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At least 1,099 records · Page 61Linked to original sources
PubMed1985

Unusual delayed onset of diabetes insipidus following closed head trauma. Case report.

A case of delayed onset of diabetes insipidus (DI), which developed 27 days after a closed head injury, is reported. The patient sustained only a minor neurological deficit and, except for antidiuretic hormone (ADH) insufficiency, hypothalamic function was intact. This selective damage of posterior pituitary function was total and permanent. Ischemia due to vascular injury may be the most likely etiology. Once the diagnosis of delayed posttraumatic DI is confirmed, the treatment of choice is DDAVP (desmopressin acetate). In contradistinction to DI immediately following minor head injury, most patients with a delayed onset of DI after trauma have permanent ADH deficiency.

Adolescent↗
PubMed2003

Diabetes insipidus and Langerhans cell histiocytosis: a case report of reversibility with 2-chlorodeoxyadenosine.

Diabetes insipidus (DI) is the most common manifestation of central nervous system involvement in Langerhans cell histiocytosis (LCH). Patients with LCH involving the head and neck region are reported to have about a 40% lifetime chance of developing DI. The clinical and biochemical diagnosis of DI is sometimes supported by the absence of the posterior pituitary bright signal on magnetic resonance images. Cladribine (2-chlorodeoxyadenosine, 2-CDA) has been reported as an active drug in children and adults with relapsed or refractory LCH. The authors report the successful reversal of DI in a 3-year-old child with established LCH using 2-CDA.

Cladribine↗
PubMed1999

Nephrogenic diabetes insipidus.

In spite of its rare incidence, the inherited renal tubular disorder nephrogenic diabetes insipidus (NDI) has in the past 10 years attracted the attention of a varied group of medical doctors and basic scientists. With the identification of the two genes involved in NDI, namely the vasopressin type-2 receptor (V2R) and the aquaporin-2 water channel (AQP2) genes, the identification of a large number of different mutations in these genes, and the subsequent functional characterization of mutant V2Rs and AQP2s, our insight into the renal cellular mechanisms involved in diuresis and antidiuresis has increased considerably. We are now entering an exciting new period in the development of new therapeutic strategies for disorders of water balance.

Amino Acid Sequence↗
PubMed2004

Accurate patient history contributes to differentiating diabetes insipidus: a case study.

This case study highlights the important contribution of nursing in obtaining an accurate health history. The case discussed herein initially appeared to be neurogenic diabetes insipidus (DI) secondary to a traumatic brain injury. The nursing staff, by reviewing the patient's health history with his family, discovered a history of polydipsia and long-standing lithium use. Lithium is implicated in drug-induced nephrogenic DI, and because the patient had not received lithium since being admitted to the hospital, his treatment changed to focus on nephrogenic DI. By combining information from the patient history, the physical examination, and radiologic and laboratory studies, the critical care team demonstrated that the patient had been self-treating his lithium-induced nephrogenic DI and developed neurogenic DI secondary to brain trauma. Thus successful treatment required that nephrogenic and neurogenic DI be treated concomitantly.

Aged↗
PubMed1991

Autosomal recessive inheritance of vasopressin-resistant diabetes insipidus.

We report on 2 intellectually normal sisters with vasopressin-resistant (nephrogenic) diabetes insipidus (NDI). The sex of the patients, the history of parental consanguinity, and the fact that both parents formed normally concentrated urine suggested that the NDI in the 2 sisters was the result of inheritance of an autosomal recessive mutation affecting renal tubular water reabsorption. The results of DNA analysis of the DXS52 locus with the use of St14 as probe, shown by Knoers et al. [1988] to be tightly linked to the NDI locus on the X-chromosome, showed that each girl inherited different Xq28 regions of the maternal X chromosomes, ruling out a diagnosis of classical X-linked NDI.

Consanguinity↗
PubMed1994

Nephrogenic diabetes insipidus secondary to lithium therapy in the postoperative patient: a case report.

Nephrogenic diabetes insipidus (NDI) presents a rarely encountered but challenging fluid management problem in the perioperative period. This case is that of a patient with a perforated duodenal ulcer and previously undiagnosed NDI who received standard preoperative and postoperative hydration with normal saline, causing hypernatremia and an inappropriate diuresis. The resulting hypernatremia and hyperosmolality required aggressive hypotonic fluid replacement to return to preoperative values. Though refractory to 1-desamino-8-D-argenine-vasopressin (dDAVP), thiazide diuretics and nonsteroidal anti-inflammatory agents have a role in managing selected patients. Early diagnosis with careful fluid and electrolyte management are critical in successful management of these patients in the perioperative period.

Adult↗
PubMed1995

[Diabetes insipidus disclosing metastasis of breast adenocarcinoma].

We are reporting on a case of diabetes insipidus (DI) and anterior pituitary failure revealing a breast cancer metastasis. Ten years after being diagnosed with a unilateral breast cancer, the patient presented with asthenia, thirst, polyuria and nocturia improved by subcutaneous DDAVP. MRI revealed a thickened pituitary stalk. DI is uncommon, late and usually asymptomatic in breast cancer. The association with an anterior pituitary failure is even more rare. In our patient the metastasis is in the pituitary stalk and seems to be due to meningeal deposits. MRI appears to be the best procedure to perform, showing a thickening stalk. Extension to the pituitary gland is related to direct tumor invasion from adjacent structures rather than haematogenous spread.

Adenocarcinoma↗
PubMed1973

Familial ADH-responsive diabetes insipidus: response to thiazides and chlorpropamide.

Twenty cases of familial ADH-responsive diabetes insipidus were identified within five generations, and eight patients were studied by one of two established dehydration protocols. In each case there was partial to total failure of response to the initial administration of ADH which was slowly corrected by continued administration. This initial failure can lead to misinterpretation of the dehydration test unless the medullary solute washout effect is taken into account in chronically polyuric patients.Treatment consisted of thiazides and/or chlorpropamide. All cases responded well.The response to chlorpropamide suggests that the failure of ADH production is not complete in these patients, and that the major defect is a failure of ADH release in response to normal stimuli. Chlorpropamide may act by either facilitating ADH release or by synergistically interacting with available ADH at the tubular level.

Adolescent↗
PubMed1998

Central diabetes insipidus with spontaneous remission. A case report.

We report a case of central diabetes insipidus with spontaneous remission 8 months after clinical beginning of the disease. A 20 years-old man developed polydipsia and polyuria in October 1994. A water deprivation study showed a defect in the urine concentrating function, which was corrected by vasopressine. A Magnetic Resonance imaging of the skull revealed a thickening of the pituitary stalk. His condition was well controlled by nasal DDAVP administration and 6 months later patient reduced spontaneously medication dose without clinical worsening. 8 months after clinical beginning, patient has become completely free from the need for medication to control clinical symptoms and urine concentrating function, as demonstrated by a re-evaluation study with water deprivation. A control Magnetic Resonance showed the regression of stalk enlargement. The clinical and radiological features of this case are discussed.

Adult↗
PubMed1995

Development of hypercalcemic crisis in a Graves' hyperthyroid patient associated with central diabetes insipidus.

A 26-year-old man with Graves' hyperthyroidism associated with central diabetes insipidus (DI), initially showed hypercalcemic crisis. Initially, very low serum levels of intact parathyroid hormone (PTH) and 1,25-dihydroxy vitamin D3 and a moderate rise of serum C-terminal PTH related protein (C-PTHrP) were observed which strongly suggested a humoral hypercalcemia of malignancy due to PTHrP. However, the serum C-PTHrP level later became normal. Mild hyperprolactinemia, no responses of growth hormone (GH) to insulin-induced hypoglycemia despite a normal growth hormone releasing hormone (GRH) test and mild thickening of the pituitary stalk on magnetic resonance imaging were observed. Thus, an autoimmune nature of his central DI is considered; it is noteworthy that the serum C-PTHrP level may be elevated by renal failure in patients with hypercalcemia due to causes other than PTHrP.

Acute Disease↗
PubMed1992

Contractile effect and tissue content of arginine vasopressin in the urinary bladder of Brattleboro rats with hereditary diabetes insipidus.

1. Urinary bladders from male rats of the Brattleboro strain with hereditary diabetes insipidus (DI) were analyzed for presence of immunoreactive arginine vasopressin (ir-AVP). Healthy rats were used as controls. 2. Bladders from the DI rats were heavier than controls. Concentration of ir-AVP was lower in DI bladders, but total amount of ir-AVP was similar to that in controls. 3. EC50 values for the AVP concentration-response relations were similar for control and DI bladder strips. Maximum response to AVP relative to response to K+ high solution was lower in the DI group. 4. An AVP receptor antagonist that significantly blocked response to exogenous AVP had no effect on response to field stimulation. 5. We suggest that AVP is synthetized locally and that AVP is not the non-adrenergic non-cholinergic transmitter responsible for the atropine resistant contraction in rat bladder.

Animals↗
PubMed2006

[Polyuria and polydipsia due to renal diabetes insipidus during the use of lithium].

Polyuria, thirst and polydipsia due to renal diabetes insipidus (RDI) are common side effects of long-term lithium treatment. In a man aged 56 years, the polyuria could be reduced considerably by diuretics. However, as shown in the case of a 49-year-old man, such treatment carries the risk of acute lithium intoxication due to volume depletion and reduced renal lithium clearance. A reduction in the dose of lithium prior to diuretic treatment is therefore mandatory. Although polyuria and polydipsia are generally mainly a nuisance, the condition may become life-threatening when free access to fluids is impossible. This is demonstrated by the case of a 46-year-old man who was on chronic lithium treatment with probable RDI and who developed fatal severe dehydration and hypernatraemia after traumatic brain injury. Awareness of the possibility of RDI in patients on chronic lithium treatment is therefore important.

Diabetes Insipidus, Nephrogenic↗