Communication patterns in families affected by parental cancer from the healthy parents' perspective-process evaluation of the complex intervention Family-SCOUT.

PURPOSE: Within families affected by parental cancer, open communication impacts the well-being of parents and their children; however, limited research exists on communication patterns in these families. This sub-study addresses this through the Family-SCOUT study, a multicenter, prospective, interventional, and non-randomized investigation with intervention (IG) and control group (CG). The purpose of this sub-study was to identify and compare the differences in communication patterns between the IG and CG as part of the process evaluation. The research question was addressed in both groups: What communication patterns do healthy parents perceive within their families? METHODS: Using a qualitative approach, the study involved interviewing healthy parents as surrogates for their families. The interviews were audio-recorded, transcribed, and coded using a template analysis. The resulting data were analyzed at the group level. RESULTS: Twenty-three interviews were conducted in the IG and 27 interviews in the CG. The analysis of themes centered on communication patterns as seen in the family structure. Both groups exhibited instances of open communication about fears and wishes as well as the use of child-friendly language when discussing cancer. Notable differences were observed: challenges in open communication with children were sorely reported in CG interviews, and "the illness is discussed when necessary" was sorely described in IG interviews. CONCLUSION: This study underscores the need to address and encourage open communication within families with parental cancer.

Effectiveness of a comprehensive support program for families with parental cancer (Family-SCOUT): results of a multicenter non-randomized controlled trial.

BACKGROUND: Cancer patients with minor children but also their families suffer from significant psychological distress and comorbidity. Protective factors predicting successful coping are well known. Corresponding systematic interventions are rare and limited by access barriers. We developed a comprehensive family-centered intervention for cancer patients with at least one dependent minor. PATIENTS AND METHODS: Family-SCOUT represents a multicentric, prospective, interventional, and controlled study for families with parental cancer and their minor children. In the intervention group (IG), all family members were addressed using a care and case management approach for nine months. Families in the control group (CG) received standard of care. Participating parents were asked to complete the Hospital-Anxiety-Depression-Scale (HADS) questionnaire at enrolment (T0) and after 9 months (T2). The primary outcome was a clinically relevant reduction of distress in at least one parent per family, measured as minimal important difference (MID) of ≥1.6 in the HADS total score. The percentage of families achieving MID is compared between the IG and CG by exact Fisher's test, followed by multivariate confounder analyses. RESULTS: T0-questionnaire of at least one parent was available for 424 of 472 participating families, T2-questionnaire after 9 months was available for 331 families (IG n = 175, CG n = 156). At baseline, both parents showed high levels of distress (HADS total: sick parents IG: 18.7 ± 8.1; CG: 16.0 ± 7.2; healthy partners: IG: 19.1 ± 7.9; CG: 15.2 ± 7.7). The intervention was associated with a significant reduction in parental distress in the IG (MID 70.4% in at least one parent) compared with the CG (MID 55.8%; P = 0.008). Adjustment for group differences from specific confounders retained significance (P = 0.047). Bias from other confounders cannot be excluded. CONCLUSIONS: Parental cancer leads to a high psychosocial burden in affected families. Significant distress reduction can be achieved through an optimized and structured care approach directed at the family level such as family-SCOUT.

Atherosclerosis and vascular calcification in uraemia - a new experimental model.

Cardiovascular disease (CVD) is the most frequent cause of morbidity and mortality in chronic renal failure (CRF) patients. Accelerated calcifying atherosclerosis, medial calcification, and valvular calcification are hallmarks of CVD in the dialysis population. The mechanisms by which uraemia promotes vascular calcification and the relationship between arterial wall calcification and atherosclerosis are poorly understood. We surgically induced CRF in apolipoprotein E knockout (apoE-/-) mice to study a possible acceleration of aortic atherosclerosis, the degree and type of vascular calcification as well as factors involved in the calcification process. Finally we investigated appropriate treatment measures. Atherosclerotic lesions in the thoracic aorta were significantly larger in uraemic apoE-/- mice than in non-uraemic controls. The relative proportion of the calcified area to the total surface area of both atherosclerotic lesions and lesion-free vascular tissue was increased in the aortic root of uraemic apoE-/- mice when compared with controls. The accelerated atherosclerosis was associated with an increase in aortic nitrotyrosine expression, indicating enhanced oxidative stress, and an increase in plaque collagen content, indicating changes in plaque composition. N-acetylcysteine (NAC) treatment slowed the rapid progression of atherosclerotic lesions and reversed the increase in plaque collagen content compared with placebo treatment. NAC-treatment also reduced nitrotyrosine expression in uremic apoE-/- mice whereas the degree of macrophage infiltration was unchanged. Sevelamer treatment delayed not only vascular calcification but also atherosclerotic lesion progression in uraemic apoE-/- mice. These treatment effects also were associated with diminished oxidative stress and were independent of cholesterol lowering. We anticipate that this experimental model will prove to be useful to test other treatment strategies aimed at decreasing the accelerated atherosclerosis and arterial calcification of the uraemic state.