Biomedical subjects

A M Gutiérrez-Alvarez

Publications and source records attributed to A M Gutiérrez-Alvarez.

5 recordsLinked to original sources

PubMed2007

Do your patients suffer from excessive yawning?

OBJECTIVE: Yawning has been described in relation to drugs such as serotonin reuptake inhibitors, levodopa, dopamine agonists, MAO B inhibitor, morphine, methadone, buprenorphine, dextromethorphan, benzodiazepine, lidocaine, and flecaine. This is a report of two patients, on long-term escitalopram therapy (more than 8 weeks) with stable dosing, who presented excessive yawning. Escitalopram is widely used in major depressive disorder and generalized anxiety disorder. METHOD: A clinical description of two cases. RESULTS: Two females (62 and 59 years old, respectively) developed excessive daytime yawning. It was not associated with sedation or a feeling of needing sleep. The dosage was reduced and yawning disappeared some hours later. The patients' depression did not recur. CONCLUSION: Yawning has been described in relation to different selective serotonin reuptake inhibitors and remitted following their discontinuation; it is interesting that the reported yawning in these two cases disappeared with the reduction of dosage, rather than the interruption of treatment.

Antidepressive Agents, Second-Generation↗

PubMedDate not supplied

[Use of anticonvulsive drugs during pregnancy and the risk of malformations in the newborn: a meta-analysis].

OBJECTIVE: To determine the risk, if any, of anticonvulsants use on the foetus with respect to major malformations. MATERIALS AND METHODS: MEDLINE, EMBASE, SCISEARCH and programs as ProQuest, HINARI and Ovid were searched for human studies. Studies that examined the effects of systematic exposure to any anticonvulsant during pregnancy (any dose, any duration, indicated for any type of epilepsy) were eligible. Studies that assessed major malformations in the infants were eligible. Major malformations were defined using the criteria described by Holmes. The number of neonates exposed to anticonvulsants who did and did not exhibit major malformations, and the number of neonates not exposed to anticonvulsants who did and did not exhibit major malformations, were extracted in the form of 2 x 2 tables. The odds ratio (OR), relative risk and 95% confidence interval (CI) was calculated for each of the studies. RESULTS: Ten cohort studies and four case control studies were included. A total of 2,509 cases and 433,890 controls were included. Major malformations were found in 9.8% among the exposed children and 7.4% among the non exposed. (OR: 2.7; CI 95%: 2.062-3.641; p<0.000). There was no evidence of an association between any anticonvulsant and a specific major malformation. CONCLUSIONS: The available epidemiological data support the hypothesis that anticonvulsants increase the risk of major malformations by an order of 2- to 3-fold.

Abnormalities, Drug-Induced↗

PubMedDate not supplied

[Changes in selenium levels in epilepsy].

INTRODUCTION: It has been suggested that antiepileptic drug therapies deplete total body selenium stores and failure to give appropriate selenium supplementation, especially to patients receiving valproic acid during pregnancy may increase the risk of neural tube defects or other free radical mediated damage. Selenium is essential for the synthesis of selenoproteins, including glutathione peroxidase. AIMS: To review the present state of knowledge about selenium behaviour in people with epilepsy taking antiepileptic drugs and to develop guidelines for the appropriate use of selenium supplements. DEVELOPMENT: Databases such as Medline, Embase, Scisearch and Lilacs were consulted to have access to literature. A search in said databases was performed in order to find articles published from January 1966 to August 2004. All articles published in English and Spanish were considered. A manual review of the references present in each produced article was done in order to identify the articles that the electronic search may have not found itself. The title and abstract of the potential articles were analyzed before asking for the complete article. However, articles which seemed ambiguous were completely analyzed later to establish their relevance. CONCLUSIONS: There is insufficient evidence to fully evaluate the effect of selenium supplementation. The possible beneficial effects on pregnancy need to be evaluated in further studies.

Anticonvulsants↗

PubMedDate not supplied

[The risk of defects in the neural tube caused by valproic acid and carbamazepine].

OBJECTIVE: To determine the risk, if any, of carbamazepine and valproic acid use on the foetus with respect to neural tube defects. MATERIALS AND METHODS: Databases such as MEDLINE, EMBASE, SCISEARCH, The Cochrane Library and LILACS were consulted to have access to published literature from January 1966 to September 2004. All articles published in English and Spanish were considered. A manual review of the references presented in each produced article was done in order to identify the articles that the electronic search may have not found itself. However, articles which seemed ambiguous as to the title and/or abstract were completely analyzed to establish their relevance. Studies that examined the effects of systematic exposure to carbamazepine or valproic acid during pregnancy and that assessed neural tube defects in the infants were eligible. The data was extracted in the form of 2 x 2 tables. The odds ratio (OR), relative risk (RR) and 95% confidence interval (CI) was calculated for each of the studies. RESULTS: The pooled relative risk of neural tube defects among the exposed to valproic acid was 0.61 (95% CI: 0.06-6.72). The risk among the exposed to carbamazepine was 1.10 (95% CI: 0.16-7-75). CONCLUSIONS: Due to the methodologic limitations of most of the studies where the data was insufficient, only three studies could be included in the meta-analysis. There is not enough evidence to establish the risk raised in the objective of the study.

Anticonvulsants↗

PubMedDate not supplied

[Zinc and epilepsy: is there a causal relation between them?].

INTRODUCTION: Zinc is a fundamental trace element for an adequate nervous system function. It has been suggested that in the brain, a zinc homeostasis alteration may be associated with the genesis of epilepsy, although it is not yet determined if concentrations of zinc are a cause or a consequence of seizures. Another poorly studied aspect is the relationship between antiepileptic drugs and the neuronal zinc behaviour. DEVELOPMENT: We perform a systematic review of the literature to evaluate the role that zinc plays in epilepsy as well as the antiepileptic effect of zinc concentrations. Databases such as MEDLINE, EMBASE, SCISEARCH and LILACS were consulted from January 1974 to July 2005. All articles published in English and Spanish were considered. A manual review of the references present in each article was done in order to identify the articles that the electronic search may have not found itself. The title and abstract of the potential articles were analyzed before asking for the complete article. However, articles that seemed ambiguous were completely analyzed later to establish their relevance. CONCLUSIONS: Clinical research in epilepsy presented contradictory results. In fact, the reviewed studies, both animal and human, did not give enough evidence to determine if organic zinc variations are directly related to epilepsy. Most of them gave not statistically significant results.

Animals↗