Background Patients with advanced cancer often experience frequent and prolonged hospitalizations; however factors associated with greater healthcare utilization have not been described. We sought to investigate the relationship between patients’ physical and psychological symptom burden and healthcare utilization. Methods We enrolled patients with advanced cancer and unplanned hospitalizations from September 2014-May 2016. Upon admission, we assessed physical (Edmonton Symptom Assessment System [ESAS]) and psychological symptoms (Patient Health Questionnaire 4 [PHQ-4]). We examined the relationship between symptom burden and healthcare utilization using linear regression for hospital length of stay (LOS) and Cox regression for time to first unplanned readmission within 90 days. We adjusted all models for age, sex, marital status, comorbidity, education, time since advanced cancer diagnosis, and cancer type. Results We enrolled 1,036 of 1,152 (89.9%) consecutive patients approached. Over half reported moderate/severe fatigue, poor well-being, drowsiness, pain, and lack of appetite. Using the PHQ-4, 29% and 28% of patients had depression and anxiety symptoms, respectively. Mean hospital LOS was 6.3 days and 90-day readmission rate was 43.1%. Physical symptoms (ESAS: B=0.06, P<.001), psychological distress (PHQ-4 total: B=0.11, P=.040), and depression symptoms (PHQ-4 depression: B=0.22, P=.017) were associated with longer hospital LOS. Physical (ESAS: HR=1.01, P<.001) and anxiety symptoms (PHQ-4 anxiety: HR=1.06, P=.045) were associated with a higher likelihood for readmission. Conclusions Hospitalized patients with advanced cancer experience a high symptom burden, which is significantly associated with prolonged hospitalizations and readmissions. Interventions are needed to address the symptom burden of this population to improve healthcare delivery and utilization.
AimsPatients with chronic heart failure (CHF) show impaired health-related quality of life (HRQoL), an important target for therapeutic intervention. Impaired iron homeostasis may be one mechanism underlying the poor physical condition of CHF patients. This detailed subanalysis of the previously published FAIR-HF study evaluated baseline HRQoL in iron-deficient patients with CHF and the effect of intravenous ferric carboxymaltose (FCM) on HRQoL.Methods and resultsFAIR-HF randomized 459 patients with reduced left ventricular ejection fraction and iron deficiency, with or without anaemia, to FCM or placebo (2:1). Health-related quality of life was assessed at baseline and after 4, 12, and 24 weeks of therapy using the generic EQ-5D questionnaire and disease-specific Kansas City Cardiomyopathy Questionnaire (KCCQ). Baseline mean Visual Analogue Scale (VAS) score was 54.3 ± 16.4 and KCCQ overall summary score was 52.4 ± 18.8. Ferric carboxymaltose significantly improved VAS and KCCQ (mean differences from baseline in KCCQ overall, clinical and total symptom scores, P< 0.001 vs. placebo) at all time points. At Week 24, significant improvement vs. placebo was observed in four of the five EQ-5D dimensions: mobility (P= 0.004), self-care (P< 0.001), pain/discomfort (P= 0.006), anxiety/depression (P= 0.012), and usual activity (P= 0.035). Ferric carboxymaltose improved all KCCQ domain mean scores from Week 4 onward (P≤ 0.05), except for self-efficacy and social limitation. Effects were present in both anaemic and non-anaemic patients.ConclusionsHRQoL is impaired in iron-deficient patients with CHF. Intravenous FCM significantly improved HRQoL after 4 weeks, and throughout the remaining study period. The positive effects of FCM were independent of anaemia status.
Chronic lymphocytic leukemia (CLL), the most common leukemia worldwide, is associated with increased COVID-19 mortality. Previous studies suggest only a proportion of vaccinated CLL patients develop SARS-CoV-2 spike antibodies. Whether the elicited antibodies are functional and/or accompanied by functional T-cell responses is unknown. This prospective cohort study (NCT05007860) included patients with CLL who received SARS-CoV-2 and PCV13 vaccines (not concurrently). The primary cohort included adults with CLL off therapy. Co-primary outcomes were serologic response to SARS-CoV-2 (receptor binding domain [RBD]-immunoassay) and PCV13 vaccines (23-serotype IgG assay). Characterization of SARS-CoV-2 antibodies and their functional activity and assessment of functional T-cell responses were performed. Sixty percent (18/30) of patients demonstrated serologic responses to SARS-CoV-2 vaccination, appearing more frequent among treatment-naïve patients (72%). Among treatment-naïve patients, an absolute lymphocyte count ≤24,000/uL was associated with serologic response (94% vs 14%, p<0.001). On interferon gamma release assays, 80% (16/20) of patients had functional spike-specific T-cell responses, including 78% (7/9) with a negative RBD-immunoassay, a group enriched for prior B-cell depleting therapies. A bead-based multiplex immunoassay identified antibodies against wildtype and variant SARS-CoV-2 (alpha, beta, gamma, and delta) in all tested patients, and confirmed Fc-receptor binding and effector functions of these antibodies. Of 11 patients with negative RBD-immunoassay post-vaccination, 6 (55%) responded to an additional mRNA-based vaccine dose. The PCV13 serologic response rate was 29% (8/28). Our data demonstrate that SARS-CoV-2 vaccination induces functional T-cell and antibody responses in CLL patients and provides the framework for investigating the molecular mechanisms and clinical benefit of these responses. This trial is registered at www.clinicaltrials.gov as NCT05007860.
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