Homelessness is a public health crisis. Homeless individuals have significantly worse health outcomes than the general population. We have begun examining challenges of caring for homeless patients with rheumatic and musculoskeletal diseases. Difficulties include physical environment, food and financial insecurity, access to healthcare, low health literacy, and comorbid mental illness, and substance abuse. Based on known prevalences of rheumatic and musculoskeletal diseases (RMSDs), we extrapolate that there are thousands of homeless with rheumatoid arthritis (RA), systemic lupus erythematosus, psoriatic arthritis, gout, and osteoarthritis. We present preliminary observations of disparities in the care of homeless patients with RA seen at the Los Angeles County Medical Center of the Keck School of Medicine of the University of Southern California. They tended to be African American males, missed appointments, utilized emergency services frequently, tended not to be on medications, and exhibited severe disease. We reviewed the available literature on homelessness and homeless healthcare to consider what further studies might be helpful and what interventions might improve the care of patients with RMSDs. We identified several aspirational and practical recommendations. These include ensuring access to healthcare for the homeless (indeed for all); reducing disparities through policy, tailored care, and enhanced social services; and recognizing and treating disease early. Developing better approaches for the care of these homeless has obvious and important implications for other underserved populations needing rheumatologic care, patients with early arthritis, or situations where rheumatologists are unavailable. We believe that physicians have a special responsibility to mitigate inequities in this particularly disadvantaged population.

BackgroundThe objective of this study was to identify serum biomarkers capable of predicting clinical outcomes in previously-treated NSCLC patients with wild-type for EGFR activating mutations or insufficient tissue for mutation status determination.MethodsSixty-six Luminex immunoassays representative of biological themes that emerged from a re-analysis of transcriptome data from the Cancer Genome Atlas (TCGA) were evaluate against pretreatment serum specimens from previously-treated advanced NSCLC patients received either cytotoxic chemotherapy (n=32) or erlotinib (n=79). Known EGFR mutation positive cases were excluded from analysis. Associations of biomarkers with outcome parameters and their differential interaction with treatment for survival outcomes were assessed using multivariate Cox PH analyses.ResultsOur EMT-based transcriptomic analysis revealed a range of biological processes associated with angiogenesis, apoptosis, cachexia, inflammation, and metabolism emerging as those most highly associated with patient outcome. These processes were evaluated via surrogate serum biomarkers. A treatment-biomarker interaction analysis revealed that higher pretreatment levels of c-Met signaling biomarkers (i.e. HGF levels), pro-inflammatory/ pro-cachexia (e.g. IL-8, sIL-2Rα, FGF-2) processes and a pro-angiogenic (e.g. TGF-α, IL-8, VEGF) milieu were associated with inferior survival (HR=0.35, 0.29, 0.58, 0.50, 0.61, 0.45, respectively; all p<0.05) for patients receiving chemotherapy, relative to erlotinib. In contrast, high levels of decoy receptor for IL-1, sIL-1RII, and a high tissue vimentin/E-cadherin ratio were associated with a poor OS (HR=3.78; p=0.00055) in the erlotinib cohort.ConclusionsContemporary precision medicine initiatives that pair patient tumor characteristics with the optimal therapy type may maximize the use of agents targeting EGFR in the treatment of NSCLC.

There is a well-known increased risk for cardiovascular disease that contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Major adverse cardiovascular events and subclinical atherosclerosis are both increased in this patient population. While traditional cardiac risk factors do contribute to the increased risk that is seen, lupus disease-related factors, medications, and genetic factors also impact the overall risk. SLE-specific inflammation, including oxidized lipids, cytokines, and altered immune cell subtypes all are likely to play a role in the pathogenesis of atherosclerotic plaques. Research is ongoing to identify biomarkers that can help clinicians to predict which SLE patients are at the greatest risk for cardiovascular disease (CVD). While SLE-specific treatment regimens for the prevention of cardiovascular events have not been identified, current strategies include minimization of traditional cardiac risk factors and lowering of overall lupus disease activity.