Publications

OBJECTIVE

To examine the relationship between cardiac self-efficacy and health status, including symptom burden, physical limitation, quality of life, and overall health among outpatients with stable coronary heart disease (CHD). We hypothesized that lower self-efficacy would predict worse health status, independent of CHD severity and depression.

METHODS

We performed a cross-sectional study of 1024 outpatients with CHD, who were recruited between 2000 and 2002 for the Heart and Soul Study. We administered a validated measure of cardiac self-efficacy, assessed cardiac function using exercise treadmill testing with stress echocardiography, and measured depressive symptoms using the Patient Health Questionnaire. Health status outcomes (symptom burden, physical limitation, and quality of life) were assessed using the Seattle Angina Questionnaire, and overall health was measured as fair or poor (versus good, very good, or excellent).

RESULTS

After adjustment for CHD severity and depressive symptoms, each standard deviation (4.5-point) decrease in self-efficacy score was independently associated with greater symptom burden (adjusted odds ratio (OR) = 2.1, p = .001), greater physical limitation (OR = 1.8, p < .0001), worse quality of life (OR = 1.6, p < .0001), and worse overall health (OR = 1.9, p < .0001). Depressive symptoms and poor treadmill exercise capacity were also associated with poor health status, but left ventricular ejection fraction and ischemia were not.

CONCLUSIONS

Among patients with CHD, low cardiac self-efficacy is associated with poor health status, independent of CHD severity and depressive symptoms. Further study should examine if self-efficacy constitutes a useful target for cardiovascular disease management interventions.

OBJECTIVES

ABCB1 encodes the efflux transporter P-glycoprotein (P-gp), which regulates the intracellular concentration of many xenobiotics, including several HIV protease inhibitors (PIs). Exposure to some xenobiotics, such as the antibiotic rifampicin, increases P-gp expression. In the present study, we investigated the effect of the HIV PIs saquinavir and atazanavir on the expression and function of ABCB1 and P-gp in primary and cultured lymphocytes, as well as the molecular interactions between these drugs and P-gp. ABCB1 and P-gp expression and function were examined in lymphocyte samples from healthy subjects before and after atazanavir-boosted saquinavir treatment. Expression and function were also studied in CEM cells following exposure to atazanavir and saquinavir. The inhibitory effects of these drugs were investigated in ABCB1-transfected HEK293T cells.

METHODS

P-gp expression and function were measured by flow cytometry. ABCB1 mRNA expression was evaluated using quantitative RT-PCR.

RESULTS

There were no overall changes in ABCB1 or P-gp expression or function after saquinavir-atazanavir treatment in primary lymphocyte samples. However, there was considerable interindividual variability in baseline lymphocyte ABCB1 expression, as well as in the degree of change in ABCB1 expression after saquinavir-atazanavir administration. In cell culture, 5 microM saquinavir increased ABCB1 levels, although it did not affect P-gp expression. Atazanavir inhibited P-gp function at concentrations above therapeutic levels.

CONCLUSIONS

Differences in lymphocyte ABCB1 expression, which may be caused by genetic polymorphisms in ABCB1 or its regulatory partners, are a likely cause of interindividual variation in the disposition and efficacy of clinically relevant P-gp substrates, including HIV PIs.

Little is known about practice patterns regarding the diagnosis and management of idiopathic pulmonary fibrosis (IPF). This study attempts to define the practice patterns of academic pulmonologists caring for patients with IPF. Academic pulmonologists in the United States were surveyed electronically. Completed surveys were received from 272 respondents (representing approximately 10% of academic pulmonologists). The majority agreed that high-resolution computed tomography can establish the diagnosis of IPF, and that surgical lung biopsy is indicated when the diagnosis remains unclear. Bronchoscopy is little utilized. Most respondents treat patients with medications, but there is no consensus regarding treatment regimen. These results suggest there is general consensus regarding the approach to diagnosis, but that there is no consensus about medical management in IPF.

HIV-1 persists in peripheral blood monocytes in individuals receiving highly active antiretroviral therapy (HAART) with viral suppression, despite these cells being poorly susceptible to infection in vitro. Because very few monocytes harbor HIV-1 in vivo, we considered whether a subset of monocytes might be more permissive to infection. We show that a minor CD16+ monocyte subset preferentially harbors HIV-1 in infected individuals on HAART when compared with the majority of monocytes (CD14highCD16-). We confirmed this by in vitro experiments showing that CD16+ monocytes were more susceptible to CCR5-using strains of HIV-1, a finding that is associated with higher CCR5 expression on these cells. CD16+ monocytes were also more permissive to infection with a vesicular stomatitis virus G protein-pseudotyped reporter strain of HIV-1 than the majority of monocytes, suggesting that they are better able to support HIV-1 replication after entry. Consistent with this observation, high molecular mass complexes of apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G) were observed in CD16+ monocytes that were similar to those observed in highly permissive T cells. In contrast, CD14highCD16- monocytes contained low molecular mass active APOBEC3G, suggesting this is a mechanism of resistance to HIV-1 infection in these cells. Collectively, these data show that CD16+ monocytes are preferentially susceptible to HIV-1 entry, more permissive for replication, and constitute a continuing source of viral persistence during HAART.

OBJECTIVE

To evaluate the associations between Medicaid insurance and distance traveled by patients to treating physicians and health care utilization for patients with systemic lupus erythematosus (SLE).

METHODS

A total of 982 adults with SLE were recruited between 2002 and 2004. We calculated the distance between patient homes and physicians using Mapquest, an Internet mapping program. We then assessed the association between Medicaid status and distance traveled to the primary SLE provider, presence of > or =1 physician visits, and the number of all physician visits, with and without adjustment for demographic and medical covariates.

RESULTS

On an unadjusted basis, Medicaid patients traveled longer distances to see their primary SLE provider. This effect was pronounced for patients under the care of a rheumatologist. Adjustment reduced, but did not eliminate, these differences. With adjustment for covariates, Medicaid patients were equally as likely to see a rheumatologist as non-Medicaid patients. However, Medicaid patients were more likely to be seen by a general practitioner or in the emergency room for their SLE, and reported more visits to general practitioners and the emergency room for SLE.

CONCLUSION

Medicaid patients with SLE traveled longer distances to see an SLE physician, especially rheumatologists. They also reported a different pattern of health care utilization. These results suggest that Medicaid patients may face barriers in obtaining comprehensive medical services in proximity to their residences.