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PubMed1988

Vasopressin gene expression in hypertensive, normotensive, and diabetes insipidus rats.

This investigation examined the presence and abundance of vasopressin-gene messenger ribonucleic acid (mRNA) transcripts in hypothalamic tissue from five strains of rats: Long Evans, Wistar-Kyoto, and diabetes insipidus (Brattleboro) rats, stroke-prone spontaneously hypertensive rats, and cross-bred diabetes insipidus x stroke-prone spontaneously hypertensive rats. A single-stranded RNA probe complementary to exon C of the vasopressin gene was utilized for in situ hybridization and identified hypothalamic 'vasopressinergic' neurons in tissue from all five strains of rats. The results obtained by solution and in situ hybridization suggested the cross-bred diabetic-hypertensive rat exhibits a level of vasopressin-gene messenger ribonucleic acid similar to diabetes insipidus rats. This observation is consistent with previous physiological data which suggests cross-bred diabetic-hypertensive rats inherit the mutated vasopressin gene of the Brattleboro rat.

Animals↗
PubMed1979

Diabetes insipidus following obstetric shock.

The first known case of obstetric shock followed by diabetes insipidus without anterior pituitary deficiency is presented. A patient developed extreme thirst and polyuria after massive bleeding and prolonged shock due to placenta previa percreta with bladder invasion. Evaluation confirmed diabetes insipidus sensitive to vasopressin administration. Anterior pituitary deficiency could not be identified, either acutely or 6 months later.

Adult↗
PubMed1984

Diabetes insipidus in preleukaemic phase of acute myeloid leukaemia in 2 patients with empty sella turcica. A report of 2 cases.

2 patients with diabetes insipidus established in the preleukaemic phase of acute myeloid leukaemia are described. Both patients had probably coincidentally an empty sella turcica showed by a computerized tomography. In one of them, leukaemia developed secondary to a cytostatic therapy for a vesical cancer. In this patient, blast cells appeared in cerebrospinal fluid after the patients had become polyuric and later on autopsy findings showed a peripituitary leukaemic infiltrate. In the other patient, diabetes insipidus and the acute phase of leukaemia developed after a long period with a dysmyelopoietic syndrome. Hormonal tests suggested a hypothalamic injury in both patients due to a leukaemic infiltrate at least in the former of them. It is concluded that diabetes insipidus as a consequence of hypothalamic lesion may develop in the preleukaemic phase of acute myeloid leukaemia and become evident before any other symptoms of leukaemia have manifested.

Anemia, Aplastic↗
PubMedDate not supplied

Diabetes insipidus versus syndrome of inappropriate antidiuretic hormone.

Diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone (SIADH) are two endocrine disorders presenting a challenge to the critical care nurse. The challenge lies in the recognition and assessment of the effects on the patient's fluid balance and in the planning of interventions to prevent complications.

Diabetes Insipidus↗
PubMed1975

Dental fluorosis associated with hereditary diabetes insipidus.

Among the characteristics of hereditary pituitary diabetes insipidus are polydipsia and polyuria from early infancy. Drinking of large amounts of water, even with lower than accepted fluoride content, can produce fluorosis of the teeth. A mother and her four children affected by this disorder presented different degrees of fluorosis directly related to the stage at which hormonal therapy was introduced.

Adolescent↗
PubMedDate not supplied

[Abnormal sweat test in patient with Diabetes Insipidus unresponsive to ADH].

Increased sweat concentrations (92, 76 and 80 mEq/l) were observed in a 7-year-old boy with pitressin-resistant diabetes insipidus. All previous observations of elevated sweat electrolytes in diabetes insipidus have been in infants less than 10 months of age. The sweat test is an exceptionally reliable, sensitive and specific test for the diagnosis of Cystic Fibrosis. Pitressin-resistant diabetes insipidus is one of the diseases associated with elevated sweat test results.

English Abstract↗
PubMedDate not supplied

[A case of acute leukemia with a diabetes insipidus syndrome and thrombocytosis].

A case is described of acute leukosis presenting with unusual clinical picture. In a female patient aged forty nine presenting with signs of diabetes insipidus, blood count revealed thrombocytosis together with alterations suggesting acute leukosis. Bone marrow blasts showed the typical morphological features of megakaryoblasts. Institution of chemotherapy made for dispelling of diabetes-insipidus manifestations. To the authors' thinking, they observed a rare megakaryoblastic variety of acute leukosis caused by leukotic infiltration of the hypothalamohypophyseal zone in a patient wasted by heavy urination as is common in diabetes insipidus.

Acute Disease↗
PubMed2002

Transient hypothalamic hypothyroidism and diabetes insipidus after electrical injury.

Transient or permanent diabetes insipidus (DI) due to damage in vasopressinergic neurons--which may be hereditary or caused by head injury, brain surgery, tumors, granulomatous disorders, infections, vascular disorders, autoimmunity, and idiopathic causes--is not rare. Hypothalamic hypothyroidism is due to decreased thyrotropin-releasing hormone secretion and is seen rarely. We report a case of transient hypothalamic hypothyroidism and transient DI due to electrical injury.

Adult↗
PubMed1988

Localization of the gene for X-linked nephrogenic diabetes insipidus to Xq28.

X-linked nephrogenic diabetes insipidus (NDI) was segregating in a large Indiana family. It was tested for linkage of the NDI gene to X-chromosome molecular markers. Maximum lod scores of 3.15 and 3.01 (theta = 0) obtained for the molecular markers F8A (F8C) and DXS15 (DX13) respectively, indicate that the NDI gene is located in Xq28. A lod score of 3.61 (theta = 0) was obtained with multipoint linkage analysis of F8A and DXS15.

Chromosome Mapping↗
PubMed1998

Aquaporin-2, a vasopressin-sensitive water channel, and nephrogenic diabetes insipidus.

Two cases of autosomal recessive nephrogenic diabetes insipidus (NDI) were evaluated. Both cases were found to be compound heterozygote for missense mutations in the aquaporin-2 (AQP2) gene. To determine the structural-functional relationship, the mutated AQP2 proteins, T125M, G175R, A190T, and P262L, were expressed in Xenopus oocytes and examined by measurement of water permeability, immunoblot, and immunocytochemistry. Our results suggest that T125M and G175R are nonfunctional water channels, whereas the translocation to the plasma membrane is impaired in A190T and P262L.

Amino Acid Sequence↗
PubMed1997

[Temporal hemianopia and diabetes insipidus following head injury].

Bitemporal hemianopia and diabetes insipidus following head injury are caused by a lesion in the center of the optic chiasm, together with injury to the adjacent pituitary stalk or the hypothalamus. This combination was thought to be a rare complication of severe head injury. The case of a 16-year-old male is presented, which together with recent reports suggests that this relatively under-recognized syndrome is not infrequent, that it may follow even minor head injury, and that magnetic resonance imaging can demonstrate the chiasmal lesion.

Adolescent↗
PubMed1964

DIABETES INSIPIDUS.

Explore the source record for details and available documents.

Arginine Vasopressin↗
PubMed1997

Persistent high MR signal of the posterior pituitary gland in central diabetes insipidus.

We describe three cases of central diabetes insipidus, each with a different pathogenesis, in which unexpected hyperintensity of the posterior pituitary gland was seen on T1-weighted MR images obtained at the time of presentation. In the first case (idiopathic), the posterior pituitary signal persisted more than 10 years; in the second case (Langerhans cell histiocytosis), the signal disappeared within 3 months, despite early specific chemotherapy with etoposide; and in the third case (transient), the posterior signal disappeared within 1 year, but it was documented at the time of spontaneous reversal of polyuria and polydipsia.

Adolescent↗
PubMed1991

Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction.

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.

Diabetes Insipidus↗