NASAL SPRAY TREATMENT OF DIABETES INSIPIDUS.
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Alteration of posterior pituitary function in the empty sella syndrome is rare. A case of central diabetes insipidus and clear-cut deficiency of gonadotropins associated with an empty sella is described. Although computed tomographic scan revealed a defect of the diaphragma sellae, other pathogenic mechanisms are considered. Previously documented cases of empty sella syndrome associated with diabetes insipidus are reviewed.
A 17-month-old boy presented with failure to thrive, polyuria, and vomiting. He had been diagnosed clinically with nephrogenic diabetes insipidus and treated by amiloride and hydrochlorothiazide combination without a satisfactory outcome at another center since 1 year of age. The diagnosis was confirmed by genetic analysis (AVPR2mutation), and the treatment was modified to include rofecoxib (a selective cyclooxygenase-2 inhibitor) in addition to hydrochlorothiazide and amiloride. This combination along with a low-salt diet resulted in a dramatic decrease in urinary free-water loss, while no side effect was noted. Because of prohibition of rofecoxib, it had to be substituted first by indomethacin and then by ibuprofen. However, both drugs were ineffective in controlling water diuresis. Thus, we had to replace these drugs by celecoxib (another selective cyclooxygenase-2 inhibitor). We conclude that the combination hydrochlorothiazide/amiloride/cyclooxygenase-2 inhibitor could be successfully used to treat congenital nephrogenic diabetes insipidus.
The very rare occurrence of an ADH-producing small cell carcinoma of the lung in a 52 year old male patient with cranial diabetes insipidus since childhood is described. In this case diabetes insipidus disappeared concomitantly with development of lung cancer and re-appeared with shrinkage of the lung tumour by radiation therapy. Further progressive expansion of the primary and metastatic tumours induced the syndrome of inappropriate ADH secretion once again (SIADH). This deterioration in the clinical course was reflected in the plasma levels of ADH and neurophysins. The existence of vasopressin in the tumour tissue was also demonstrated by means of an immunohistochemical staining technique combined with anti-vasopressin serum.
Neuroendocrine dysfunctions are among the various complications that occur after traumatic brain injury. We report a case of onset of diabetes insipidus during acute rehabilitation of a 20-yr-old patient with a traumatic brain injury caused by a gunshot wound. Our case is the latest onset of diabetes insipidus after traumatic brain injury that has been reported in the literature.
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The Brattleboro rat with hypothalamic diabetes insipidus (BDI) has an abnormal aversion to drinking quinine-adulterated water compared with normal rats of the parent Long Evans (LE) strain. This BDI animal tolerates marked hypovolemia and decreased body weight in preference to drinking the quinine-adulterated fluid, indicative of a reduced motivation to drink. Acute or chronic treatment of BDI rats with desamino-8D arginine vasopressin (DDAVP) restored to normal their drinking response to quinine solution. Partial restoration of fluid turnover in BDI rats with hydrochlorothiazide, which has an antidiuretic effect in diabetes insipidus (when vasopressin is absent), failed to abolish the abnormal drinking response to quinine-adulterated solution in 8 out of 12 animals. In contrast, induction of diabetes mellitus in LE rats, which resulted in a marked polydipsia and polyuria even though vasopressin was still present, did not impair the drinking response to quinine solutions. These results suggest that the abnormal drinking response to quinine-adulterated fluid in BDI rats is reversed by treatment with the vasopressin V2-receptor agonist DDAVP but is unlikely to be a consequence of the restoration of fluid turnover to normal levels by a renal action. A possible central action involving vasopressin and the motivation to drink is discussed.
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These experiments studied the behavior of an inbred strain of vasopressin-deficient rat, the Roman high avoidance rat homozygous for diabetes insipidus (RHA: di/di). The RHA: di/di rat has been bred to be congenic with the parent normal Roman high avoidance (RHA: +/+) strain, differing from it only by the gene(s) coding for diabetes insipidus. Therefore, the RHA: +/+ strain represents an improved model system with which to study the behavioral effects of vasopressin-deficiency, given recent findings suggesting that considerable behavioral variation exists within the Long-Evans derived Brattleboro strain of vasopressin-deficient rat. We examined the behavior of RHA: di/di and RHA: +/+ rats in the open field and on tests of approach-avoidance, spatial memory and passive avoidance. RHA: di/di rats showed retarded habituation of ambulation and elevated incidence of rearing, defecation, and ambulation in the central area of the open field, relative to RHA: +/+ rats. The RHA: di/di and RHA: +/+ rat did not differ on measures of adaptation to a novel straight runway and both groups increased latencies to enter the goal box of the runway following shock, indicating memory. RHA: di/di rats did exhibit substantial recovery of goal-approach following shock, whereas RHA: +/+ rats did not. Both groups were able to solve a delayed non-match to sample task to receive reward. RHA: di/di rats showed a slower acquisition of the contingency and significantly faster run times of choice trials of the paired run procedure. No differences were evident between groups in memory of passive avoidance. The results of these experiments suggest that hereditary deficiency of vasopressin may influence physiological processes which determine arousal or attentiveness. The effects of vasopressin deficiency on performance of memory-indicating tasks appears to be secondary to modulations in arousal.
In LCH extended disease CNS involvement in is not infrequent. Diabetes insipidus, due to the affectation of hypothalamus-hypophysis axis, is its most frequent finding. The solitary affectation of hypothalamus-hypophysis axis is exceptional. At times, it's a difficult diagnosis and could precede the diagnosis of LCH several years. Usually, CAT and NMR show morphologic lesions. We report a patient who was diagnosed of idiopathic diabetes insipidus when he was 16 years old. Seven year later, he was diagnosed of LCH after underwent a bone marrow biopsy examination, just when the disease involved the bone and lung. Cerebral CAT and NMR didn't show morphologic lesions. In the presence of morphologic lesions in hypothalamus and/or hypophysis, proved by cerebral CAT and NMR, or a clinical setting of DI, the possibility of LCH must be considered.
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This case study details the use of arginine vasopressin in a pediatric organ donor. Although arginine vasopressin is primarily administered for its antidiuretic effects in the treatment of diabetes insipidus, the study demonstrates the often overlooked vasoactive effect of arginine vasopressin and its use in a patient without diabetes insipidus.
Renal toxicity of long-term lithium therapy is a common problem. Nephrogenic diabetes insipidus is the most frequently encountered complication, but often remains unrecognised because of the rather benign symptoms. We present a patient with long-term lithium therapy who developed life-threatening hypernatraemia due to insufficient oral fluid intake after elective spinal surgery. Careful daily substitution of up to 25 l of hypotonic fluids led to full recovery within 9 days. Nephrogenic diabetes insipidus should always be considered in lithium-treated patients undergoing elective surgery in order to avoid severe hypernatraemia.