Publications

OBJECTIVE

This study examined the contribution of perceived social support to the presence of anxiety in persons with chronic obstructive pulmonary disease (COPD).

METHODS

A cross-sectional survey sample of 452 persons with COPD (61.3% female; 53.5% older than 65; 70.8% without a college degree or higher educational achievement, and 54.8% with household income of $40,000 or less) completed a telephone survey. Measures included the anxiety subscale of the Hospital Anxiety and Depression Scale (HADS-A), 5 social support subscales from the Positive and Negative Social Exchanges (PANSE) Scale, a COPD Severity Score (CSS; a weighted algorithmic combination of symptoms and the need for various COPD medical interventions), and the Geriatric Depression Scale, Short Form (GDS-SF). Zero order correlations and a series of multiple regression analyses were calculated.

RESULTS

Multiple regression analysis revealed that the receipt of instrumental support, feeling let down by the failure of others to provide needed help, and unsympathetic or insensitive behavior from others each positively predicted a higher level of patient anxiety in COPD patients, after controlling for demographic variables, smoking status, comorbid depression (GDS) and severity of illness (CSS). Additionally, the control variable of depression was the strongest predictor of anxiety, suggesting a high degree of co-morbidity in this sample.

CONCLUSION

Anxiety and depression are serious co-morbid mental health concerns for persons with COPD. It is important to examine both positive and negative aspects of perceived social support for COPD patients and how they may impact or interact with these mental health concerns.

Systemic lupus erythematosus (SLE) is a chronic, disabling, progressive disease, with many associated comorbidities, affecting patients during prime working years resulting in a high economic burden on society, producing high direct, indirect and intangible costs. In this article, our goals are two-fold. First, we review and discuss studies published in the period 2002-2012 concerning costs of SLE and point out gaps in the published literature. Second, we propose further research studies to advance our understanding of the economic perspective in SLE in the current area of new and emerging therapies. The literature evaluating disease costs in SLE remains limited and to date has only included a small number of countries. Despite these limitations, available studies indicate that SLE has significant socio-economic ramifications. Future studies are needed, especially to assess novel biologic therapies which have been made available or currently under investigation for SLE. An interesting approach in these new economic evaluations in SLE may be represented by the selection of the targets of the treatment to include in the cost-effectiveness and cost-utility analyses. Future treat-to-target strategies will likely include evaluation of their pharmacoeconomic implications.

Viremic slow progressors (VSP) are a rare subset of HIV-infected persons who exhibit slow immunologic progression despite high viremia. The mechanisms associated with this slow progression remain to be defined. Clinical characteristics of VSP are similar to those of natural hosts for simian immunodeficiency virus (SIV), such as sooty mangabeys (SM) and African green monkeys (AGM), who maintain near-normal CD4 counts despite high-level viremia but maintain low immune activation. Immune activation is a powerful predictor of disease progression, and we hypothesized that low immune activation might also explain the VSP phenotype. Using multiparameter flow cytometry, we assessed levels of T cell activation and regulatory T cells (Treg) in blood and rectal mucosa of VSP, typical progressors, virologic controllers, and seronegative controls. We also assessed Treg function and CD4 T cell proliferative capacity in VSP. Contrary to expectations, we found that VSP subjects have high levels of T cell activation in the gastrointestinal mucosa. The ratio of Treg to CD3+ T cells in the mucosa of VSP was relatively low, potentially contributing to increased immune activation. Nonetheless, CD4+CD25- T cells isolated from these individuals displayed a comparatively weak proliferative response to anti-CD3 stimulation. These data reveal that the VSP phenotype is associated with elevated markers of mucosal immune activation and low numbers of mucosal Treg, suggesting that factors other than immune activation account for this phenotype.