يعرض 1 - 5 نتائج من 5 نتيجة بحث عن '"Cinzia Costa"', وقت الاستعلام: 0.87s تنقيح النتائج
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    الوصف: The efficacy of levetiracetam (LEV) in controlling seizures in patients with brain tumor-related epilepsy (BTRE) depends on tumoral expression of synaptic vesicle protein 2A (SV2A). Although LEV is generally well tolerated, neuropsychiatric adverse events (NPAEs) might occur, limiting compliance and seizure control. We aimed to assess the influence of tumoral SV2A expression on the occurrence of LEV-related NPAEs in patients with glioma.Specimens from patients enrolled in the multicenter COMPO study, with glioma and BTRE treated with LEV, undergoing neurosurgery were retrieved. Immunohistochemistry-based expression of SV2A in tumoral and peritumoral tissue was scored in a four-point scale from absent (score = 0) to strong (score = 3). Low immunoreactivity (IR) corresponded to scores 2. Staining ratios (tumoral SV2A IR/peritumoral SV2A IR) were grouped into low (≤ 0.5) and high ( 0.5). NPAEs were assessed longitudinally with the Neuropsychiatry Inventory 12 test (NPI-12).Overall, 18 patients were eligible for analysis. All received LEV monotherapy, with 67% developing NPAEs. Patients with NPAEs had significantly lower median SV2A intensity score compared to patients without NPAEs (score 1 vs 0, p = 0.025). Low staining ratio (≤ 0.5) associated with higher NPAE occurrence compared to SR 0.5 (85.7% vs 0%, p 0.01). A SR ≤ 0.5 predicted a consistent increase in risk of NPAEs (OR 45.0; 95% CI 1.8-1128; p = 0.02).Our results suggest that SV2A expression in tumoral and peritumoral tissue correlates with the occurrence of LEV-related NPAEs. Thus, considering that SV2A expression also influences LEV effectiveness, SV2A staining might help in tailoring treatment to patients.

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    الوصف: Background and purpose We assessed the prevalence and magnitude of neuropsychiatric adverse events (NPAEs) associated with antiepileptic drugs (AEDs) among patients with brain tumour-related epilepsy (BTRE). Methods This observational, prospective, multicentre study enrolled 259 patients with BTRE after neurosurgery. All patients received AED monotherapy. Efficacy was assessed through clinical diaries, whereas NPAEs were collected using the Neuropsychiatric Inventory Test-12 questionnaire at baseline and after 5 months. Results Tumour localization in the frontal lobe was associated with a higher prevalence of NPAEs (odds ratio, 7.73; P < 0.001). Independent of tumour localization, levetiracetam (LVT) treatment was associated with higher prevalence and magnitude of NPAEs (odds ratio, 7.94; P < 0.01) compared with other AEDs. Patients with oligodendroglioma reported more NPAEs than patients with other tumour types. NPAEs were not influenced by chemotherapy, radiotherapy or steroid treatment. Evaluating non-neurobehavioural adverse events of AEDs, no significant differences were found among AEDs, although patients treated with old AEDs had a higher prevalence of adverse events than those treated with new AEDs. Conclusions Both tumour localization in the frontal lobe and LVT treatment are associated with a higher risk of NPAEs in patients with BTRE. LVT is regarded as a first-line option in patients with BTRE because of easy titration and few significant drug-to-drug interactions. Thus, as NPAEs lead to poor compliance and a high dropout rate, clinicians need to accurately monitor NPAEs after AED prescription, especially in patients with frontal lobe tumours receiving LVT.

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    المساهمون: Belcastro, V, Striano, P, Gorgone, G, Costa, C, Ciampa, C, Caccamo, D, Pisani, Lr, Oteri, G, Marciani, Mg, Aguglia, U, Striano, Salvatore, Ientile, R, Calabresi, P, Pisani, F.

    مصطلحات موضوعية: Male, Homocysteine, medicine.medical_treatment, Pharmacology, Gastroenterology, chemistry.chemical_compound, Folate deficiency, genetics, Oxcarbazepine, biology, Triazines, drug effects/genetics, Middle Aged, adverse effects/therapeutic use, Vitamin B 12, Carbamazepine, Neurology, Enzyme Induction, Phenobarbital, Anticonvulsants, Female, Levetiracetam, medicine.drug, Topiramate, Adult, medicine.medical_specialty, Hyperhomocysteinemia, Adolescent, Genotype, Fructose, Lamotrigine, adverse effects/analogs /&/ derivatives/therapeutic use, Folic Acid, Genetic, blood, Internal medicine, medicine, blood/drug therapy/enzymology/genetics, Humans, Polymorphism, Methylenetetrahydrofolate Reductase (NADPH2), Polymorphism, Genetic, Epilepsy, business.industry, Hepatic enzyme induction, Adolescent, Adult, Anticonvulsants, adverse effects/therapeutic use, Carbamazepine, adverse effects/analogs /&/ derivatives/therapeutic use, Enzyme Induction, drug effects/genetics, Epilepsy, blood/drug therapy/enzymology/genetics, Female, Folic Acid, blood, Fructose, adverse effects/analogs /&/ derivatives/therapeutic use, Genotype, Humans, Hyperhomocysteinemia, blood/chemically induced/genetics, Male, Methylenetetrahydrofolate Reductase (NADPH2), genetics, Middle Aged, Phenobarbital, adverse effects/therapeutic use, Polymorphism, Genetic, Triazines, adverse effects/therapeutic use, Vitamin B 12, medicine.disease, blood/chemically induced/genetics, Anticonvulsant, chemistry, Methylenetetrahydrofolate reductase, biology.protein, Neurology (clinical), business

    الوصف: Summary Purpose: Older enzyme-inducing antiepileptic drugs (AEDs) may induce supraphysiologic plasma concentrations of total (t) homocysteine (Hcy). The aim of the present study was to investigate the effect of new AEDs on plasma tHcy levels. Methods: Patients 18–50 years of age, on AEDs monotherapy, with no other known cause of hyper-tHcy were enrolled. Plasma tHcy, folate, vitamin B12, and AEDs levels were determined by standard high-performance liquid chromatography (HPLC) methods. Methylenetetrahydrofolate-reductase (MTHFR) polymorphisms were checked using Puregene genomic DNA purification system (Gentra, Celbio, Italy). A group of healthy volunteers matched for age and sex was taken as control. Results: Two hundred fifty-nine patients (151 on newer and 108 on older AEDs) and 231 controls were enrolled. Plasma tHcy levels were significantly higher [mean values, standard error (SE) 16.8, 0.4 vs. 9.1, 0.2 μm; physiologic range 5–13 μm] and folate lower (6.3, 0.1 vs. 9.3, 0.1 nm; normal > 6.8 nm) in patients compared to controls. Patients treated with oxcarbazepine, topiramate, carbamazepine, and phenobarbital exhibited mean plasma tHcy levels above the physiologic range [mean values (SE) 16 (0.8), 19.1 (0.8), 20.5 (1.0), and 18.5 (1.5) μm, respectively]. Conversely, normal tHcy concentrations were observed in the lamotrigine and levetiracetam groups [both 11.1 (0.5) μm]. Discussion: Oxcarbazepine and topiramate might cause hyper-tHcy, most likely because of the capacity of these agents to induce the hepatic enzymes. Because literature data suggest that hyper-tHcy may contribute to the development of cerebrovascular diseases and brain atrophy, a supplement of folate can be considered in these patients to normalize plasma tHcy.

    وصف الملف: ELETTRONICO

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    المصدر: Stroke. 35(2)

    الوصف: Background and Purpose— The possible neuroprotective effect of endogenous γ-aminobutyric acid (GABA) on the irreversible electrophysiological changes induced by in vitro ischemia on striatal neurons was investigated. In particular, the aim of the study was the characterization of the neuroprotective action of 2 antiepileptic drugs increasing GABAergic transmission such as tiagabine, a GABA transporter inhibitor, and vigabatrin, an irreversible inhibitor of GABA transaminase. Methods— Extracellular field potential recordings were obtained from rat corticostriatal slice preparations. In vitro ischemia was delivered by switching to an artificial cerebrospinal fluid solution in which glucose was omitted and oxygen was replaced with N 2 . Results— An irreversible loss of the field potentials recorded from striatal neurons was observed after 10 minutes of ischemia in control solution. Conversely, tiagabine and vigabatrin partially prevented the ischemia-induced field potential loss. Surprisingly, both GABA A and GABA B receptor antagonists blocked these effects. Accordingly, neuroprotection could be obtained only when GABA A and GABA B receptor agonists were coapplied, but not when a single agonist was given in isolation. Conclusions— Antiepileptic drugs targeting GABAergic transmission can exert neuroprotective effects against ischemia by increasing endogenous GABA levels and via the activation of both GABA A and GABA B receptors.