1/31. Hyponatraemia associated with lamotrigine in cranial diabetes insipidus.We report the cases of two children with cranial diabetes insipidus who were treated with lamotrigine for seizures and who had accompanying changes in desmopressin requirements. Lamotrigine is a new anticonvulsant chemically unrelated to other existing antiepileptic drugs. Studies suggest it acts at voltage-sensitive sodium channels and also decreases calcium conductance. Both of these mechanisms of action are shared by carbamazepine, which can cause hyponatraemia secondary to inappropriate secretion of antidiuretic hormone. It is possible that the effect of lamotrigine on fluid balance in the cases described is also centrally mediated.- - - - - - - - - - ranking = 1keywords = antidiuretic hormone, antidiuretic, hormone, secretion (Clic here for more details about this article) |
2/31. A missense mutation encoding cys(67) --> gly in neurophysin ii is associated with early onset autosomal dominant neurohypophyseal diabetes insipidus.Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is an inherited disorder in which progressive degeneration of magnocellular neurons of the hypothalamus impairs production of arginine vasopressin (AVP). ADNDI is caused by mutations in the arginine vasopressin-neurophysin II (AVP-NPII) gene. These mutations are hypothesized to trigger neurodegeneration via disruption of preproAVP-NPII processing. Affected individuals usually develop diabetes insipidus between 1 and 6 years of age. Here we report a novel mutation of the AVP-NPII gene in a family with unusually early presentation of ADNDI. The index case developed symptoms of diabetes insipidus at 1 month of age, her mother at 9 months of age, and the maternal grandfather in early childhood. Each was found to be heterozygous for the missense mutation 1665T > G encoding the amino acid substitution C67G within NPII. This mutation helps to define two homologous regions of the AVP-NPII precursor bounded by disulfide bridges between C13 and C27 and between C61 and C73 that have structural homology and contain the majority of amino acid substitutions associated with ADNDI. The early onset of symptomatic diabetes insipidus in this family suggests that the C67G substitution may be particularly deleterious to magnocellular neurons and may provide a valuable model for study of dominantly inherited neurodegeneration.- - - - - - - - - - ranking = 1.3221440741713keywords = vasopressin (Clic here for more details about this article) |
3/31. A clinical feature of hyperlipidemia in patients with central diabetes insipidus.In this study, we analyzed plasma lipid and lipoprotein levels before and after treatment with 1-desamino-8-D-arginine vasopressin (DDAVP) in subjects with partial and complete central diabetes insipidus (DI) in order to determine how a shortage and supplement of this hormone affect plasma lipid metabolism. The subjects consisted of 6 patients with partial and 6 with complete central DI. After treatment with DDAVP through nasal cavity, plasma total cholesterol (TC) level did not decrease either in complete or partial form. plasma triglyceride (TG) levels decreased from 306 /-175 mg/dl to 198 /-91 (35% decrease, p=0.027) in complete form, while TG did not change significantly in partial form. A detailed investigation of plasma lipoprotein metabolism during treatment with DDAVP was carried out in 3 of the 6 subjects with complete form of DI. lipoprotein lipase activity and mass in post-heparin plasma from those three subjects tended to increase after treatment with DDAVP, along with the complete disappearance of an unusual lipoprotein between low density lipoprotein (LDL) and very low density lipoprotein (VLDL) as analyzed by polyacrylamide gel electrophoresis. These results suggest that the DDAVP treatment has a favorable effect on lipid and lipoprotein metabolism, especially triglyceride-rich lipoproteins, either directly or through modifying factors contributing to lipid metabolism.- - - - - - - - - - ranking = 0.66961018331347keywords = vasopressin, hormone (Clic here for more details about this article) |
4/31. hyponatremia and polyuria in children with central diabetes insipidus: challenges in diagnosis and management.Five patients with well-controlled, long-standing, central diabetes insipidus had acute development of dehydration, hyponatremia, and inappropriate natriuresis in the setting of polyuria resistant to exogenous antidiuretic hormone. hyponatremia and dehydration worsened with fluid restriction or use of exogenous antidiuretic hormone. We discuss the challenges in diagnosis and management of probable salt wasting in children with central diabetes insipidus.- - - - - - - - - - ranking = 1.2503506530012keywords = antidiuretic hormone, antidiuretic, hormone (Clic here for more details about this article) |
5/31. Perioperative management of central diabetes insipidus in kidney transplantation.Central diabetes insipidus is clinically masked in dialysis patients. We report a 12-year-old girl receiving a living-related donor graft for renal failure from Alport syndrome, in whom a craniopharyngioma had been resected 6 months before transplantation. Pretransplant evaluation had documented central hypothyroidism, growth hormone deficiency, and presumptive hypogonadotropic hypogonadism. The corticotropin-releasing factor test had been normal. Four hours after transplantation, urine output exceeded 1,000 ml/h without diuretic therapy. serum sodium concentration was 155 mmol/l, serum osmolality 333 mmol/kg, and plasma antidiuretic hormone 4.9 ng/l, while urine osmolality was 233 mmol/kg. Desmopressin acetate was started by continuous intravenous infusion at 1 microgram/day. serum electrolytes rapidly normalized, urine output stabilized at 2 l/day. The patient was discharged 4 weeks after transplantation with good allograft function, receiving intranasal desmopressin acetate 10 micrograms twice daily. Pre-existing central diabetes insipidus is unmasked after successful kidney transplantation, leading to rapid dehydration and hypernatremia, which can be prevented by prompt institution of desmopressin therapy.- - - - - - - - - - ranking = 1.0005192236778keywords = antidiuretic hormone, antidiuretic, hormone (Clic here for more details about this article) |
6/31. 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.- - - - - - - - - - ranking = 0.99198107745004keywords = antidiuretic hormone, antidiuretic, hormone (Clic here for more details about this article) |
7/31. diabetes insipidus secondary to penetrating spinal cord trauma: case report and literature review.STUDY DESIGN: Case report. OBJECTIVE: To present a case of central diabetes insipidus (CDI) that developed after a gunshot injury to the thorax and thoracic spinal cord and to discuss the disease process in light of the relevant literature. SUMMARY OF BACKGROUND DATA: Antidiuretic hormone (ADH) abnormalities may develop after spinal trauma and/or surgery. Although there are published reports of inappropriate adh syndrome arising in this clinical picture, CDI is rare. methods: A 33-year-old woman with hemopneumothorax and a gunshot wound to her thoracic spine was treated with chest tube drainage. No surgery was performed for the spinal injury. The patient was paraplegic on admission and rapidly developed excessive urine output. Testing revealed that her serum ADH level was low, consistent with CDI. Desmopressin acetate nasal spray was the prescribed treatment. RESULTS: The patient responded well to the desmopressin acetate spray. CONCLUSIONS: CDI is a complicated hormonal disorder characterized by excessive urine output. It is typically linked to an abnormality in the hypothalamohypophyseal axis that markedly reduces ADH production. The most common inciting causes are craniocerebral trauma, brain tumor and/or surgery, and central nervous system infection. Although uncommon, CDI should be considered when a spinal trauma patient develops excessive urine output.- - - - - - - - - - ranking = 0.0085381462278071keywords = hormone (Clic here for more details about this article) |
8/31. Identification of a novel mutation in the arginine vasopressin-neurophysin II gene in familial central diabetes insipidus.Familial central diabetes insipidus is an inherited disease of predominant autosomal dominant trait characterized by a deficiency of arginine vasopressin. The arginine vasopressin-neurophysin II ( AVP-NPII) gene consists of three exons and is located on chromosome 20p13 encoding for the precursor protein of AVP. We investigated two Caucasian families with a typical autosomal dominant trait of familial central diabetes insipidus, defined by deficiency of arginine vasopressin. After PCR amplification of exon 1 and exon 2/3, fragments were pooled and purified. Nucleotide sequencing was performed with the Taq DyeDeoxy-terminator cycle sequencing method using nested primers. Two mutations in the coding region of NPII were identified. In family C we found a heterozygous G ==> C missense mutation (AA61) in exon 2 leading to the substitution of cystein with serine. In family D a novel heterozygous nonsense mutation in exon 3 (AA 83, GAG ==> TAG) was indentified, leading to a stop codon instead of glutamine. Both mutations were confirmed by restriction analysis and were found in all affected but not in healthy family members or control subjects. We therefore have identified a missense mutation of the AVP-NPII gene and a novel mutation predicting a truncated protein.- - - - - - - - - - ranking = 4.6275042595997keywords = vasopressin (Clic here for more details about this article) |
9/31. A missense mutation encoding Cys73Phe in neurophysin II is associated with autosomal dominant neurohypophyseal diabetes insipidus.Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is an inherited disease caused by progressive deficiency of the hormone arginine vasopressin (AVP) that typically becomes clinically apparent in the first decade of life. The genetic locus of ADNDI is the arginine vasopressin-neurophysin II (AVP-NPII) gene and mutations that cause ADNDI have been found in the nucleotides encoding the signal peptide, vasopressin, and neurophysin II peptides. In this study we have analyzed the AVP-NPII gene in a 20-year-old female who was diagnosed with ADNDI at 2 years of age. A heterozygous missense mutation (1684G>T) was found in exon 2 that predicts replacement of cysteine with phenylalanine at position 73 of neurophysin II. The mutation was confirmed by subcloning exon 2 PCR products to sequence each allele independently. Two out of four clones were found to have the missense mutation and two have the normal sequence, confirming the presence of the mutation and heterozygosity. Neurophysin II is an intracellular carrier protein for AVP during axonal transport from the hypothalamus to the posterior pituitary and contains 14 cysteine residues forming 7 disulfide bonds. This mutation is predicted to disrupt the disulfide bridge between Cys73 and Cys61 within the neurophysin II moiety. This finding of a novel mutation substituting cysteine with phenylalanine in one AVP-NPII gene allele supports the hypothesis that inability to form normal disulfide bonds in neurophysin II leads to ADNDI.- - - - - - - - - - ranking = 1.9917542574848keywords = vasopressin, hormone (Clic here for more details about this article) |
10/31. postpartum hemorrhage complicated with irreversible renal failure and central diabetes insipidus.Sheehan's syndrome is a rare complication of pregnancy with multiple hormone deficiency. The exact pathogenetic mechanism is not well understood, because such endocrine abnormalities are not obvious in most women with severe hemorrhage. Central diabetes insipidus with fluid and sodium disturbances occurred in about 5% of the patients. [1,2] There are very few existing literature discussing concomitant Sheehan's syndrome and acute renal failure. The following case reports a patient showing Sheehan's syndrome, irreversible acute renal failure and central diabetes insipidus concurrently.- - - - - - - - - - ranking = 0.0085381462278071keywords = hormone (Clic here for more details about this article) |
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