Publication: Tratamiento con heparina tópica en pacientes con síndrome eritrosidestésico palmo plantar asociado a capecitabina y estudio de su mecanismo fisiopatológico
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2017-02-24
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Universidad Complutense de Madrid
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Abstract
El síndrome palmo-plantar (SPP) es un efecto adverso, asociado a distintas quimioterapias sistémicas, más frecuentemente secundario a fluoropirimidinas orales como Capecitabina (Xeloda®). Su incidencia se estima entre un 36 y un 68 % de los pacientes sometidos a este tratamiento. Generalmente no amenaza la vida del paciente y rara vez requiere hospitalización.(Childress and Lokich, 2003, Abushullaih et al., 2002) El tratamiento es la suspensión del quimioterápico, modificación de dosis hasta mejoría sintomática y medidas de soporte.(Gressett et al., 2006) La discontinuación del agente causal determina la regeneración de la piel en 1 a 2 semanas, en función del grado y estadio. La fisiopatología del SPP no está establecida. Los cambios clínicos e histológicos que se observan son compatibles con daños en la barrera fisiológica de la piel.(Degen et al., 2010) Entre los hallazgos anatomopatológicos descritos se encuentran cambios inflamatorios inespecíficos como infiltración linfocitaria, dilatación de vasos sanguíneos y edema, marcada hiperqueratosis con paraqueratosis y queratinocitos apoptóticos. (Gressett et al., 2006, Scotte et al., 2005, Scheithauer and Blum, 2004)...
The Hand Foot Syndrome or Palmar–Plantar Erythrodysesthesia Syndrome (PPS) is an adverse effect, associated with various systemic chemotherapy, as Capecitabine (Xeloda). Incidence is estimated between 36 and 68% of patients undergoing this treatment. Usually it is not life threatening for the patient and rarely requires hospitalization. (Childress and Lokich, 2003, Abushullaih et al., 2002) Treatment is chemotherapy discontinuation, dose modification to symptomatic improvement and supportive measures. (Gressett et al., 2006) Discontinuing the causal agent determines skin regeneration in 1 to 2 weeks, depending on the grade and stage. The pathophysiology of PPS is not established. Clinical and histological changes observed are consistent with damage to the physiological barrier of the skin. (Degen et al., 2010). Among the pathologic findings are described as nonspecific inflammatory changes, lymphocytic infiltration, dilation of blood vessels and edema, marked hyperkeratosis with parakeratosis and apoptotic keratinocytes. (Gressett et al., 2006, Scotte et al., 2005, Scheithauer and Blum, 2004) The selective engagement of the dermis of palms and soles, with epithelial cell damage, suggesting a direct toxic effect on keratinocytes of the basal layer. Probably the main pathophysiological mechanism of PPS, although there are different theories. (Gressett et al., 2006, Narasimhan et al., 2004) The first theory relates PPS with increased levels of the enzyme Thymidine Phosphorylase (TP) in specialized skin cells (keratinocytes) that determines the accumulation of active metabolites of Capecitabine in the epidermis, leading to an increased chance of developing this side effect...
The Hand Foot Syndrome or Palmar–Plantar Erythrodysesthesia Syndrome (PPS) is an adverse effect, associated with various systemic chemotherapy, as Capecitabine (Xeloda). Incidence is estimated between 36 and 68% of patients undergoing this treatment. Usually it is not life threatening for the patient and rarely requires hospitalization. (Childress and Lokich, 2003, Abushullaih et al., 2002) Treatment is chemotherapy discontinuation, dose modification to symptomatic improvement and supportive measures. (Gressett et al., 2006) Discontinuing the causal agent determines skin regeneration in 1 to 2 weeks, depending on the grade and stage. The pathophysiology of PPS is not established. Clinical and histological changes observed are consistent with damage to the physiological barrier of the skin. (Degen et al., 2010). Among the pathologic findings are described as nonspecific inflammatory changes, lymphocytic infiltration, dilation of blood vessels and edema, marked hyperkeratosis with parakeratosis and apoptotic keratinocytes. (Gressett et al., 2006, Scotte et al., 2005, Scheithauer and Blum, 2004) The selective engagement of the dermis of palms and soles, with epithelial cell damage, suggesting a direct toxic effect on keratinocytes of the basal layer. Probably the main pathophysiological mechanism of PPS, although there are different theories. (Gressett et al., 2006, Narasimhan et al., 2004) The first theory relates PPS with increased levels of the enzyme Thymidine Phosphorylase (TP) in specialized skin cells (keratinocytes) that determines the accumulation of active metabolites of Capecitabine in the epidermis, leading to an increased chance of developing this side effect...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Medicina, Departamento de Medicina, leída el 25-01-2016