Safety of percutaneous injection of bovine dermal crosslinked collagen for glottic insufficiency.

OBJECTIVE: Our aim was to review the safety of percutaneous injection laryngoplasty using bovine crosslinked collagen, focusing specifically on two often-stated concerns: injecting patients who are taking the anticoagulant medication warfarin, and injecting patients without prior skin hypersensitivity testing. STUDY DESIGN AND SETTING: Retrospective chart review of injection laryngoplasty performed between 1997 and 2006 at the University of California, Los Angeles. RESULTS: The study group consisted of 895 patients who underwent 1290 injection laryngoplasty procedures. No bleeding complications were noted in 59 patients taking warfarin. No allergic complications were reported in 845 patients who did not undergo skin hypersensitivity testing before injection laryngoplasty. CONCLUSION: Percutaneous bovine crosslinked collagen injection laryngoplasty is safe in patients taking warfarin. Skin testing for hypersensitivity does not appear to be necessary before injection. SIGNIFICANCE: Patients on warfarin are candidates for injection laryngoplasty without the need to discontinue the medication. Eliminating skin hypersensitivity testing before percutaneous bovine crosslinked collagen injection laryngoplasty allows for a prompt treatment of glottic insufficiency

Efeitos comportamentais, cognitivos e psicofisiológicos dos canabinoides: relevância para a psicose e a esquizofrenia Behavioral, cognitive and psychophysiological effects of cannabinoids: relevance to psychosis and schizophrenia

Avanços recentes no conhecimento sobre a função do receptor de canabinoide renovaram o interesse na associação entre cannabis e psicose. Linhas convergentes de evidências sugerem que os canabinoides podem produzir uma ampla gama de sintomas transitórios positivos, negativos e cognitivos assemelhados aos de esquizofrenia. Os canabinoides também produzem alguns déficits psicofisiológicos sabidamente presentes na esquizofrenia. É igualmente claro que em indivíduos com um transtorno psicótico estabelecido, os canabinoides podem exacerbar sintomas, desencadear recaídas e ter consequências negativas no curso da doença. Evidências crescentes sugerem que a exposição precoce e pesada à cannabis pode aumentar o risco de se desenvolver um transtorno psicótico como a esquizofrenia. A relação entre exposição à cannabis e esquizofrenia preenche alguns, mas não todos os critérios usuais de causalidade. Porém, a maioria das pessoas que utilizam cannabis não desenvolve esquizofrenia e muitas pessoas diagnosticadas com esquizofrenia nunca utilizaram cannabis. Portanto, é provável que a exposição à cannabis seja uma "causa componente" que interage com outros fatores para "causar" esquizofrenia ou outro transtorno psicótico, mas não é nem necessária nem suficiente para fazê-lo sozinha. No entanto, na ausência de causas conhecidas da esquizofrenia e com as implicações de políticas de saúde pública, se tal vínculo for estabelecido, as causas componentes, tais como a exposição a canabinoide, devem continuar sendo um foco de estudos futuros. Finalmente, são necessárias mais pesquisas para identificar os fatores subjacentes à vulnerabilidade à psicose relacionada a canabinoide e para elucidar os mecanismos biológicos subjacentes a esse risco.<br>Recent advances in knowledge about cannabinoid receptor function have renewed interest in the association between cannabis and psychosis. Converging lines of evidence suggest that cannabinoids can produce a full range of transient schizophrenia-like positive, negative and cognitive symptoms. Cannabinoids also produce some psychophysiological deficits also known to be present in schizophrenia. Also clear is that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Increasing evidence suggests that early and heavy cannabis exposure may increase the risk of developing a psychotic disorder such as schizophrenia. The relationship between cannabis exposure and schizophrenia fulfills some, but not all, of the usual criteria for causality. However, most people who use cannabis do not develop schizophrenia, and many people diagnosed with schizophrenia have never used cannabis. Therefore, it is likely that cannabis exposure is a "component cause" that interacts with other factors to "cause" schizophrenia or other psychotic disorder, but is neither necessary nor sufficient to do so alone. In the absence of known causes of schizophrenia, however, and the implications for public health policy should such a link be established the role of component causes such as cannabinoid exposure should remain a focus of further study. Finally, further work is necessary to identify the factors that underlie individual vulnerability to cannabinoid-related psychosis and to elucidate the biological mechanisms underlying this risk