PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DIABETES INSIPIDUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1996

A novel mutation in the coding region for neurophysin-II is associated with autosomal dominant neurohypophyseal diabetes insipidus.

OBJECTIVE: Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is a rare cause of diabetes insipidus, in which AVP serum levels are insufficient. AVP is synthesized along with neurophysin-II (NPII) as an AVP-NPII precursor polypeptide in the hypothalamus. After proteolytic cleavage during axonal transport, AVP and NPII are reassembled and stored loosely bound to each other in the posterior pituitary until both are released into the circulation. In this study, we investigated the genetic basis of ADNDI in a German kindred with 10 affected members spanning three generations. DESIGN: Genomic DNA was isolated from peripheral blood leucocytes. The entire coding region of the AVP-NPII gene of one of the affected persons was amplified by polymerase chain reaction (PCR) and subjected to nucleotide sequence analysis. Sequencing results were confirmed by restriction enzyme analysis of PCR products. PATIENTS: Six affected and two unaffected members of a family with ADNDI and 54 unrelated healthy control subjects were studied. RESULTS: The index patient was found by direct sequencing to be heterozygous for a G to T transversion at nucleotide position 1884 (exon 2) of the AVP-NPII gene. This mutation introduced a new recognition site for the restriction enzyme Ava II, which was used to test for the presence of the mutation in other family members and in control subjects. The mutation was detected in all family members with ADNDI, but was not found in unaffected family members or in control subjects. The mutation encodes a valine in place of the normal glycine at amino acid 65 of NPII, which is known to be highly conserved during evolution. CONCLUSIONS: In this family, the autosomal dominant neurohypophyseal diabetes insipidus phenotype cosegregates with a point mutation in a region of the AVP-neurophysin-II gene which codes for the carboxy-terminal domain of neurophysin-II. Although the altered amino acid is not directly involved in AVP binding, the mutation might lead to conformational changes that impair the dimerization of neurophysin-II molecules. This could in turn affect the AVP binding affinity of neurophysin-II or might interfere with the transport of the AVP-neurophysin-II precursor in the AVP-producing cells of the hypothalamus.

Base Sequence↗
PubMed1995

Differential diagnosis and pathophysiology of diabetes insipidus.

Differential diagnosis of diabetes insipidus has been discussed in this paper in terms of pathophysiological aspects. Three points are emphasized: (1) we should include dipsogenic D.I. as one form of diabetes insipidus; (2) the water deprivation test is inconclusive in approximately 25% of patients, where the main difficulty is to distinguish between partial neurogenic D.I. and dipsogenic D.I.; and (3) this difficulty cannot be solved by a single determination of plasma vasopressin. Pathophysiology of inherited neurogenic D.I. and nephrogenic D.I. are also discussed.

Animals↗
PubMed1976

Diabetes insipidus in hypoxemic encephalopathy.

Diabetes insipidus developed in two patients who experienced severe hypoxemia as a consequence of drug-induced respiratory failure. Post-mortem examination revealed generalized cerebral edema, encephalomalacia, and a profound and diffuse loss of neurons. Hypoxemia-induced diabetes insipidus may indicate that the patient is suffering from severe brain damage.

Adult↗
PubMed1979

Diabetes insipidus and breast cancer.

Diabetes insipidus, resulting from metastatic involvement of the neurohypophysial system, is a rare complication of breast cancer. This review examined the clinical features, metastatic pattern, and radiological and postmortem findings of 39 breast cancer patients with this complication. All patients had polyuria and polydipsia, and all had evidence of advanced metastatic breast cancer. A high incidence of meningeal carcinoma carcinomatosis and/or sellar metastases was observed. In view of the anatomical proximity of the posterior pituitary to the dura mater and the sella turcica, our findings suggest that metastases to the neurohypophysis can occur not only as a result of hematogenous dissemination of malignant cells, but also from direct tumor extension and/or invasion from adjacent structures. Although satisfactory symptomatic relief can be obtained with vasopressin tannate, complete resolution of the diabetic insipidus syndrome was evident only in those patients who had achieved control of the underlying breast disease.

Adult↗
PubMedDate not supplied

[Fertile amenorrhea associated to diabetes insipidus].

A case of diabetes insipidus is presented which appeared in a 13 year old girl associated with hormone-resistant amenorrhea; she went through two normal pregnancies and partutition at 22 and 25, indicating a fertile amenorrhea. During a total of 17 years of observation the amenorrhea persisted, with the exception of a few normal menstruation periods at the beginning of the disease. She remained permanently under treatment with pitressin tannate. Repeated administrations of estrogens, gestagens and chorionic gonadotrophin, had no effect. An endometrial biopsy revealed a presecretory phase. Acidophilic index in vaginal smears as well as serial determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of urinary pregnanodiol indicated cyclic changes. Daily determinations of plasma gonadotrophins during 28 days revealed normal levels, with normal FSH pulse and ovulatory type peak of LH. An LH-RH test gave marked and characteristic increase of both hormones. The data indicate the integrity of the hypothalamo-hypophyso-ovaric system, with cyclic changes and formation of corpus luteum, vaginal trophism and endometrial changes, concordant with the two normal pregnancies. In this case, the amenorrhea can only be explained by alteration of the usual endometrial vascular changes. The coexistence of diabetes insipidus and fertile amenorrhea is discused in relation with the possible participation of vasopressin in the mechanism of menstruation.

Adult↗
PubMedDate not supplied

Central diabetes insipidus following carbon monoxide poisoning.

Diabetes insipidus is a rare complication after carbon monoxide poisoning. We report on a woman and her daughter who were noted to have polyuria and hypernatremia after exposure to carbon monoxide. Both patients were responsive to desmopressin therapy, and the diagnosis of central diabetes insipidus was made. The development and correction of hypernatremia further complicated the neurological damages caused by carbon monoxide poisoning. These cases illustrate the possibility of central diabetes insipidus and hypernatremia after carbon monoxide poisoning and the importance of immediate antidiuretic hormone treatment and careful fluid therapy.

Adult↗
PubMed2002

Diabetes insipidus in children: pathophysiology, diagnosis and management.

In diabetes insipidus, the amount of water ingested and the quantity and concentration of urine produced needs to be carefully regulated if fluid volume and osmolality are to be maintained within the normal range. One of the principal mechanisms controlling urine output is vasopressin which is released from the posterior pituitary gland and enhances water reabsorption from the renal collecting duct. In diabetes insipidus, the excessive production of dilute urine, and the causes of this clinical picture can be divided into three main groups: the first is primary polydipsia where the amount of fluid ingested is inappropriately large; the second group is cranial diabetes insipidus where the production of vasopressin is abnormally low; and, the third group is nephrogenic diabetes insipidus where the kidney response to vasopressin is impaired. The history and examination may suggest an underlying explanation for diabetes insipidus but a range of baseline and more extensive investigations may be required before a diagnosis can be reached. These investigations are not without risk, and the results need to be interpreted carefully because children do not always segregate neatly into a particular diagnostic category on the basis of one test alone. Children with cranial diabetes insipidus typically respond to arginine vasopressin or its manufactured analogue, desmopressin, with an increase in urine osmolality and an associated reduction in urine output. Such children usually require neuroimaging to look for evidence of evolving CNS pathology, such as an intracranial tumour. Vasopressin "replacement" with desmopressin is the treatment of choice in patients with cranial diabetes insipidus although extreme caution is required when treating babies or small children because of the danger of fluid overload. Abnormal production of other pituitary hormones in children with CNS disease can also influence fluid balance. Nephrogenic diabetes insipidus can be due to abnormal electrolyte concentrations, therefore these should be measured as part of the initial assessment. In a small number of children the defect is a primary abnormality of the vasopressin receptor or one of the water channel proteins (aquaporins) involved in water transport. The treatment of these patients is difficult and typically involves therapy with a diuretic such as chlorothiazide, as well as indomethacin. These agents enhance urine osmolality by their effect on circulating volume and renal solute and water handling. The fluid intake of most young children with primary polydipsia can be safely reduced to a more appropriate level.

Adolescent↗
PubMed1992

Diabetes insipidus: another cause of hormonal hyperthermia.

Diabetes insipidus is not generally recognized as a possible cause of etiologically obscure fever. We describe a female patient who presented with fever and polyuria and was shown to have idiopathic partial neurogenic diabetes insipidus. The fever was subsequently demonstrated to be caused by diabetes insipidus per se. The mechanism for the production of fever in this patient was most likely a defect in peripheral heat dissipation secondary to inadequate hydration. We conclude that diabetes insipidus is another cause of hormonal hyperthermia and should be considered in the differential diagnosis of etiologically obscure fever.

Adolescent↗
PubMed2003

Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy.

BACKGROUND: Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin. CASE: While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. Urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. CONCLUSION: Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.

Adult↗
PubMed1982

Recognition of diabetes insipidus in postpartum hypopituitarism.

The association of diabetes insipidus with postpartum hypopituitarism is unusual. This report presents a patient with both conditions. Evidence pointing to the pathogenesis of the diabetes insipidus is discussed. This case and selected others illustrate the wide spectrum in the severity of diabetes insipidus encountered in postpartum hypopituitarism, as well as the masking of symptoms caused by concomitant glucocorticoid insufficiency. Histopathologic and experimental evidence suggests that patients with hypopituitarism occurring postpartum might also display mild diabetes insipidus if challenged with antidiuretic stimuli. Diabetes insipidus may be a feature of postpartum hypopituitarism that is infrequently recognized.

Adult↗
PubMed1997

The management of diabetes insipidus in adults.

The management of patients with diabetes insipidus can be confusing because of the disorder's variable pathophysiology, the numerous medications used, and the possible complications related to their use. Nevertheless, the primary care physician, rather than the subspecialist, will increasingly be called on to manage patients with such relatively uncommon conditions in the future. If a few basic facts and principles are kept in mind, the care of most patients with diabetes insipidus can be successful. A comprehensive, practical review of the short- and long-term therapy for patients with diabetes insipidus, including central diabetes insipidus, nephrogenic diabetes insipidus, and the "excessive vasopressinase syndrome," is presented. The use of single and multidrug regimens, and of the newly marketed oral formulation of desmopressin acetate, is described for common clinical settings.

Acute Disease↗
PubMed1996

Diabetes insipidus, acute myelogenous leukemia, and monosomy 7.

Diabetes insipidus together with acute myelogenous leukemia has rarely been seen. Still rarer is the occurrence of monosomy 7 with the two diseases (only six cases reported). A patient who had diabetes insipidus develop before the diagnosis of acute myelogenous leukemia was found at karyotyping to have monosomy 7. Although a specific mechanism whereby monosomy 7 would cause diabetes insipidus has been proposed, some have suggested that monosomy 7 may have its effect by altering cell wall membranes. Others have suggested that acute myelogenous leukemia causes diabetes insipidus by causing infiltrates in the hypothalamus or posterior lobe of the pituitary gland. Magnetic resonance imaging of the patient's brain showed no abnormalities of the hypothalamus or pituitary gland. Lumbar puncture revealed no leukocytes in the cerebrospinal fluid. The authors believe that the cause of diabetes insipidus can be explained in patients with acute myelogenous leukemia by checking for monosomy 7 during karyotyping. Because karyotyping is now more frequently performed in evaluation of patients for chemotherapy or bone marrow transplantation, genetic abnormalities such as monosomy 7 will become increasingly apparent.

Anti-Bacterial Agents↗
PubMed1985

Transient nephrogenic diabetes insipidus associated with pregnancy.

The coexistence of diabetes insipidus and pregnancy is uncommon and can be associated with worsening of the diabetes insipidus. We report a patient who developed a transient nephrogenic diabetes insipidus associated with a pregnancy complicated by preeclampsia. The diabetes insipidus resolved spontaneously within several days after delivery.

Adult↗
PubMed2004

Diabetes insipidus: historical aspects.

The contributions to our present knowledge and understanding of diabetes insipidus are briefly surveyed. Though a disease presenting with polyuria and thirst had been recognized since Antiquity, it was not until the 17. Century the distinction was made between diabetes insipidus and diabetes mellitus. At the beginning of the 20. Century almost nothing was known about the function of the pituitary. It was generally believed that diabetes insipidus was a renal disease. Two clinical observations in 1912 suggested an association between the hypophysis and diabetes insipidus. This view was supported by the recognition in 1913 that extract of the posterior lobe of the pituitary was effective in diabetes insipidus. Despite much evidence to the contrary, it was assumed that the antidiuretic hormone was produced in the intermediate lobe of the pituitary. Around 1950 it was finally established that 'the posterior lobe hormones' are in fact secreted in the hypothalamus. At the same time the antidiuretic hormone was isolated and synthesized. More recently, progress within genetics has made it possible to characterize in details other rare types of diabetes insipidus.

Diabetes Insipidus↗
PubMed1999

Drug-induced diabetes insipidus: incidence, prevention and management.

Drug-induced diabetes insipidus is always of the nephrogenic type, i.e. unresponsiveness of the kidneys to the action of antidiuretic hormone. This condition is easily diagnosed by measuring urinary concentrating capacity during a thirst test (e.g. 12 hours of water deprivation) or by administration of a modified antidiuretic hormone, desmopressin, to demonstrate the renal unresponsiveness. Drug-induced nephrogenic diabetes insipidus is not a common disorder except in patients receiving treatment with lithium salts for affective disorders where it may affect about 10% of patients treated long term (15 years). Drug-induced nephrogenic diabetes insipidus caused by other drugs usually occurs in critically ill patients in intensive care units receiving a multitude of drugs dominated by antimicrobials and cytostatics. A search of the World Health Organization's adverse effect database revealed 359 reports of drug-induced diabetes insipidus. Lithium was the most common cause (159 reports) followed by foscarnet (15) and clozapine (10). Treatment is symptomatic in most patients and the offending drug should be stopped. If urine volumes exceed 4 L/day, treatment with thiazides and amiloride has been advocated, and nonsteroidal anti-inflammatory drugs, such as indomethacin, may be tried in severe cases. Prevention of lithium-induced nephrogenic diabetes insipidus is an important aspect of the treatment of affective disorders. In patients treated long term it appears to be only partly reversible upon lithium discontinuation. Close monitoring of the treatment aiming at 12-hour trough value of 0.4 to 0.6 mmol/L is recommended. Yearly measurement of the urinary volume/day is effective in making both the patient and the physician aware of the development of the drug-induced nephrogenic diabetes insipidus. The condition is a serious adverse effect because of the risk of developing dehydration and aggravation of drug intoxications.

Animals↗
PubMed1989

Diabetes insipidus with spontaneous remission.

Pathogenesis of idiopathic diabetes insipidus is unknown and the clinical course of the disease is permanent. However, we observed one patient who was diagnosed of idiopathic diabetes insipidus spontaneously reverted after approximately 13 months. The cause and pathogenesis of the disease were not evident. However, some reversible abnormalities should have been encountered in the hypothalamic-neurohypophyseal system. It is suggested that some unknown reversible impairments of the supraopticohypophyseal tract can cause diabetes insipidus. This case represents a well-documented description of idiopathic diabetes insipidus with spontaneous remission.

Adult↗
PubMed1998

[Diabetes insipidus with a hypothalamo-hypophyseal morphologic anomaly during a pregnancy].

BACKGROUND: Diabetes insipidus is uncommon in pregnancy. Despite physiological modifications in hydroelectrolytic balance during normal pregnancy, the capacity of the kidney to concentrate urine is preserved, partially due to lower vasopressin secretion. CASE REPORT: A young woman developed diabetes insipidus during the third trimester of normal pregnancy. The disease regressed totally after delivery. However, magnetic resonance imaging revealed a persistent expansive intrasellar image with a high-intensity signal. DISCUSSION: Onset of diabetes insipidus is usually rapidly progressive in pregnancy. Occurring generally during the third trimester in normal pregnancies, diabetes insipidus is generally well tolerated and responds to dDAVP, usually without pituitary abnormally, and regresses after delivery. Two types are distinguished: partially latent diabetes insipidus occurring during pregnancy and due to a central rather than nephrogenic origin; and excessive vasopressinase activity leading to diabetes insipidus usually associated with liver anomalies and high frequency of pre-eclampsia. During normal pregnancy, the size of the anterior pituitary increases and the normal high-intensity signal in the posterior pituitary seen on MRI usually regresses or disappears. In diabetes insipidus, the posterior pituitary hypersignal image generally disappears, reflecting reduced vasopressin storage. Few observations of diabetes insipidus occurring during pregnancy have been reported with morphological explorations. Most have described a "normal" aspect of the pituitary, specifically in the post partum period. In our patient, the weak vasopressin response to the end of water restriction at post partum when the diabetes insipidus symptoms had disappeared would suggest partial central diabetes insipidus revealed by pregnancy. Other pathologies involving this region could also be involved due to the unusual and persistent sellar image, with an expansive process showing a high intensity signal on MRI. An asymptomatic craniopharyngioma cyst was hypothesized and would be more compatible with the observed symptoms.

Adult↗