Impact of caregiver burden on health-related quality of life and family functioning of carers of children with epilepsy at the Charlotte Maxeke Johannesburg Academic Hospital, South Africa

Background. The impact of caring for a child with a chronic disease on caregivers and their family functioning contributes to the child's adaptation to the disease.Objectives. To determine the impact of caregiver burden on the health-related quality of life (HRQOL) and family functioning of carers of children with epilepsy (CWE), and to determine factors associated with a high impact of caregiver burden.Method. A cross-sectional study was conducted among primary caregivers of CWE attending the Charlotte Maxeke Johannesburg Academic Hospital, South Africa. Participants had been involved in childcare for at least 6 months before study enrolment and all gave informed consent. Data regarding sociodemographic and epilepsy-related variables were obtained from questionnaires, including the 36-item family impact module of the Pediatric Quality of Life assessment tool. Scores in the lower quartile were considered indicative of a negative impact on HRQOL and poor family functioning.Results. Participants identified as experiencing a high impact of paediatric epilepsy care reported raw scores ≤31.3 for both caregiver burden and family functioning. The family functioning score correlated strongly with the caregivers' HRQOL score (p=0.78; p<0.001). Multivariate analysis identified a low level of education among caregivers and a high seizure frequency in patients as independent predictors of caregiver burden associated with a negative impact.Conclusion. Our findings suggest that the burden of caregiving in paediatric epilepsy among our study population impacts negatively on family functioning. The burden of care was associated with a low level of caregiver education and a high seizure frequency in their children

Reduction in lactate accumulation correlates with differentiation-induced terminal cell division of leukemia cells.

Lactate accumulation in the medium and glucose utilization decreased during the induction of in vitro differentiation of mouse erythroleukemia (MEL) and human myeloid leukemia (HL-60) cells. The decrease in lactate accumulation occurred as early as 24 h after inducer treatment was initiated and occurred prior to the decrease in glucose utilization. The decrease in lactate accumulation was greater than that predicted by the decrease in glucose utilization, i.e., the ratio of glucose used glycolytically, as measured by lactate accumulation, to glucose used in other pathways ('glycolytic ratio') markedly decreased during differentiation in these cell lines. Differentiation correlated with the abrogation of the high levels of lactate accumulation first described by Warburg as characteristic of some transformed and neoplastic cells. Studies on both parental and differentiation-resistant variant MEL cell lines indicated that the changes in lactate accumulation were not dependent on the changes in glucose utilization and could be dissociated from them. Moreover, the changes in lactate accumulation only occurred in cells able to undergo differentiation-induced terminal cell division. This regulatable expression of lactate accumulation in MEL and HL-60 cells in vitro may make them useful model systems for the elucidation of the molecular mechanisms controlling lactate formation in malignant cells.