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M B Sánchez

Publications and source records attributed to M B Sánchez.

8 recordsLinked to original sources
PubMed2006

[Mechanism of action of antiepileptic drugs and new antiepileptic drugs].

INTRODUCTION: Although 10 second generation new antiepileptic drugs are currently available on the market, 30% of patients are resistant to pharmacological treatment. In addition, today's antiepileptic drugs avert or suppress seizures but do not prevent the appearance of epilepsy or its progression. DEVELOPMENT: The foundations of the aetiopathogenesis of epilepsy and the main targets of antiepileptic drugs are described. Describing the important role of gamma-aminobutyric and glutamic acid in the genesis and proliferation of the seizures has allowed for the development of new antiepileptic drugs that increase the inhibitory tone of GABA or inhibit the excitatory tone of glutamate. The discovery that some epilepsies may be due to channelopathies is now making it possible to conduct research into drugs that inhibit calcium channels, activate potassium channels or inhibit abnormal AMPA/KA receptor channels. Recent reports describing a specific attachment of some antiepileptic drugs to the a2d subunits of the calcium channel and to the synaptic vesicles proteins SV2A open up new perspectives. Moreover, research is also being carried out on new drugs that are capable of preventing epileptogenesis, stemming the progression of epilepsy or overcoming the resistance to pharmacological treatment displayed by some epilepsies. CONCLUSIONS: The identification of new pharmacological targets in the aetiopathogenesis of epilepsies has made it possible to develop second generation antiepileptic drugs and it is allowing for the development of third generation antiepileptic drugs.

Anticonvulsants↗
PubMed2006

Risk factors for bacteremia in patients with limb cellulitis.

The aim of this study was to identify the risk factors for bacteremia in patients with limb cellulitis. Using the administrative and microbiology laboratory databases of a community teaching hospital, a review was conducted of all cases of community-acquired limb cellulitis that occurred during the period 1997-2004 and in which blood cultures had been performed. A comparison of demographical, clinical, and analytical data of patients with bacteremia versus patients without bacteremia was performed by univariate and multivariate analyses. Of 2,678 patients with cellulitis who presented to the hospital's emergency department, 308 were diagnosed with limb cellulitis and had blood cultures. Of these, 57 (18.5%) had bacteremia. In 24 of the 57 (42.1%) patients with bacteremia, the microorganism isolated in blood cultures was non-group-A beta-hemolytic Streptococcus, and in another 14 (24.6%), the microorganism identified was a gram-negative bacterium. Staphylococcus aureus was determined as the cause of bacteremia in just 6 (10.5%) patients and group A Streptococcus in 2 (3.5%). By logistic regression analysis, the following factors were associated with bacteremia: absence of previous antibiotic treatment (OR 5.3, 95% CI 1.4-20.3), presence of two or more comorbid factors simultaneously (OR 4.3, 95% CI 1.6-11.7), length of illness<2 days OR 2.44, 95% CI 1.07-5.56), and proximal limb involvement (OR 6, 95% CI 3.03-12.04). Patients with limb cellulitis who exhibit any of these characteristics are at increased risk of bacteremia. In such patients, it is imperative that blood cultures be performed.

Adolescent↗
PubMed2003

Incidence of neutropenia during treatment of bone-related infections with piperacillin-tazobactam.

Of 41 patients with bone-related infections who were treated for > or =10 days with piperacillin-tazobactam, 14 (34%) developed neutropenia. Cumulative doses of piperacillin administered to neutropenic patients were higher than those administered to nonneutropenic ones (330 vs. 237 g; P=.008), and an inverse correlation was detected between the absolute neutrophil count at the end of treatment and the cumulative dose of piperacillin (r=-0.47, P=.002). Moreover, the incidence of piperacillin-tazobactam-induced neutropenia increased with an increase in the cumulative dose of piperacillin: 0% of patients in the first quartile of cumulative piperacillin doses, 33.3% in the second quartile, 40% in the third quartile, and 66.7% in the fourth quartile.

Age Factors↗
PubMed1992

[Postoperative gallbladder and systemic candidiasis].

Gangrenous cholecystitis occurred in an immunodepressed patient with generalized neoplasia. Evolution was rapid and severe. Emergency cholecystectomy and systemic treatment with Anphotherycin were life-saving.

Adult↗
PubMedDate not supplied

[Use of antiepileptic drugs in bipolar disorder].

OBJECTIVE: Bipolar disorder is a chronic disease difficult to treat that generates a high degree of incapacity. Although lithium remains the first choice drug, some patients do not respond and others show adverse reactions. One alternative to lithium is the use of certain antiepileptic drugs. Data on the efficacy of old and new antiepileptic drugs in bipolar disorder obtained in controlled clinical trials are reviewed. DEVELOPMENT: Results in many clinical trial support the use of some old antiepileptic drugs such as carbamazepine and sodium valproate in monotherapy in the acute treatment of severe, mixed or mild manic episodes as well as in the management treatment of bipolar disorder. Overall, new antiepileptic drugs show a better profile of adverse reactions with fewer interactions than lithium, but data on their efficacy in bipolar disorder remain scarce. Oxcarbazepine efficacy in mania is similar to that of the carbamazepine. Lamotrigine is becoming the best alternative to lithium in depressive episodes. Topiramate does not appear to be effective in acute treatment of manic episodes. Levetiracetam seems to produce some benefits, but controlled, randomized and double blind clinical trials are not yet available. Data on gabapentin efficacy are controversial. CONCLUSIONS: Although lithium is still the first choice for the treatment of bipolar disorder, carbamazepine and valproate are also first choice drugs. Oxcarbazepine and lamotrigine may be a good option in some patients. Other new antiepileptic drugs may also be effective in bipolar disorder but more solid evidence of their efficacy is needed.

Anticonvulsants↗
PubMedDate not supplied

[The interactions of antiepileptic drugs in oncology practice].

AIMS: Antiepileptic drugs, which often have to be used in patients with cancer, can have important effects on the results offered by antineoplastic agents. Here, we review the influence of antiepileptic drugs on antineoplastic agents and the influence of antineoplastic agents on antiepileptic drugs; measures to prevent such interactions are also suggested. DEVELOPMENT: Antiepileptic drugs that induce cytochrome P450, such as carbamazepine, phenytoin and phenobarbital, can reduce the levels and effects of antineoplastics that metabolise by means of this enzyme, for example, taxanes, Vinca alkaloids, methotrexate, teniposide and camptothecin. Furthermore, enzyme-inducing antiepileptic drugs diminish the levels and effects of many other drugs that can be administered to oncology patients, such as other antiepileptic drugs used in polytherapy, narcotic analgesics, antidepressants, antipsychotics or antibiotics. In contrast, valproate can increase the toxicity of etoposide or nitrosoureas. Moreover, antineoplastic agents like cisplatin or corticoids can lower the effectiveness of phenytoin and methotrexate has a similar effect on valproate. In contrast, 5-fluorouracil can increase the toxicity of phenytoin. Pharmacodynamic interactions are also possible. CONCLUSIONS: Information about the clinical consequences of the interactions between antiepileptics and antineoplastic agents is often based on cases or series of cases, but a growing body of evidence from pharmacokinetic studies shows that enzyme-inducing antiepileptics exert an important influence on the effectiveness of the antineoplastic agents. It is therefore recommendable to avoid them and replace them with non-enzyme-inducing antiepileptics, such as gabapentin, lamotrigine, levetiracetam, pregabalin, topiramate or zonisamide. When enzyme-inducing antiepileptics have to be used, it is likely that higher doses of antineoplastic agents or other inducible drugs will have to be utilised.

Anticonvulsants↗