Parental distress - a predictor of treatment adherence in pediatric neuroblastoma: a cross-sectional study of chinese families.
This cross-sectional study examined whether parental distress is associated with treatment adherence in children with neuroblastoma and identified specific parental psychological factors as independent risk markers for non-adherence.
Three hundred fifty families from four tertiary medical centers in China were enrolled. Parents completed the Parenting Stress Index-Short Form (PSI-SF), Medication Adherence Rating Scale (MARS-5), Beck Depression Inventory-II (BDI-II), and Family Assessment Device-General Functioning (FAD-GF). Path analysis examined associations between parental distress, family functioning, disease risk, and treatment adherence. Common method bias was assessed using Harman's single-factor test. Sensitivity analyses examined MARS-5 cutoff robustness using median split and MARS-5 < 18 thresholds.
Parental distress was significantly associated with lower treatment adherence (beta = -0.35, p = 0.002). Family functioning was statistically consistent with partial mediation (indirect beta = -0.12, p = 0.003), though causal interpretation is precluded by the cross-sectional design. Paternal depressive symptoms emerged as the strongest independent risk marker for non-adherence (OR = 2.2, 95% CI 1.18-4.09, p = 0.013). Mothers reported significantly higher parenting stress than fathers (Bonferroni-corrected p < 0.008; Cohen's d = 0.37-0.62). Families with poor functioning were 2.8 times more likely to exhibit suboptimal adherence. Harman's single-factor test yielded 8 factors with eigenvalues > 1.0, with the first factor explaining 28.4% of total variance-below the 40% threshold indicative of substantial common method bias. Sensitivity analyses using alternative MARS-5 cutoffs confirmed the robustness of paternal depression and family functioning as predictors.
Parental distress, particularly paternal depressive symptoms, represents a modifiable risk marker associated with treatment non-adherence. Screening for paternal psychological distress and family dysfunction may support treatment adherence in pediatric neuroblastoma. Given the cross-sectional design, these associations should be interpreted as concurrent rather than causal.
Three hundred fifty families from four tertiary medical centers in China were enrolled. Parents completed the Parenting Stress Index-Short Form (PSI-SF), Medication Adherence Rating Scale (MARS-5), Beck Depression Inventory-II (BDI-II), and Family Assessment Device-General Functioning (FAD-GF). Path analysis examined associations between parental distress, family functioning, disease risk, and treatment adherence. Common method bias was assessed using Harman's single-factor test. Sensitivity analyses examined MARS-5 cutoff robustness using median split and MARS-5 < 18 thresholds.
Parental distress was significantly associated with lower treatment adherence (beta = -0.35, p = 0.002). Family functioning was statistically consistent with partial mediation (indirect beta = -0.12, p = 0.003), though causal interpretation is precluded by the cross-sectional design. Paternal depressive symptoms emerged as the strongest independent risk marker for non-adherence (OR = 2.2, 95% CI 1.18-4.09, p = 0.013). Mothers reported significantly higher parenting stress than fathers (Bonferroni-corrected p < 0.008; Cohen's d = 0.37-0.62). Families with poor functioning were 2.8 times more likely to exhibit suboptimal adherence. Harman's single-factor test yielded 8 factors with eigenvalues > 1.0, with the first factor explaining 28.4% of total variance-below the 40% threshold indicative of substantial common method bias. Sensitivity analyses using alternative MARS-5 cutoffs confirmed the robustness of paternal depression and family functioning as predictors.
Parental distress, particularly paternal depressive symptoms, represents a modifiable risk marker associated with treatment non-adherence. Screening for paternal psychological distress and family dysfunction may support treatment adherence in pediatric neuroblastoma. Given the cross-sectional design, these associations should be interpreted as concurrent rather than causal.