Role of urinary concentrating ability in the generation of toxic papillary necrosis

Role of urinary concentrating ability in the generation of toxic papillary necrosis. We studied the pathogenesis of chemically induced papillary necrosis in six groups of rats. Papillary necrosis was produced by a single injection of 2-bromoethylamine hydrobromide (BEA), 50 mg, i.v.; the animals were followed for 7 to 10 days after the administration of the compound. Following BEA, heterozygous Brattleboro rats developed all the functional and morphologic lesions of papillary necrosis that we previously described in Sprague-Dawley rats. They were unable to maintain sodium balance when dietary sodium was withdrawn. Homozygous Brattleboro rats, on the other hand, developed none of the manifestations of papillary necrosis (that is, animals with central diabetes insipidus were protected completely from the nephrotoxic effects of BEA). They adapted normally to a zero sodium diet. Chronic administration of vasopressin to homozygous Brattleboro rats fully restored the toxic effects of BEA. Lowering urinary concentrating ability by inducing a water diuresis in Sprague-Dawley rats completely protected against BEA-induced papillary necrosis. Decreasing papillary solute concentration by furosemide or increasing urine flow after abrupt withdrawal of vasopressin to homozygous Brattleboro rats did not protect against BEA-induced papillary necrosis. We conclude that the combination, but not either alone, of increased urine flow and decreased papillary solute concentration protects against the development of BEA-induced papillary necrosis.Rôle du pouvoir de concentration urinaire sur l'apparition d'une nécrose papillaire toxique. Nous avons étudié la physiopathologie d'une nécrose papillaire induite chimiquement chez six groupes de rats. La nécrose papillaire était produite par une injection unique de 2-bromoéthylamine hydrobromide (BEA), 50 mg, i.v.; les animaux étaient suivis pendant 7 à 10 jours après administration du produit. Après le BEA, des rats Brattleboro hétérozygotes ont développé toutes les lésions fonctionnelles et morphologiques d'une nécrose papillaire telles que nous les avions déjà décrites chez des rats Sprague-Dawley. Ils n'étaient pas capables d'assurer l'équilibre de la balance sodée lorsque le sodium alimentaire était supprimé. Par ailleurs, des rats Brattleboro homozygotes n'ont développé aucune des manifestations de nécrose papillaire (c'est-à-dire que les animaux ayant un diabète insipide central étaient complètement protégés des effets néphrotoxiques du BEA). Ils s'adaptaient normalement à un régime sans sodium. L'administration chronique de vasopressine à des rats Brattleboro homozygotes a totalement restauré l'effet toxique du BEA. Le fait d'abaisser la capacité de concentration des urines en induisant une diurèse aqueuse dans les rats Sprague-Dawley a complètement protégé contre la nécrose papillaire induite par le BEA. La diminution de la concentration de solutés papillaires par le furosémide ou l'augmentation du débit urinaire après arrêt brutal de la vasopressine chez des rats Brattleboro homozygotes ne protégeait pas contre la nécrose papillaire induite par le BEA. Nous concluons que la combinaison, mais non chaque facteur séparément, d'une augmentation du débit urinaire et d'une diminution de la concentration de solutés papillaires protègent contre le développement d'une nécrose papillaire induite par le BEA

Congenital laryngeal webs: Surgical course and outcomes

Objectives: We compare the success of different surgical options in the treatment of laryngeal webs. Methods: We performed a retrospective study spanning the years 1980 to 2005. Results: Eighteen patients were identified. The average age at diagnosis was 6 months (range, 1 day to 2.5 years). The presenting symptoms included weak cry, stridor, airway obstruction, and difficulty breathing. Associated cardiac defects consistent with the diagnosis of 22q-syndrome were present in 7 patients. Webs were classified as grade I (5 patients), grade II (2 patients), grade III (10 patients), or grade IV (1 patient) according to the Cohen classification. In 5 patients, only endoscopic lysis was required. The remaining 13 patients underwent open procedures; 9 patients in this group required tracheotomy. An average of 1.3 open airway procedures was necessary to achieve a decannulation rate of 89%. After operation, 34% of patients had residual webbing and 20% had a weak or aphonic voice. Conclusions: Management of laryngeal webs is dependent on the severity of airway obstruction. Grade I and II webs can be treated endoscopically; more severe laryngeal webs usually require tracheotomy and open airway reconstruction. © 2010 Annals Publishing Company. All rights reserved

Spastic diplegia and other motor disturbances in infants receiving interferon-alpha

Objective: To determine how frequently the use of -interferon (-IFN) is associated with the development of spastic diplegia. Study Design and Methods: Meta-analysis of 600 English manuscripts published January 1991 to June 2002 reporting -IFN use in infants/ children. We identified 3,113 children 18 years of age or younger and an estimated 3,055 children 12 years of age or younger who received -IFN therapy. Sixty-nine percent were treated for chronic hepatitis and 14% for vascular neoplasms. Outcome Measure: Neurologic examination to confirm spastic diplegia or a motor developmental disturbance other than spastic diplegia such as hyperactive deep tendon reflexes, gait disturbances, or impaired fine motor control. Results: Including our index case, 11 of 441 children with vascular lesions developed spastic diplegia and an additional 16 of 441 developed a motor developmental disturbance. All of these children were less than 1 year of age at initiation of therapy. Mean age of initiation and duration of -IFN therapy were not significantly different between groups (P \u3e .05); however, motor developmental disturbances improved with cessation of therapy, whereas spastic diplegia did not. No child receiving treatment for chronic hepatitis developed neurologic complications; however, only 49 children were less than 1 year of age at initiation of therapy. Conclusion: -IFN should not be used in infants under 1 year of age unless life-threatening conditions do not respond to any other form of treatment. If -IFN must be used, children should have monthly neurologic examinations. If a motor developmental disturbance is detected and -IFN therapy can be discontinued, it should be