Effects of lifestyle intervention on health care costs: Improving Control with Activity and Nutrition (ICAN).

OBJECTIVE: To evaluate program and health care costs of a lifestyle intervention in a high-risk obese population. DESIGN: Twelve-month randomized controlled trial comparing lifestyle case management to usual care. SUBJECTS/SETTING: Health plan members (n=147) with obesity (body mass index >/=27) and type 2 diabetes. INTERVENTION: Lifestyle case management entailed individual and group education, support, and referrals by registered dietitians. Those in the usual-care group received educational material. MAIN OUTCOME MEASURES: Medical and pharmaceutical health care costs reimbursed by the participant's primary insurance company. STATISTICAL ANALYSIS: Total costs were modeled using the four-equation model using previous year cost as a predictor. RESULTS: Net cost of the intervention was $328 per person per year. After incorporating program costs, mean health plan costs were $3,586 (95% confidence interval [CI]: -$8,036, -$25, P<0.05) lower in case management compared to usual care. The difference was driven by group differences in medical (-$3,316, 95% CI: -$7,829 to -$320, P<0.05) but not pharmaceutical costs (-$239, 95% CI: -$870 to $280, not statistically significant), with fewer inpatient admissions and costs among case management compared with usual care (admission prevalence: 2.8% vs 22.5% respectively, P<0.001). CONCLUSION: Addition of a modest-cost, registered dietitian-led lifestyle case-management intervention to usual medical care did not increase health care costs and suggested modest cost savings among obese patients with type 2 diabetes. Larger trials are needed to determine whether these results can be replicated in a broader population. The findings can be judiciously applied to support that the addition of a registered dietitian-led lifestyle case-management program to medical care does not increase health care costs.

Uptake rates for breast cancer genetic testing: a systematic review.

PURPOSE: Individuals and families dealing with the possibility of hereditary cancer risk face numerous decisions, including whether to obtain genetic testing. The purpose of this article is to determine what is known about the rate at which people obtain cancer genetic testing. METHODS: Using MEDLINE, CINAHL, and PSYCHINFO plus reviewing reference lists of relevant articles, we identified 40 studies in May 2002 that addressed breast cancer-related decisions, enrolled adult participants, were published in 1990 or more recently, were peer-reviewed primary clinical studies, addressed genetic testing either alone or in combination with genetic counseling, and reported rates at which participants showed interest in and/or underwent cancer genetic testing. Information regarding study design, participants, and genetic testing uptake rates was recorded. Each article was reviewed for methodologic quality using a flexible quality review system applicable to all study types. RESULTS: Of the 40 studies, 25 provided information about hypothetical genetic testing decisions, 14 about real decisions, and 1 about both. Mean hypothetical uptake was 66% (range, 20-96%) and real uptake was 59% (range, 25-96%). Multivariate logistic regression analyses found that decision type (real/hypothetical), personal and family history of breast cancer, and variability in sampling strategy, recruitment setting, and criteria for real and hypothetical uptake were independently associated with uptake. Our systematic review identified additional explanations for uptake variability (investigator influences, small sample sizes, variability in target populations, lack of clearly described sampling strategies, sampling methods open to bias, and variability in reporting associated risk factors). CONCLUSION: In addition to clinical characteristics, research methodologic issues are likely to be major determinants of variability in published breast cancer genetic testing uptake rates. An understanding of these issues will clarify to clinicians why their clinical experience may not be congruent with published rates and help guide future research.

Spatial analysis of prostate cancer incidence and race in Virginia, 1990-1999.

BACKGROUND: Racial disparities exist in prostate cancer incidence. An important contributor to these disparities may be socioeconomic status. METHODS: Virginia Cancer Registry data, 1990-1999 (37,373 cases) were geocoded to the Census tract and county level. The annualized, age-adjusted incidence rates for African Americans and whites were calculated, and crude and smoothed maps of these rates were produced. Statistical tests for clustering of cases were conducted. Prostate cancer incidence was statistically modeled as a function of area-based measures of poverty, median household income, education, rural status, ratio of physicians to population in each county, percentage of men in each county obtaining prostate cancer screening with the prostate-specific antigen (PSA) test, and percent of households headed by females. RESULTS: Prostate cancer incidence was elevated in the eastern and central portions of the state. Statistical tests for clustering were highly significant (Tango's test, p<0.008; spatial scan statistic, p<0.001). Poverty and lower education were associated with a decreased incidence among whites but not African Americans. Median household income and urban status were positively associated with incidence for both populations. Among whites, increased percent of female heads of households and ratio of physicians per population were associated with increased incidence. Associations between predictor variables and prostate cancer incidence were seen only in the census tract level analyses. CONCLUSIONS: Overall, the findings support the argument that area measures of poverty and education do not explain the increased incidence of prostate cancer among African Americans. Other factors, such as dietary practices, may help explain racial disparities in prostate cancer incidence. Because of the large differences between tract and county level results, the time and expense of obtaining data geocoded to the tract level seems worthwhile.

Geographic bias related to geocoding in epidemiologic studies.

BACKGROUND: This article describes geographic bias in GIS analyses with unrepresentative data owing to missing geocodes, using as an example a spatial analysis of prostate cancer incidence among whites and African Americans in Virginia, 1990-1999. Statistical tests for clustering were performed and such clusters mapped. The patterns of missing census tract identifiers for the cases were examined by generalized linear regression models. RESULTS: The county of residency for all cases was known, and 26,338 (74%) of these cases were geocoded successfully to census tracts. Cluster maps showed patterns that appeared markedly different, depending upon whether one used all cases or those geocoded to the census tract. Multivariate regression analysis showed that, in the most rural counties (where the missing data were concentrated), the percent of a county's population over age 64 and with less than a high school education were both independently associated with a higher percent of missing geocodes. CONCLUSION: We found statistically significant pattern differences resulting from spatially non-random differences in geocoding completeness across Virginia. Appropriate interpretation of maps, therefore, requires an understanding of this phenomenon, which we call "cartographic confounding."

Plaque blush, branch location, and calcification are angiographic predictors of progression of mild to moderate coronary stenoses.

BACKGROUND: Angiographic predictors of plaque progression are weak and few: length, irregular surface, turbulence, low shear, and (in some studies) eccentricity and calcification. Having noted plaques that briefly retained dye after angiography, we interpreted these as plaques with a fissured surface or neovascularization and hypothesized that progression would be predicted by "plaque blush." METHODS: Plaques (<50% diameter stenosis) in 68 pairs of angiograms, 5.6 +/- 4.8 months apart, were reviewed by 2 blinded observers. The presence of plaque blush, calcification, clot (mobile defect), eccentricity, and a branch point location were compared between progressing (> or =20% stenosis increase) and nonprogressing plaques. RESULTS: Sixteen lesions in 15 patients progressed from 29% +/- 13% to 68% +/- 14% over a period of 8.1 +/- 7.9 months. Patients with and without progression were similar in sex, age, congestive heart disease risk factors, medications, interval between angiograms, clinical presentation, and initial stenosis severity. By logistic regression, plaque blush (BL) (P =.002), calcification (CA) (P =.024), and a branch (BR) point location (P =.001) predicted plaque progression. The odds ratio for plaque progression (ORp) was calculated as ORp = e(2.5 x BL + 1.8 x CA + 2.6 x BR). Using an ORp of 1/3, the model has 81% sensitivity and 77% specificity. A second analysis in which each progressive lesion was compared with proximal and distal lesions and with one in a different coronary artery yielded similar results. CONCLUSIONS: In mild to moderate coronary stenoses, studied retrospectively, plaque blush (a new sign) and a branch point location were strong predictors of plaque progression, whereas calcification was a weak predictor of progression.

Influenza infection exerts prominent inflammatory and thrombotic effects on the atherosclerotic plaques of apolipoprotein E-deficient mice.

BACKGROUND: The role of infection in the development and complications of atherosclerosis has been the focus of much attention. We reported previously that influenza vaccination was associated with reduced risk of recurrent myocardial infarction. Here, we report the effect of influenza A virus on the apolipoprotein E-deficient (apoE(-/-)) mouse, an animal model of atherosclerosis. METHODS AND RESULTS: Twenty-four apoE(-/-) mice >24 months old were injected with 1 LD(50) (lethal dose 50) of influenza A virus. Ten wild-type C57BL/6 infected mice and 11 noninfected age-matched apoE(-/-) mice served as controls. Multiple aortic sections were studied histologically 3, 5, and 10 days later. The infected mice showed markedly increased intimal cellularity compared with the noninfected apoE(-/-) mice. No aortic abnormalities were seen in infected wild-type mice. Ten infected apoE(-/-) mice had a significant subendothelial infiltrate composed of a heterogeneous group of cells that stained positively for smooth muscle cell actin, F4/80 (macrophages), and CD3 (T lymphocytes). One case of subocclusive platelet and fibrin-rich thrombus was seen. CONCLUSIONS: This study shows that influenza infection promotes inflammation, smooth muscle cell proliferation, and fibrin deposition in atherosclerotic plaques.