RÉSUMÉ
One of the mechanisms of action of non steroid antiinflammatory drugs (NSAIDs) consists of inhibition of prostaglandin synthesis. This explains many of the pharmacological effects and adverse events observed in medical practice. Administration of NSAIDs to patients with hemostatic disorders or perioperative conditions entails the risk of bleeding due to inhibition of platelet function. This study deals with platelet changes induced by lysine clonixinate vs diclofenac, ibuprofen and aspirin in classical tests such as platelet count, platelet factor 3 (PF3) activity and platelet aggregation with various inductors and more recent procedures such as P-selectin measurement by flow cytometry. Unlike control drugs, lysine clonixinate did not induce changes in platelet count or function when administered to healthy volunteers at the commonly used therapeutic doses.
Sujet(s)
Anti-inflammatoires non stéroïdiens/pharmacologie , Plaquettes/effets des médicaments et des substances chimiques , Clonixine/analogues et dérivés , Clonixine/antagonistes et inhibiteurs , Lysine/analogues et dérivés , Lysine/antagonistes et inhibiteurs , Agrégation plaquettaire/effets des médicaments et des substances chimiques , Adulte , Analyse de variance , Acide acétylsalicylique/pharmacologie , Clonixine/administration et posologie , Diclofenac/pharmacologie , Cytométrie en flux , Humains , Ibuprofène/pharmacologie , Lysine/administration et posologie , Mâle , Sélectine P , Numération des plaquettes , Tests fonctionnels plaquettairesRÉSUMÉ
One of the mechanisms of action of non steroid antiinflammatory drugs (NSAIDs) consists of inhibition of prostaglandin synthesis. This explains many of the pharmacological effects and adverse events observed in medical practice. Administration of NSAIDs to patients with hemostatic disorders or perioperative conditions entails the risk of bleeding due to inhibition of platelet function. This study deals with platelet changes induced by lysine clonixinate vs diclofenac, ibuprofen and aspirin in classical tests such as platelet count, platelet factor 3 (PF3) activity and platelet aggregation with various inductors and more recent procedures such as P-selectin measurement by flow cytometry. Unlike control drugs, lysine clonixinate did not induce changes in platelet count or function when administered to healthy volunteers at the commonly used therapeutic doses.
Sujet(s)
Humains , Nouveau-né , Nourrisson , Enfant , Adolescent , Adulte , Arrêt cardiaque , Réanimation cardiopulmonaire , Réanimation , Épinéphrine , LidocaïneSujet(s)
Réanimation cardiopulmonaire/normes , Arrêt cardiaque/thérapie , Soins de maintien des fonctions vitales/normes , Adolescent , Adulte , Algorithmes , Réanimation cardiopulmonaire/méthodes , Enfant , Enfant d'âge préscolaire , Arrêt cardiaque/mortalité , Humains , Nourrisson , Nouveau-né , Soins de maintien des fonctions vitales/méthodes , PronosticRÉSUMÉ
We evaluated 17 children with primary intracranial neoplasms for subarachnoid metastatic disease (SAMD) using myelography with computed tomographic follow-up (Myelo + CT) and cerebrospinal fluid (CSF) histopathologic examination, as well as magnetic resonance imaging with gadolinium DTPA (MRI + Gd), between December 1988 and December 1989. There were 12 boys, and the median age was 5.7 years (range, 0.8 to 21.8 years). Tumor histology included 8 primitive neuroectodermal tumors (PNETs), 3 ependymomas, 2 low-grade astrocytomas, 1 anaplastic astrocytoma, 1 glioblastoma multiforme, 1 atypical rhabdoid tumor, and 1 malignant fibrous histiocytoma. Thirteen tumors originated in the posterior fossa, 2 were supratentorial, and 2 were in the spinal cord. The median interval between the 2 diagnostic tests was 2 days. MRI + Gd was positive in 11 (65%), Myelo + CT in 8 (47%), and CSF in 5 (29%) cases. MRI + Gd was superior in delineating spinal cord nodules and "sugar coating" whereas Myelo + CT more readily revealed nerve root sleeve filling defects. There was no case in which Myelo + CT was positive that MRI + Gd did not reveal SAMD. MRI + Gd is a safe, noninvasive test that should be used as the initial imaging modality for the presence of SAMD.