Promoting health equity in the health-care system: How can we identify potentially vulnerable patients?

BACKGROUND: There is documented social inequality in cancer. The health-care system may contribute to health equity by targeting interventions to potentially vulnerable patients who may be at risk of not receiving optimal treatment and care. AIM: This study aimed to develop and pilot test a tool to identify patients who may need additional support. METHOD: The study took place in a department of palliative medicine and in a team for head and neck cancer within an oncology department. The tool to identify potentially vulnerable patients was developed based on literature reviews and interviews with patients and health-care personnel. It was pilot tested in a six-month period, with subsequent interviews with health-care personnel. RESULTS: In total, 212 consecutive patients referred to the departments were systematically screened with the tool by health-care personnel. Of these, 74 (35%) patients were considered potentially vulnerable. The most frequently reported sign of vulnerability was 'few supportive relations' (47% of the vulnerable patients). Most health-care personnel found it relevant to focus systematically on these patients. However, some were concerned that using the tool could prove to be stigmatising and were critical of attributing the vulnerability to the individual. CONCLUSIONS: Most patients were considered in need of additional support because they lacked a social network or had difficulties communicating with health-care personnel. Applying a tool to identify potentially vulnerable patients was feasible and increased attention to this group of patients. However, the screening procedure was also questioned.

Trafficking, localization and degradation of the Na+,HCO3- co-transporter NBCn1 in kidney and breast epithelial cells.

The Na+;HCO3- co-transporter NBCn1 (SLC4A7) is a major regulator of intracellular pH yet its trafficking and turnover are essentially unstudied. Here, we used MDCK-II and MCF-7 cells to investigate these processes in epithelial cells. GFP-NBCn1 membrane localization was abolished by truncation of the full NBCn1 C-terminal tail (C-tail) yet did not require the C-terminal PDZ-binding motif (ETSL). Glutathione-S-Transferase-pulldown of the C-tail followed by mass spectrometry analysis revealed putative interactions with multiple sorting-, degradation- and retention factors, including the scaffolding protein RACK1. Pulldown of FLAG-tagged deletion constructs mapped the RACK1 interaction to the proximal NBCn1 C-tail. Proximity Ligation Assay and co-immunoprecipitation confirmed that native NBCn1 interacts with RACK1 in a cellular context. Consistent with a functional role of this complex, RACK1 knockdown reduced NBCn1 membrane localization without affecting total NBCn1 expression. Notably, only non-confluent cells exhibited detectable NBCn1-RACK1 plasma membrane co-localization, suggesting that RACK1 regulates the trafficking of NBCn1 to the membrane. Whereas total NBCn1 degradation was slow, with a half-life of more than 24 h, one-third of surface NBCn1 was constitutively endocytosed from the basolateral membrane within 60 min. This suggests that a fraction of NBCn1 exhibits recycling between the basolateral membrane and intracellular compartment(s). Our findings have important implications for understanding NBCn1 regulation as well as its dysregulation in disease.