary volume of 26-44%. Hyperelectrolytaemia disappeared and a normal thriving could be achieved. Later an additional treatment with indomethacin (2 mg/kg/d) was necessary in 3 boys because of an increase of polyuria; there was a further reduction of the daily urinary volume of 50-60%. The combination of hydrochlorothiazide and indomethacin in the treatment of the congenital nephrogenic diabetes insipidus was well tolerated and seems to be--especially during the first few years of life--a necessary and effective treatment which allows a normal thriving and psychointellectual development.

Adolescent↗
PubMedDate not supplied

[Growth in children with diabetes insipidus].

Commercial preparations of vasopressin for the treatment of diabetes insipidus are not available in Mexico. Besides, the hormone is useless in the nephrogenic variety. In the department of Endocrinology at the Hospital Infantil de Mexico, a preparation containing hydrochlorothiazide, aminopyrine and potassium chloride, which reduces urinary volumes in about two thirds, is employed in all varieties of the disease. Growth in stature was investigated in 44 patients under treatment, attending the Endocrine Outpatient Clinic since 1967 for a period of 2 to 12 years. Clinical material included 29 males and 15 females. There were 23 idiopathic, 7 histiocytosis, 5 nephrogenic, 4 craniopharyngiomas, 2 psychogenic polydipsia, 2 traumatic and 1, as a sequel of tuberculous meningoencephalitis. Six idiopathic, 2 nephrogenic, 2 traumatic, 1 histiocytosis, and 1 psychogenic proceeded between percentiles 3 and 97, parallel to the nearest line of reference along the whole period of study. Two nephrogenic, 2 histiocytosis, 1 psychogenic, 1 post-meningoencephalitis and 14 idiopathic, grew below the third percentile, but parallel to it. One nephrogenic, 4 histiocytosis, 4 craniopharyngioma and 3 idiopathic progressively departed from the initial centile. Two of the latter had growth hormone deficiency, and 1 had been very irregularly treated. It is concluded that the therapy employed limits stature impairment but does not produce catch-up growth. Accordingly, it is proposed that the treatment of diabetes insipidus should be started as early as possible, and that if progress in stature is appreciably deteriorated, the presence of additional pathology should be suspected.

Age Determination by Skeleton↗
PubMed1979

The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus.

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.

Body Water↗
PubMed1985

Familial cranial diabetes insipidus: a report of five families. Genetic, diagnostic and therapeutic aspects.

Five families were studied in which cranial diabetes insipidus occurred. In the pedigrees presented, the disease clearly followed an autosomal dominant mode of inheritance. Linkage analysis was performed in one large family by calculating lod scores for linkage between loci for cranial diabetes insipidus and 18 polymorphic markers and chromosome heteromorphisms. No significant genetic linkage was found and only one of the polymorphic markers gave a positive hint of linkage. A water deprivation test was performed in nine patients from three of the families and in healthy control subjects. The plasma concentration of arginine vasopressin was very low or undetectable in the patients, and unlike the control subjects did not increase significantly during water deprivation. Arginine vasopressin and serum osmolality (Sosm) were significantly positively correlated in the controls, but not in the patients. The results indicated that an arginine vasopressin-level lower than 2 pg/ml strongly suggests a diagnosis of cranial diabetes insipidus if at the same time Sosm is higher than 295 mosmol/kg. Studies with different intranasal dosages of 1-deamino-D-arginine-vasopressin (DDAVP) given once or twice a day showed that 20 micrograms effectively reduced urinary output and that administration once a day could be sufficient.

Adolescent↗
PubMed1981

Vasopressin secretion in primary polydipsia and cranial diabetes insipidus.

Vasopressin secretion was studied in a group of 18 patients with polydipsia (urine volume greater than 21/24 h) in whom nephrogenic diabetes insipidus had been excluded. Osmoregulation of vasopressin release was defined by hypertonic saline infusion, and three independent non-osmotic tests of vasopressin release were also applied. A wide spectrum of abnormalities in vasopressin secretion was observed. Four patients seem to have primary polydipsia, since they showed a normal response to osmotic stimulation, but non-osmotic vasopressin release was subnormal in two. The remaining 14 patients had cranial diabetes insipidus, as judged by subnormal or absent vasoprsssin responses to hypertonic saline infusion. Of these 14, five had undetectable vasopressin during osmotic stimulation, but each mounted a response to the non-osmotic stimuli; three of these had familial polyuria. Three further patients appeared to have isolated osmoreceptor defects, showing normal responses to non-osmotic stimuli but none to osmotic stress. Four patients with partial cranial diabetes insipidus, as judged by subnormal vasopressin response to osmotic stimuli, seemed to have normal osmoreceptor function but deficient vasopressin release. There was no correlation between the degree of vasopressin response to osmotic stimuli and the three non-osmotic tests of vasopressin release, and in particular vasopressin release should not replace osmotic tests to define cranial diabetes insipidus.

Adult↗
PubMed1989

[Diabetes insipidus as the first cause of myelodysplastic syndrome].

The concurrent occurrence of myelodysplastic syndrome and diabetes insipidus is very rare. In the available literature so far only three cases were described. In acute leukaemia the concurrence of the two diseases is rare. The authors describe two cases of concurrent diabetes insipidus and myelodysplastic syndrome with typical clinical and laboratory symptoms. A 27-year-old man with refractory anaemia (according to the FAB classification of myelodysplastic syndrome) died after 10 months from complications of acute leukaemia. In a 58-year-old female patients with refractory anaemia after two years remission the condition deteriorated and developed into RASEB (refractory anaemia with excess of blast cells) according to the FAB classification with partial remission of the disease after cytostatic treatment. During permanent substitution treatment (Adiuretin Spofa) diabetes insipidus was compensated in both diseases.

Adult↗
PubMed1988

Familial cerebellar ataxia and diabetes insipidus.

Two sisters are reported who both developed partial cranial diabetes insipidus in their 4th decade, followed by progressive cerebellar ataxia. This appears to be the first report of cerebellar ataxia and diabetes insipidus occurring together as a genetic entity.

Aged↗
PubMed2000

Central diabetes insipidus as the first manifestation of neurosarcoidosis in a 10-year-old girl.

Central diabetes insipidus with thickening of the pituitary stalk has been demonstrated in adults with Langerhans cell histiocytosis (LCH), tuberculosis or sarcoidosis, and in children with LCH. We present a 10.5-year-old girl with central diabetes insipidus. Magnetic resonance imaging (MRI) revealed thickening of the central part of the pituitary stalk and multiple hyperintense lesions in the frontal white matter on T(2)-weighted images. Laboratory findings were normal except for an elevated serum angiotensin-converting enzyme (ACE) level. The MRI findings together with the elevated serum ACE level highly suggest the diagnosis of sarcoidosis. We conclude that central diabetes insipidus can be the first clinical manifestation of sarcoidosis in children.

Brain↗
PubMed1980

[ADH-deficient diabetes insipidus in children. A study of 93 cases (author's transl)].

Ninety three cases of diabetes insipidus are reviewed after 1 to 20 years follow-up. A codified water deprivation test realized in 50 cases revealed 31 severe cases and 19 partial forms. Apart from surgical causes of diabetes insipidus (16%), tumors represent the most frequent etiology (33.5%), essentially craniopharyngiomas and pinealomas. Histiocytosis X (16%) is also an important cause. In one third no cause could be found. Decreased secretion of anterior pituitary hormones is very common in association with surgical and tumoral causes and can also be found in idiopathic forms. Thus, in our experience, detection of a pituitary deficit is not necessarily associated with a tumor. It can be pointed out that when an etiology is found it is always discovered during the four years following the onset of diabetes insipidus. This implies that very careful neurological and neuroradiological follow-up is necessary during this period.

Adolescent↗
PubMed2002

Diabetes insipidus as a complication of cryptococcal meningitis in an HIV-infected patient.

We describe an HIV-infected patient with central diabetes insipidus as a complication of cryptococcal meningitis. Nephrogenic diabetes insipidus as a result of amphotericin B treatment is a rare but known complication. Central diabetes insipidus in cryptococcal meningitis has not been reported before. The patient responded well to desmopressin treatment.

AIDS-Related Opportunistic Infections↗
PubMed1975

Treatment of diabetes insipidus with 1-deamino-8-d-arginine vasopressin.

The effect on water metabolism of 1-deamino-8-D-arginine vasopressin and lysine vasopressin have been studied and compared in 20 vasopressin-sensitive and 2 ADH-resistant diabetes insipidus patients. In every case of ADH-sensitive diabetes insipidus, diuresis decreased and the urinary osmolality increased more markedly and for a longer time with the former than with the latter drug. Both drugs were ineffective in patients with ADH-resistant diabetes insipidus. Administration of 1-deamino-8-D-arginine vasopressin did not cause any side effect. It is concluded that 1-deamino-8-D-arginine vasopressin can successfully be employed in the treatment of ADH-sensitive diabetes insipidus.

Administration, Intranasal↗
PubMed1987

Diabetes insipidus and pregnancy.

A case of a pregnant woman with diabetes insipidus is reported. The course of the pregnancy was uneventful except for a slightly increased need for vasopressin during the last trimester. Neurophysin levels increased at a rate similar to that seen in the normal pregnant state. The combination of normal neurophysin physiology and undisturbed spontaneous labor demonstrating normal oxytocin secretion suggests that there is a singular deficiency of antidiuretic hormone in essential diabetes insipidus.

Adult↗