1/9. Pseudo-bartter syndrome in a neonate on prostaglandin infusion.We describe a case of iatrogenic pseudo-bartter syndrome caused by administration of prostaglandin E1 (PGE1 alprostadil). Although the use of i.v. PGE1 is a well-established pharmacological therapy in neonates with a ductus-dependent congenital cardiopathy to ensure ductus-dependent flow, we could only find one other report on pseudo-bartter syndrome related to PGE1 infusion. CONCLUSION: Primary bartter syndrome is associated with endogenous increased levels of prostaglandins. Therefore, we postulate that the dose of prostaglandin E1 administered, immaturity and the genetic background are all relevant factors involved in the phenotypic presentation of iatrogenic pseudo-bartter syndrome in this preterm infant.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/9. Novel mutant vasopressin-neurophysin II gene associated with familial neurohypophyseal diabetes insipidus.We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G-->A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.- - - - - - - - - - ranking = 0.14285714285714keywords = gland (Clic here for more details about this article) |
3/9. indomethacin in streptozocin-induced nephrogenic diabetes insipidus.A 14-year-old female patient with metastatic carcinoid developed streptozocin-induced glomerular, proximal, and distal tubular dysfunction. The latter was in the form of nephrogenic diabetes insipidus, with urine volumes in excess of 11 L/24 h. The prostaglandin synthetase inhibitor, indomethacin, rapidly corrected the polyuria both initially and on rechallenge, independent of change in glomerular filtration rate.- - - - - - - - - - ranking = 0.14285714285714keywords = gland (Clic here for more details about this article) |
4/9. Post-obstructive urinary concentrating defect. A case study in the role of prostaglandins.A child with post-obstructive urinary concentrating defect was studied for the possible pathophysiological role of prostaglandins and an eventual therapeutic approach. Increased urinary excretion of prostaglandins was corrected by indomethacin, with resultant increased nephrogenous cyclic amp and partial improvement in the concentrating defect. The addition of a thiazide restored urinary concentration. These results add clinical support to the conception of the important role of prostaglandins in the mechanism of post-obstructive hyposthenuria. This therapeutic regimen is advocated for prolonged post-obstructive concentrating defect.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
5/9. Idiopathic hypercalciuria associated with hyperreninemia and high urinary prostaglandin E.A patient with idiopathic hypercalciuria and some features suggestive of Bartter syndrome is reported. Excessive urinary prostaglandin E (PGE) excretion and renal calcium leak were documented in this child. Treatment with aspirin and indomethacin reduced urinary PGE excretion and was associated with a decrease in daily calcium excretion. At the lowest levels of urinary PGE, the renal calcium leak was no longer evident although mild hypercalciuria persisted. These results suggest that PGE may play a role in some cases of idiopathic hypercalciuria.- - - - - - - - - - ranking = 0.71428571428571keywords = gland (Clic here for more details about this article) |
6/9. Prostaglandin synthetase inhibitors in the treatment of nephrogenic diabetes insipidus.Two boys with classical NDI have been treated with prostaglandin synthetase inhibitors. A boy, 7 years old, was treated with low solute-load diet and diuretics from his first year of life. His main complaint was nocturnal enuresis. He responded within one day to indomethacin 25 mg twice daily, and the urine volume was reduced from 4 1/2--6 litre/day to 2 1/2--3 litre/day. There is almost no enuresis. A boy, 7 months old, had a basal daily urine volume of 1.6--1.8 litre. A low solute-load diet and diuretics reduced urine volume to 1 litre, but he still needed gastric tube feeding. With the addition of acetylsalicylic acid, 75 mg three times daily, the urine volume was reduced to 600 ml, and he needed no more tube feeding. Both boys are doing well on the above-mentioned regimens, and no side effects have been observed after 1 year of treatment.- - - - - - - - - - ranking = 0.71428571428571keywords = gland (Clic here for more details about this article) |
7/9. Conn syndrome in a child, caused by adrenal adenoma.hyperaldosteronism owing to aldosterone-producing adenoma (Conn syndrome) is a rare but potentially curable form of pediatric hypertension. The authors report on a 5-year-old girl who had symptoms of polyuria, polydipsia, and fatigue, and for whom the diagnosis of hyperaldosteronemia was suggested by a low serum potassium level and persistent hypertension. The diagnosis was confirmed by increased levels of plasma aldosterone and decreased levels of plasma renin. The tumor was localized with ultrasonography and computed tomography, which showed a 2-cm mass in the left adrenal gland. The left adrenal gland was excised, and pathological assessment showed an adenoma. Only 14 other pediatric cases (< 16 years of age) have been reported in the English-language literature.- - - - - - - - - - ranking = 0.28571428571429keywords = gland (Clic here for more details about this article) |
8/9. ketorolac appears to decrease polyuria during intracranial surgery.Two cases are described of patients, undergoing surgery for intracranial pathology, who developed polyuria intraoperatively. The urine output decreased to within normal range shortly after the administration of ketorolac, a nonsteroidal antiinflammatory drug. The possible mechanisms producing the increased urinary output and the influence of prostaglandins on renal function are discussed.- - - - - - - - - - ranking = 0.14285714285714keywords = gland (Clic here for more details about this article) |
9/9. Central diabetes insipitus in a patient with congenital toxoplasmosis.A 33-day-old male infant who developed central diabetes insipitus as a complication of congenital toxoplasmosis is presented. He had polyuria and hypernatremia on admission and responded to Intranasal desmopressin acetate with the normalization of above mentioned findings. Computed tomographic (CT) scan of the brain showed obstructive hydrocephaly with periventricular and right basal ganglion calcification. CT scan of the pituitary gland, thyroid function tests, and serum cortisol levels were all normal. This is the first report of isolated diabetes insipitus with congenital toxoplasmosis in literature and central diabetes insipitus should be remembered if polyuria and hypernatremia develops in a patient with congenital toxoplasmosis.- - - - - - - - - - ranking = 0.14285714285714keywords = gland (Clic here for more details about this article) |