RESUMEN
The experience of childhood cancer can be one of the most severe stressors that parents endure. Studies using illness-specific measures of parental stress indicate that moderate-to-severe parenting stress is quite common in the first year of childhood cancer treatment, and as many as 5% to 10% of these parents go on to develop posttraumatic stress disorder. This review of the literature suggested that although parenting stress symptoms may be relatively transitory for most parents dealing with childhood cancer, the impact of these stress symptoms on parent and child functioning is substantive and worthy of therapeutic attention. The stresses entailed in childhood cancer should be viewed as complex and varied across stages of diagnosis and treatment. Factors associated with increased risk of parental posttraumatic stress symptoms include poor social support, adverse experience with invasive procedures, negative parental beliefs about the child's illness and/or associated treatment, and trait anxiety. For those parents with risk factors that might forebode more severe and enduring stress reactions to their children's cancer, therapeutic strategies are proposed to ameliorate their stress and reduce the development and/or maintenance of posttraumatic stress symptoms.
Asunto(s)
Neoplasias/psicología , Relaciones Padres-Hijo , Padres/psicología , Estrés Psicológico , Adulto , Ansiedad , Actitud Frente a la Salud , Niño , Cultura , Femenino , Humanos , Masculino , Salud Mental , Cooperación del Paciente , Apoyo Social , Resultado del TratamientoRESUMEN
We report on a child with a family history of autoimmune defects, who presented at the age of 3(1/2) years with alopecia and Graves disease. He subsequently developed vitiligo and psoriasis. At 9(1/2) years, he developed an autoimmune form of Lambert-Eaton Myasthenic syndrome (LEMS) with a significant elevation of glutamic acid decarboxylase (GAD) autoantibodies. Shortly thereafter he developed chronic urticaria. HLA associations were present for Graves disease, vitiligo, psoriasis, and IgA deficiency. There was also evidence of autoimmunity involving the pancreatic islet cells and gastric parietal cells.