Interações medicamentosas na clínica odontológica / Drug interactions in dental clinic

A interação medicamentosa é um assunto relevante para prática odontológica. O número de interações possíveis no dia a dia do cirurgião-dentista é imenso. O levantamento adequado dos fármacos contribui para que sejam diminuídas as possibilidades de interação que causem efeitos deletérios ao paciente. Dessa forma, o objetivo dessa pesquisa foi determinar as principais interações medicamentosas relatadas na literatura na prática odontológica utilizando uma ferramenta on-line (UpToDate®). Cabe ao profissional realizar uma adequada anamnese e avaliar as potenciais interações. Ferramentas on-line e aplicativos para dispositivos móveis podem auxiliar a análise das interações medicamentosas e proporcionar mais segurança ao profissional e ao paciente.

Drug interaction is a relevant issue in dental practice. The number of possible interactions in the everyday dentist is enormous. The adequate research of drugs contributes to diminish possibilities of interactions that cause deleterious effects to the patient. Therefore, the objective of this research was to determine major drug interactions reported in the literature in dental practice using an online tool (UpTo- Date®). The professional needs to conduct a proper interview and assess potential interactions. Online tools and applications for mobile devices can facilitate the analysis of drug interactions and provide more security for the dental professional and the patient.

Antiepileptic drugs prevent changes in adenosine deamination during acute seizure episodes in adult zebrafish.

Adenosine is an endogenous modulator of brain functions, which presents anticonvulsant properties. In addition, its levels can be increased during neural injury. The modulation of extracellular adenosine levels by ectonucleotidase and adenosine deaminase (ADA) activities may represent a key mechanism in the control of epileptogenesis. In the present study, we investigated the effects of acute seizure episodes and antiepileptic drug (AED) treatments on ectonucleotidases and ADA activities in adult zebrafish brain. Our data have demonstrated that pentylenetetrazole (PTZ)-induced seizures did not alter ATP, ADP, and AMP hydrolysis in brain membrane fractions. However, there was a significant increase on ecto-ADA and soluble ADA activities in PTZ-treated animals immediately after a clonus-like convulsion and loss of posture, which are typical behavioral changes observed in Stage 3. Furthermore, our results have demonstrated that AED pretreatments prevented the stimulatory effect promoted by PTZ exposure on ADA activities. The PTZ and AED treatments did not promote alterations on ADA gene expression. Interestingly, when exposed to PTZ, animals pretreated with AEDs showed longer latency to reach the clonus-like seizure status, which is an effect that matches the suppression of the increase of ADA activity promoted by the AEDs. These data suggest that the adenosine deamination could be involved in the control of seizure development in zebrafish and may be modulated by AED treatments.

PTZ-induced seizures inhibit adenosine deamination in adult zebrafish brain membranes.

Adenosine exerts neuromodulatory functions with mostly inhibitory effects, being considered an endogenous anticonvulsant. The hydrolysis of ATP by ectonucleotidases is an important source of adenosine, and adenosine deaminase (ADA) contributes to the regulation of this nucleoside concentration through its deamination. In this study, we tested the effect of pentylenetetrazole (PTZ)-induced seizures on ectonucleotidase and ADA activities in adult zebrafish brain. Our results have demonstrated that PTZ treatments did not alter ectonucleotidase and ADA activities in membranes and soluble fraction, respectively. However, ecto-ADA activity was significantly decreased in brain membranes of animals exposed to 5mM and 15 mM PTZ treatments (22.4% and 29.5%, respectively) when compared to the control group. Semiquantitative RT-PCR analysis did not show significant changes after the PTZ exposure on ADA gene expression. The decreased adenosine deamination observed in this study suggests a modulation of extracellular adenosine levels during PTZ-induced seizures in zebrafish.