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At least 595 records · Page 33Linked to original sources
PubMed1990

Antidiuretic effect of indapamide in central diabetes insipidus.

Indapamide produced a significant decrease in urinary output in three patients with central diabetes insipidus. The 24-h urinary volume was reduced from 5 to 2.3 l in a 39-year-old woman; from 11 to 4.3 l in a 30-year-old man, and from 16 to 9.2 l in a 40-year-old man receiving 2.5 mg of indapamide per day. To our knowledge, the antidiuretic effect of indapamide in central diabetes insipidus has not been reported previously.

Adult↗
PubMed1980

[Transient diabetes insipidus following removal of a medullary thyroid carcinoma (author's transl)].

Medullary thyroid carcinoma (MTC) is a known apudoma producing calcitonin, prostaglandins and serotonin. It can present itself as a familial or sporadic form or as part of a multiple endocrine adenomatosis. We present here the case of a patient admitted with a four-year history of diarrhea, enlargement of the thyroid and palpable lymph nodes in the right side of the neck. There was no uptake of 131I in the right lobe of the thyroid and the serum calcitonin levels were very high. With the diagnosis of MTC a total thyroidectomy mas performed developping within hours of the surgical procedure a picture of diabetes insipidus with 31 liters of urine output in the first 48 hours. It responded to vasopressin and disappeared spontaneously in two weeks. We have considered the different mechanisms that could explain the development of diabetes insipidus, and after failing to find one, we especulate at prostaglandins could play an important role in the synthesis and/or release of ADH. The sudden depletion of prostaglandins after removal of the neoplasm that produced them could account for the diabetes insipidus in our patient. We have not found any similar case described in the literature. We call attention to the need for a close postoperative observation of patients operated for MTC for the possible onset of diabetes insipidus.

Adult↗
PubMed1996

[Magnetic resonance in familial central diabetes insipidus: a family study].

OBJECTIVE: To evaluate through MR the presence or absence of the normal hyper-intense signal of the posterior pituitary lobe in four patients diagnosed of familial central diabetes insipidus. PATIENTS AND METHODS: The posterior pituitary lobe was studied by magnetic resonance imaging in four patients, three children and one adult, diagnosed of familiar central diabetes insipidus. RESULTS: In none of the four patients could the normal posterior bright signal be detected. CONCLUSION: The normal hyper-intense MR image of the neurohypophysis is suggested to reflect its function and its absence is frequent in patients diagnosed of familial central diabetes insipidus.

Adult↗
PubMed1995

[Simultaneous familial occurrence of distal renal tubular acidosis, polycystic kidney and nephrogenic diabetes insipidus].

In five members of three generations in a family studied in 1972, 3 nephrological disorders occurred concurrently: distal renal tubular acidosis (dRTA), polycystic kidney and nephrogenic diabetes insipidus (with the exception of a five-year-old child in whom polycystic kidney was not detectable--yet?). Chromosoma studies revealed an increased rate of the occurrence of variations. The youngest patient was reinvestigated in 1993; the other four affected members of the family were already not alive. 7 offsprings in two generations of the 3 healthy members of the third "patient generation" were healthy. The autosomal dominant way of inheritance characteristic to both dRTA and polycystic kidney disease was obvious in this family. On the other hand the same degree of the concentrating defect found both in the patients of the familial dRTA and in 11 control patients with non familial (acquired) dRTA suggested that the nephrogenic diabetes insipidus as an acquired disorder was associated with the two congenital abnormalities. The clinical picture of the combined disease was dominated by the symptoms of polydipsia and polyuria. The vasopressin resistance with a variation in the degree interindividually seemed to be responsible for the nephrogenic diabetes insipidus. Functional insufficiency of the loop of Henle was excluded on the basis of normal responses to a "loop diuretic".

Acidosis, Renal Tubular↗
PubMed1994

Enhanced adrenocorticotrophic hormone and cortisol responses to corticotrophin-releasing hormone in central idiopathic diabetes insipidus.

It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. Moreover, there is consistent evidence that the hypothalamic AVP-secreting neurons are involved in the neuroregulation of ACTH secretion. With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 micrograms iv as a bolus) in 18 normal subjects (15 females and three males, age 22-35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16-40 years). Two patients were newly diagnosed and five had discontinued substitution therapy with desamino-D-AVP 24 h before testing. All had free access to water before and during the test period. The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean +/- SEM: 17.0 +/- 1.2 vs 7.7 +/- 0.7 pmol/l, p = 0.0003; cortisol: 611.3 +/- 59.4 vs 450.7 +/- 21.2 nmol/l, p = 0.01) or area under curve values (ACTH: 672.5 +/- 75.7 vs 364.0 +/- 33.6 pmol.l-1 x h-1, p = 0.002; cortisol: 29158.0 +/- 2937.0 vs 23236.7 +/- 1052.1 nmol.l-1 x h-1, p = 0.03). These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. This may be due to the fact that in diabetes insipidus AVP secretion from parvocellular neurons of the paraventricular nucleus in the hypophysial portal system is not impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Nephrogenic diabetes insipidus persisting 57 months after cessation of lithium carbonate therapy: report of a case and review of the literature.

OBJECTIVE: To illuminate the natural history of prolonged nephrogenic diabetes insipidus after discontinuation of lithium carbonate treatment and to assess the response to therapy with desmopressin acetate and triamterene-hydrochlorothiazide. METHODS: We analyzed sequential determinations of serum and urine osmolality, plasma arginine vasopressin, serum sodium, blood urea nitrogen, calcium, ionized calcium, parathyroid hormone, and 24-hour urine volume during a period of 57 months in a 67-year-old woman. RESULTS: Our patient experienced persistent polyuria in conjunction with having repeated serum osmolalities between 300 and 323 mOsm/kg and urine osmolalities between 130 and 208 mOsm/kg. Concomitant plasma arginine vasopressin levels were as high as 12.0 pg/mL, consistent with the diagnosis of nephrogenic diabetes insipidus. Administration of triamterene-hydrochlorothiazide reduced 24-hour urine volume and serum osmolality while increasing urine osmolality. Desmopressin acetate exhibited no effect. CONCLUSION: In this report, we describe the eighth documented case of persistent nephrogenic diabetes insipidus, lasting 57 months after cessation of lithium therapy, and demonstrate a palliative effect of triamterene-hydrochlorothiazide.

Aged↗
PubMed1998

Central diabetes insipidus and Cushing's syndrome due to ectopic ACTH production by disseminated small cell lung cancer: a case report.

The present case report describes the rare clinical presentation of diabetes insipidus in a patient with an ectopic ACTH syndrome (morning plasma cortisol 1.10 mumol/l, morning plasma ACTH 322 ng/l) due to disseminated small cell lung cancer including a metastasis in the posterior pituitary. The patient was treated by combination chemotherapy and at the same time received octreotide to control hypercortisolism and desmopressin (DDAVP) to control polyuria. Partial tumour remission was achieved resulting in decreased cortisol production and disappearance of the diabetes insipidus. Medical treatment could be discontinued. Several months later tumour regrowth occurred, with recurrence of hypercortisolism (mean morning plasma cortisol 0.74 mumol/l, mean morning plasma ACTH 112 ng/l) but without diabetes insipidus. Early treatment of hypercortisolism in patients with an ectopic ACTH syndrome and disseminated small cell lung cancer may prolong survival and improve the quality of life.

ACTH Syndrome, Ectopic↗
PubMed2005

Modern approach in treatment of diabetes insipidus.

In this paper we have reviewed the position of desmopressin in the treatment of diabetes insipidus. Desmopressin is a synthetic analog of vasopressin, with more pronounced antidiuretic effect. It is treatment of choice in substitution therapy of diabetes insipidus. Its application before sleeping time can reduce nocturnal enuresis, so it has a place in the treatment of enuresis nocturna. Antidiuretic effect of desmopressin is the result of agonistic effect on V2 receptors in the renal tubules. The efficacy and safety of desmopressin in mentioned indications was confirmed in clinical studies.

Deamino Arginine Vasopressin↗
PubMed1988

Ultrastructural markers of tubular transport within the rat nephron in experimental diabetes insipidus.

Using stereological methods mitochondrial energy states and intercellular spaces with basal infolded channels were evaluated in proximal and distal tubules in rats. The studies were performed on animals with experimental diabetes insipidus and on control rats by means of electron microscopy. No significant differences were found in mitochondrial energy states and sizes of intercellular spaces with basal infolded channels in the proximal tubules, which indicates undisturbed transport in this nephron segment. However, significant differences of these parameters were found in the distal tubules. In diabetes insipidus mitochondrial energy states approximated the condensed state, while in the control animals they were similar to the orthodox state. Intercellular spaces became significantly narrowed in diabetes insipidus in comparison with these in the controls. These observations suggest that mitochondrial energy states may be considered as ultrastructural markers of active tubular transport, while intercellular spaces with basal infolded channels may reflect ultrastructural counterparts of water transport.

Animals↗
PubMed1982

1-deamino-/4-valine-8-D-arginine/-vasopressin (dVDAVP), a new synthetic vasopressin analog for treating diabetes insipidus.

The effects of LVP, dDAVP, and dVDAVP on the water excretion of 14 vasopressin-sensitive and 2 ADH-resistant patients with diabetes insipidus were studied and compared. Findings showed that dDAVP and dVDAVP decreased the diuresis of all ADH-sensitive patients, and in those with diabetes insipidus, more markedly (7.6-fold) and for a longer duration (3.3-fold) than did LVP. From a comparison of the results, dVDAVP is at present one of the most effective preparations for reduction of polyuria in patients with ADH-sensitive diabetes insipidus.

Adult↗
PubMed1990

Causes of the urinary concentrating defect in mice with nephrogenic diabetes insipidus.

In a strain of mice called DI +/+ Severe, nephrogenic (or vasopressin-resistant) diabetes insipidus is caused by an inability of the antidiuretic hormone (ADH, or vasopressin) to increase the water permeability of the renal collecting system. That inability, in turn, arises from abnormally high activity of the enzyme cAMP-phosphodiesterase, specifically of the isozyme type III (PDE-III), which hydrolyzes cAMP and prevents the intracellular buildup of this second messenger. Two rather specific inhibitors of PDE-III, rolipram and cilostamide, used either in vitro or in vivo, reverse the deficiencies in DI +/+ Severe mice by increasing intracellular cAMP and water permeability toward or to their normal values. These results have implications for the treatment of nephrogenic diabetes insipidus in human patients.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Permanent diabetes insipidus following head trauma: observations on ten patients and an approach to diagnosis.

Permanent diabetes insipidus following head trauma is uncommon, but potentially fatal. The neurologic, roentgenographic, and endocrinologic findings in ten patients with this condition are reported. Eight of the patients were males under the age of 35 years. Unconsciousness (nine) and skull fracture (seven) were frequent findings. Cranial nerve damage (four) and anterior pituitary hormone deficiency requiring replacement (one) were less frequent. An automobile accident caused the trauma in six patients. Standard water deprivation tests revealed that five of the patients had total deficiency of antidiuretic hormone (ADH), and the other five had partial deficiency. The diagnosis of diabetes insipidus was markedly simplified by using a new screening test based on comparing urine and plasma osmolality in candidates with those of normal subjects.

Adult↗
PubMed1978

[The treatment of patients with diabetes insipidus by a synthetic analogue of vasopressin, DDAVP (author's transl)].

The effects of a synthetic analogue of vasopressin, DDAVP (1-deamino-8-D-arginine vasopressin) were investigated in 98 patients with cranial diabetes insipidus. In all patients, intranasal administration of DDAVP one to three times daily, usually twice daily, was found to be satisfactory in the control of diabetes insipidus. Thus, by DDAVP administration, daily urinary volume changed from 3520 +/- 2150 ml to 1620 +/- 830 ml (mean +/- SD), and urinary osmolarity changed from 126 +/- 75 mOsm/kgH2O to 446 +/- 194 mOsm/kgH2O (mean +/- SD). A daily dose of DDAVP ranged from 2.0 to 20 microgram in children (average dose 12.8 microgram), while 10 to 20 microgram of DDAVP was usually required in adult patients (average dose 14.2 microgram). No serious side effects have been observed. It is concluded that DDAVP is safe and effective in the treatment of cranial diabetes insipidus.

Administration, Intranasal↗
PubMed1994

[Morphological abnormalities of the pituitary stalk of unknown cause in 4 cases of diabetes insipidus in children].

BACKGROUND: Magnetic resonance imaging (MRI) is the best technique for studying hypothalamic and hypophyseal structures. CASE REPORTS: Four children aged 2 years 5 months to 8 years with idiopathic diabetes insipidus were studied. Their condition had been identified for 2-6 years. All the patients had undergone complete clinical, neurological and endocrinological investigations during the search for the cause of their diabetes insipidus. A CT scan was performed in one patient and MRI in all four; the investigations were repeated each 6 months for 4 years. RESULTS: The first examination showed complete lack of antidiuretic hormone (four patients) and growth hormone deficiency (two patients). An enlarged pituitary stalk was seen in three patients, one patient had a small anterior pituitary, and three patients gave no posterior pituitary hypersignal. Follow-up showed that three patients completely lacked of growth hormone. One was thyrotropin deficient, three had persistent enlarged pituitary stalks, three had sub-normal anterior pituitaries and all four patients produced no post-pituitary hypersignal. None of the patients developed signs of histiocytosis or germinoma. CONCLUSION: The finding of abnormal pituitary stalks by MRI raises the possibility that the apparently idiopathic diabetes insipidus is due to some type of infiltrating disease of the hypothalamus and pituitary.

Child↗
PubMed1995

Diabetes insipidus and use of desmopressin (Minirin) during pregnancy.

With the use of two central health registries in Sweden, the Hospital Discharge Registry and the Medical Birth Registry, we identified 100 infants born of women who had been hospitalized for diabetes insipidus. By checking the medical records of these women, 29 infants were identified whose mothers had diabetes insipidus prior to the pregnancy and had been treated through the pregnancy with desmopressin. These infants had a normal birth weight and gestational length; there was only one congenital malformation identified (a ventricular septum defect with a patent ductus arteriosus and simian lines). This child died at the age of 14 years in a hypophyseal disease. This is the largest material published on desmopressin during pregnancy. The results suggest that maternal diabetes insipidus and treatment with desmopressin during the whole pregnancy does not constitute a major risk for the infant.

Birth Weight↗
PubMed1993

Brain adrenocorticoid receptor binding capacity in the diabetes insipidus brattleboro rat is dependent on maternal genotype.

We examined whether a different maternal genotype might differentially affect the brain adrenocorticoid receptor in homozygous diabetes insipidus Brattleboro rats. Two distinct homozygous diabetic offsprings were studied in comparison with Long Evans (LE) rats: one born of a homozygous mother (DI/HOM MOTHER), and the other born of a heterozygous mother (DI/HET MOTHER). The number of type I adrenocorticoid receptors of DI/HET MOTHER rats was significantly lower than that of LE rats in the hippocampus and hypothalamus, while in the amygdala both type I and type II receptors decreased. Surprisingly, the binding capacity of DI/HOM MOTHER rats, notwithstanding the absence of vasopressin (VP), as in the DI/HET MOTHER, did not differ from that of LE. Superimposable results were obtained in all the brain regions examined. No differences in binding affinity values (Kd) were detected. It was hypothesized that an 'unknown factor' linked to the genotype of the homozygous diabetic mother might counterbalance the receptor deficit otherwise induced by the lack of VP. The existence of two subpopulations of diabetic Brattleboro rats, as used in this study, should prompt to reexamine the origins of some behavioral and endocrine discrepancies appearing in studies on the homozygous diabetes insipidus Brattleboro strain.

Amygdala↗