RESUMO
Objetivo: Evaluar las complicaciones asociadas a la miomectomía laparotómica y a la embolización de las arterias uterinas en mujeres con miomas sintomáticos. Métodos: Estudio descriptivo restrospectivo efectuado en el Complejo Hospitalario Universitario de Vigo desde el año 2008 al 2010. La población en estudio la conformaron aquellas mujeres sometidas a una miomectomía laparotómica o a una embolización de las arterias uterinas. Se recopilaron las complicaciones registradas en las historias clínicas de las pacientes tras las técnicas. Resultados: La tasa de complicaciones en el grupo de las pacientes sometidas a miomectomía fue de 15,2 por ciento; las más frecuentes fueron fiebre, anemia, necesidad de trasfusión y hematoma subcutáneo. La tasa de complicaciones en el grupo de embolización fue de 4,5 por ciento recogiéndose casos de síndrome postembolización, mioma parido y un caso de histerectomía. Conclusión: La adecuada indicación de cada técnica es fundamental para tener una baja tasa de complicaciones. Se debe tener en cuenta la sintomatología, tipo y número de miomas, edad y deseo genésico de cada paciente.
Objective: This study was undertaken to evaluate the complications after laparotomy myomectomy and uterine artery embolization in women with symptomatic uterine leiomyoma. Methods: This was a descriptive and retrospective study of patients who were treated with embolization and myomectomy for leiomyomas from 2008-2010. Complications were measured. Results: The rate of complications collected in the myo-mectomy group was 15.2 percent; there were cases of fever, anemia, need for transfusion and subcutaneous hematoma. The rate of complications collected in the embolization group was 4.5 percent; there were cases of embolization syndrome, transcervical fibroid expulsion and a case of hysterectomy. Conclusion: The suitable indication of every tecnic is fundamental to have a low rate of complications. It is necessary to bear in mind the symptomatology, type and number of myomas and age and reproductive desire of each patient.
Assuntos
Pessoa de Meia-Idade , Embolização da Artéria Uterina/métodos , Leiomioma/terapia , Neoplasias Uterinas/terapia , Evolução Clínica , Embolização da Artéria Uterina/efeitos adversos , Fertilidade , Tempo de Internação , Leiomioma/cirurgia , Neoplasias Uterinas/cirurgia , Complicações Pós-Operatórias , Reoperação , Estudos Retrospectivos , Resultado do TratamentoRESUMO
Hyperosmotic stress promotes rapid and pronounced apoptosis in cultured cardiomyocytes. Here, we investigated if Ca(2+) signals contribute to this response. Exposure of cardiomyocytes to sorbitol [600 mosmol (kg water)(-1)] elicited large and oscillatory intracellular Ca(2+) concentration increases. These Ca(2+) signals were inhibited by nifedipine, Cd(2+), U73122, xestospongin C and ryanodine, suggesting contributions from both Ca(2+) influx through voltage dependent L-type Ca(2+) channels plus Ca(2+) release from intracellular stores mediated by IP(3) receptors and ryanodine receptors. Hyperosmotic stress also increased mitochondrial Ca(2+) levels, promoted mitochondrial depolarization, reduced intracellular ATP content, and activated the transcriptional factor cyclic AMP responsive element binding protein (CREB), determined by increased CREB phosphorylation and electrophoretic mobility shift assays. Incubation with 1 mM EGTA to decrease extracellular [Ca(2+)] prevented cardiomyocyte apoptosis induced by hyperosmotic stress, while overexpression of an adenoviral dominant negative form of CREB abolished the cardioprotection provided by 1 mM EGTA. These results suggest that hyperosmotic stress induced by sorbitol, by increasing Ca(2+) influx and raising intracellular Ca(2+) concentration, activates Ca(2+) release from stores and causes cell death through mitochondrial function collapse. In addition, the present results suggest that the Ca(2+) increase induced by hyperosmotic stress promotes cell survival by recruiting CREB-mediated signaling. Thus, the fate of cardiomyocytes under hyperosmotic stress will depend on the balance between Ca(2+)-induced survival and death pathways.