RESUMEN
AIM: XELOX and FOLFOX4 have both been recommended as adjuvant therapy for stage III colon cancer. This study compared the two regimens in terms of monetary costs, assuming equal efficacy of the therapies. METHOD: A retrospective financial audit was conducted of the medical records of patients treated with XELOX or FOLFOX4. All itemized expenses were classified as direct (chemotherapy, hospitalization, venous access and tests), related to adverse effects due to the adjuvant therapy, or societal (travel and time costs). The cost of supportive care was not included. RESULTS: XELOX involved less total cost to the patient than FOLFOX4 (a difference of US$2857.68), fewer costs related to adverse effects ($668.97), and less travel ($26.07) and time ($390.93) expenditure per patient. CONCLUSION: The results indicate that, overall, XELOX is a more affordable option than FOLFOX4 in China.
Asunto(s)
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Quimioterapia Adyuvante/economía , Neoplasias del Colon/tratamiento farmacológico , Costo de Enfermedad , Desoxicitidina/análogos & derivados , Fluorouracilo/análogos & derivados , Hospitalización/economía , Protocolos de Quimioterapia Combinada Antineoplásica/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/economía , Capecitabina , Quimioterapia Adyuvante/efectos adversos , China , Neoplasias del Colon/economía , Desoxicitidina/efectos adversos , Desoxicitidina/economía , Desoxicitidina/uso terapéutico , Femenino , Fluorouracilo/efectos adversos , Fluorouracilo/economía , Fluorouracilo/uso terapéutico , Humanos , Leucovorina/efectos adversos , Leucovorina/economía , Leucovorina/uso terapéutico , Masculino , Persona de Mediana Edad , Compuestos Organoplatinos/efectos adversos , Compuestos Organoplatinos/economía , Compuestos Organoplatinos/uso terapéutico , Oxaloacetatos , Estudios Retrospectivos , Resultado del TratamientoRESUMEN
Familial vitamin E deficiency (AVED) causes ataxia and peripheral neuropathy that resembles Friedreich's ataxia. AVED is thought to be caused by a defect in the transport of vitamin E in liver cells, which is the probable function of alpha-tocopherol transfer protein (alphaTTP). We have cloned the cDNA and several genomic phage clones covering the entire human alphaTTP gene and determined the junctions between the five exons and four introns that composed the gene for human alphaTTP. Three mutations in three unrelated North American families with AVED were identified. Two mutations, 485delT and 513insTT, cause a frame shift and a premature stop codon and the third mutation 574G-->A would substitute Arg192 to His in alphaTTP. The 2 patients with a severe form of AVED were homozygous with 485delT and 513insTT, respectively, while the patient with a mild form of the disease was compound heterozygous with 513insTT and 574G-->A. These findings have identified the underlying genetic defect in AVED and have confirmed the role of alphaTTP in AVED.