Avaliação das alterações do sono em pacientes com doença inflamatória intestinal e a relação com períodos de remissão e atividade da doença
Data
2017-06-14
Tipo
Dissertação de mestrado
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Introdução: A patogênese da DII não está definida, entretanto, fatores genéticos, imunológicos e ambientais são reportados como possíveis desencadeadores. Distúrbios do sono com alteração no ciclo circadiano, que afetam o sistema imune, têm sido descritos como potencial gatilho e/ou fator predisponente para ativação da doença, contribuindo para a piora do quadro clínico. Dessa forma, se faz necessário caracterizar esses distúrbios nesse grupo de pacientes. Objetivo: Avaliar a qualidade do sono nos pacientes com DII e relacioná-los aos períodos de atividade ou remissão da doença. Casuística e Método: Uma amostra de conveniência com 20 participantes foi incluída, sendo 11 com RCUI e nove participantes com DC (sete com doença ativa e 13 em remissão). Foram realizados exames de polissonografia e aplicados dois questionários: índice de qualidade do sono de Pittsburgh (PSQI) e escala modificada de impacto de fadiga (MIFS). As interleucinas IL-6, IL-10 e TNF-α foram mensuradas por ELISA no soro dos participantes. Os dados foram analisados por estatística descritiva, teste de normalidade, teste Exato de Fisher, teste t/Mann Whitney e teste de correlação de Spearman. Resultados: A latência do sono nos participantes com a doença ativa foi de, em média, 133,07 minutos e em remissão, foi de 106,79 minutos. A eficiência do sono foi de 80,90% na doença ativa e 84,20% em remissão. O escore total do PSQI foi igual ou maior que cinco para todos os voluntários incluídos no estudo, o que denota uma má qualidade do sono. No MIFS, observamos diferença significativa entre doença ativa e remissão (p=0,032), onde a maioria dos participantes com a doença em remissão relataram ausência de fadiga. Na análise da dosagem das interleucinas observamos valores aumentados em ambos os grupos. Conclusão: Não houve alterações significativas na qualidade do sono dos participantes por meio do exame de polissonografia, independentemente da fase da doença. Entretanto, houve um aumento na queixa dos participantes em relação a qualidade do sono e sintomas de fadiga por meio dos questionários aplicados. Os valores séricos das citocinas IL-6 e TNF-α estão aumentados nesses pacientes, independente da fase da doença, no entanto não foi possível estabelecer correlação entre os parâmetros. Sugerimos o acompanhamento da qualidade do sono nesse grupo de pacientes e um estudo mais amplo para elucidar essas alterações.
Introduction: The pathogenesis of IBD is not well understood, but genetic, immunological and environmental factors have been linked to these diseases. Sleep disorders with alterations in the circadian cycle affect the immune system and are described as potential triggers and/or predisposing factors for activation of the disease, contributing to impair the clinical condition. Therefore, it is necessary to characterize such disorders in this group of patients. Aim: To evaluate sleep quality in patients with IBD and associate them with periods of disease. Methods: 20 participants were inlcuded in this study: 11 patients with UC and 9 patients with CD (7 with active disease and 13 in remission). Polysomnography tests were performed and two questionnaires were applied: Pittsburgh Sleep Quality Index (PSQI) and Modified Fatigue Impact Scale (MIFS). Interleukins IL-6, IL-10 and TNF-α were measured by ELISA using participant´s serum. Data were analyzed using descriptive statistics, normality test, Fisher´s exact test, t/Mann-Whitney test and Spearman´s correlation test. Results: Sleep latency in patients with active disease was, on average, 133.07 minutes while in remission was 106.79 minutes. In sleep efficiency, we observed patients with active disease presenting mean values of 80.90% while in remission was 84.20%. The assessment of sleep fragmentation (WASO), our results demonstrated mean of 76.35/min in patients with active disease and 69.81/min in remission. The total PSQI score was equal to or greater than five for all volunteers included in this study, which indicates poor sleep quality. MIFS a significant difference between active disease and remission (p = 0.032) was observed, where most of participants with disease in remission reported absence of fatigue. The analysis of the interleukin dosage showed increased values in both groups. Conclusion: There were no significant changes in sleep quality through polysomnography regardless of disease stage. However, there was an increase in participant´s complaints regarding sleep quality and fatigue symptoms through the application of questionnaires. Serum cytokines IL-6 and TNF-α were increased in these patients regardless of disease stage, however, it was not possible to establish a correlation between the parameters. We suggest the follow-up in monitoring the sleep quality of these patients as well as a large-scale study to elucidate these alterations.
Introduction: The pathogenesis of IBD is not well understood, but genetic, immunological and environmental factors have been linked to these diseases. Sleep disorders with alterations in the circadian cycle affect the immune system and are described as potential triggers and/or predisposing factors for activation of the disease, contributing to impair the clinical condition. Therefore, it is necessary to characterize such disorders in this group of patients. Aim: To evaluate sleep quality in patients with IBD and associate them with periods of disease. Methods: 20 participants were inlcuded in this study: 11 patients with UC and 9 patients with CD (7 with active disease and 13 in remission). Polysomnography tests were performed and two questionnaires were applied: Pittsburgh Sleep Quality Index (PSQI) and Modified Fatigue Impact Scale (MIFS). Interleukins IL-6, IL-10 and TNF-α were measured by ELISA using participant´s serum. Data were analyzed using descriptive statistics, normality test, Fisher´s exact test, t/Mann-Whitney test and Spearman´s correlation test. Results: Sleep latency in patients with active disease was, on average, 133.07 minutes while in remission was 106.79 minutes. In sleep efficiency, we observed patients with active disease presenting mean values of 80.90% while in remission was 84.20%. The assessment of sleep fragmentation (WASO), our results demonstrated mean of 76.35/min in patients with active disease and 69.81/min in remission. The total PSQI score was equal to or greater than five for all volunteers included in this study, which indicates poor sleep quality. MIFS a significant difference between active disease and remission (p = 0.032) was observed, where most of participants with disease in remission reported absence of fatigue. The analysis of the interleukin dosage showed increased values in both groups. Conclusion: There were no significant changes in sleep quality through polysomnography regardless of disease stage. However, there was an increase in participant´s complaints regarding sleep quality and fatigue symptoms through the application of questionnaires. Serum cytokines IL-6 and TNF-α were increased in these patients regardless of disease stage, however, it was not possible to establish a correlation between the parameters. We suggest the follow-up in monitoring the sleep quality of these patients as well as a large-scale study to elucidate these alterations.