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1.
Epilepsia ; 51(2): 274-9, 2010 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-19780797

RESUMO

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 B(12), 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 microm; physiologic range 5-13 microm] 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) microm, respectively]. Conversely, normal tHcy concentrations were observed in the lamotrigine and levetiracetam groups [both 11.1 (0.5) microm]. 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.


Assuntos
Anticonvulsivantes/efeitos adversos , Epilepsia/tratamento farmacológico , Hiper-Homocisteinemia/induzido quimicamente , Adolescente , Adulto , Anticonvulsivantes/uso terapêutico , Carbamazepina/efeitos adversos , Carbamazepina/análogos & derivados , Carbamazepina/uso terapêutico , Indução Enzimática/efeitos dos fármacos , Indução Enzimática/genética , Epilepsia/sangue , Epilepsia/enzimologia , Epilepsia/genética , Feminino , Ácido Fólico/sangue , Frutose/efeitos adversos , Frutose/análogos & derivados , Frutose/uso terapêutico , Genótipo , Humanos , Hiper-Homocisteinemia/sangue , Hiper-Homocisteinemia/genética , Lamotrigina , Masculino , Metilenotetra-Hidrofolato Redutase (NADPH2)/genética , Pessoa de Meia-Idade , Oxcarbazepina , Fenobarbital/efeitos adversos , Fenobarbital/uso terapêutico , Polimorfismo Genético , Topiramato , Triazinas/efeitos adversos , Triazinas/uso terapêutico , Vitamina B 12/sangue
3.
Blood Coagul Fibrinolysis ; 26(6): 685-6, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-26126167

RESUMO

Mondor's disease is a rare entity, characterized by sclerosing thrombophlebitis classically involving one or more of the subcutaneous veins, including the anterior chest wall. It is usually a self-limited, benign condition, although it may be rarely associated with cancer. The intramuscular administration of botulinum toxin type A (BoNT-A), and also, more recently, type B, is a well-established treatment of many neurological, other medical and cosmetic disorders, including strabismus, blepharospasm, cervical and other focal/segmental dystonia, and also hyperhidrosis. Herein, we describe a case of thrombosis of the subcutaneous anterior chest veins, known as Mondor's disease, following botulinum toxin treatment for armpits hyperhidrosis.


Assuntos
Toxinas Botulínicas Tipo A/efeitos adversos , Tromboflebite/etiologia , Trombose/etiologia , Adulto , Feminino , Humanos , Injeções Intramusculares
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