Redefining Disease Severity with Special Area Involvement and Reflecting on Treatment Patterns in a Real-World Psoriasis Population.

BACKGROUND: The International Psoriasis Council (IPC) recommends an approach that considers body surface area (BSA), involvement in special areas, and treatment history for classifying patients as candidates for topical or systemic treatment. This study aimed to quantify the burden of psoriasis by describing BSA distribution, special area involvement, and treatments in a real-world population. METHODS: This retrospective cohort study included patients with psoriasis from the Optum® deidentified Electronic Health Records database with a BSA value (< 3%, 3-10%, and > 10%) recorded between 1 March 2014 and 1 September 2020. Treatments and special area involvement (face, scalp, palms/soles, nails, genitals) were identified within 90 days of the BSA value and stratified by BSA category. RESULTS: Among eligible patients (N = 5120), mean age was 51.4 years and 49.3% were women. The majority of patients (78.9%) were treated with any topical. Proportions of patients with BSA < 3%, 3-10%, and > 10% were 23.4%, 41.9%, and 34.6%, respectively; proportions with 0, 1, and 2+ special areas were 21.6%, 31.6%, and 45.7%, respectively; and 44.4%, 45.7%, and 45.9% of patients with BSA < 3%, 3-10%, and > 10%, respectively, had 2+ special areas. CONCLUSION: The IPC classification can likely identify many more patients who may benefit from systemic therapy than BSA alone.

Obesity, physical activity and the development of metabolic syndrome: the Atherosclerosis Risk in Communities study.

BACKGROUND: The objective of this study is to determine the impact of body weight and physical activity on the development of metabolic syndrome (MetS). DESIGN AND METHODS: We used the public use data from the Atherosclerosis Risk in Communities study. From the baseline cohort, we identified, as the study population, 9359 individuals who did not have MetS and who completed the second follow-up examination in 1993-1995. RESULTS: In 6 years of follow-up, 1970 individuals (25%) developed MetS. Compared with normal weight group [body mass index (BMI)<25 kg/m], the odds ratios [95% confidence interval (CI)] of incident MetS were 2.81 (95% CI: 2.50-3.17) and 5.24 (95% CI: 4.50-6.12) for the overweight (BMI: 25-30 kg/m) and the obese groups (BMI>or=30 kg/m), respectively. Compared with persons in the lowest quartile of leisure-time physical activity, the odds ratios (95% CI) of incident MetS were 0.80 (95% CI: 0.71-0.91) and 0.92 (95% CI: 0.81-1.04) for persons in the highest and the middle quartiles of leisure-time physical activity, respectively. Our results indicated that at any level of physical activity, there is a graded increase in the risk of incident MetS with an increase in BMI, in contrast to a lack of graded association between physical activity and the incidence of MetS in all categories of BMI. CONCLUSION: This study highlights the need to target obesity more than physical activity in preventing the development of MetS.

Interaction of ambient air pollution with asthma medication on exhaled nitric oxide among asthmatics.

The interaction between ambient air pollution and asthma medication remains unclear. The authors compared airway inflammation response to air pollution among asthmatics. Increases of 10 ppb of nitrogen dioxide (NO2) and of 10 microg/m3 of particulate matter < 10 micron in diameter (PM10) daily concentrations were associated with an increase in exhaled nitric oxide (eNO) of 0.13 ppb (95% confidence interval = 0.06, 0.19) and of 0.07 ppb (95% confidence interval = 0.02, 0.12), respectively, in models adjusted for important covariates. The results show that the medication could not counteract airway inflammation effects of air pollution. Specifically, the patients on triamcinolone decreased the sensitivity to PM10 but increased the sensitivity to NO2. The patients on salmeterol were more vulnerable to both NO2 and PM10. This study indicates that the current pollution levels may still enhance airway inflammation among patients with persistent asthma even when they are on asthma medications.

Ambient particulate air pollution and ectopy--the environmental epidemiology of arrhythmogenesis in Women's Health Initiative Study, 1999-2004.

The relationships between ambient PM(2.5) and PM(10) and arrhythmia and the effect modification by cigarette smoking were investigated. Data from U.S. Environmental Protection Agency (EPA) air quality monitors and an established national-scale, log-normal kriging method were used to spatially estimate daily mean concentrations of PM at addresses of 57,422 individuals from 59 examination sites in 24 U.S. states in 1999-2004. The acute and subacute exposures were estimated as mean, geocoded address-specific PM concentrations on the day of, 0-2 d before, and averaged over 30 d before the electrocardiogram (ECG) (Lag(0); Lag(1); Lag(2); Lag(1-30)). At the time of standard 12-lead resting ECG, the mean age (SD) of participants was 67.5 (6.9) yr (84% non-Hispanic White; 6% current smoker; 15% with coronary heart disease; 5% with ectopy). After the identification of significant effect modifiers, two-stage random-effects models were used to calculate center-pooled odds ratios and 95% confidence intervals (OR, 95% CI) of arrhythmia per 10 mug/m(3) increase in PM concentrations. Among current smokers, Lag(0) and Lag(1) PM concentrations were significantly associated ventricular ectopy (VE)-the OR (95% CI) for VE among current smokers was 2 (1.32-3.3) and 1.32 (1.07-1.65) at Lag(1) PM(2.5) and PM(10), respectively. The interactions between current smoking and acute exposures (Lag(0); Lag(1); Lag(2)) were significant in relationship to VE. Acute exposures were not significantly associated with supraventricular ectopy (SVE), or with VE among nonsmokers. Subacute (Lag(1-30)) exposures were not significantly associated with arrhythmia. Acute PM(2.5) and PM(10) exposure is directly associated with the odds of VE among smokers, suggesting that they are more vulnerable to the arrhythmogenic effects of PM.

Associations between air pollution and peak expiratory flow among patients with persistent asthma.

Responses of patients with persistent asthma to ambient air pollution may be different from those of general populations. For example, asthma medications may modify the effects of ambient air pollutants on peak expiratory flow (PEF). Few studies examined the association between air pollution and PEF in patients with persistent asthma on well-defined medication regimens using asthma clinical trial data. Airway obstruction effects of ambient air pollutants, using 14,919 person-days of daily self-measured peak expiratory flow (PEF), were assessed from 154 patients with persistent asthma during the 16 wk of active treatment in the Salmeterol Off Corticosteroids Study trial. The three therapies were an inhaled corticosteroid, an inhaled long-acting beta-agonist, and placebo. The participants were nonsmokers aged 12 through 63 yr, recruited from 6 university-based ambulatory care centers from February 1997 to January 1999. Air pollution data were derived from the U.S. Environmental Protection Agency Aerometric Information Retrieval System. An increase of 10 ppb of ambient daily mean concentrations of NO2 was associated with a decrease in PEF of 1.53 L/min (95% confidence interval [CI] -2.93 to -0.14) in models adjusted for age, gender, race/ethnicity, asthma clinical center, season, week, daily average temperature, and daily average relative humidity. The strongest association between NO2 and PEF was observed among the patients treated with salmeterol. Negative associations were also found between PEF and SO2 and between PEF and PM(10), respectively. The results show that the two medication regimens protected against the effects of PM(10). However, salmeterol increased the sensitivity to NO2 and triamcinalone enhanced the sensitivity to SO2.

Metabolic syndrome clusters and the risk of incident stroke: the atherosclerosis risk in communities (ARIC) study.

BACKGROUND AND PURPOSE: Little is known about the metabolic syndrome (MetS) and the risk of incident stroke. This study is designed to identify particular clusters of MetS components that carry the highest risk of incident stroke. METHODS: We analyzed the public use data from the population-based Atherosclerosis Risk in Communities study. At baseline, 14 993 stroke-free middle-aged individuals were followed-up over 9 years for incident stroke. MetS components were defined according to the National Heart, Lung, and Blood Institute/American Heart Association criteria. Incident stroke was identified using a standardized incident events identification and classification protocol. Proportional hazard models were used to assess the RRs and 95% CIs of ischemic stroke associated with MetS and its different clusters. RESULTS: At baseline, the prevalence of MetS was 39%. The mean age was 54, with 26% blacks and 55% females. The hazard ratio of incident ischemic stroke associated with MetS among women (hazard ratio, 2.41; 95% CI, 1.69 to 3.49) and men (hazard ratio, 2.11; 95% CI, 1.56-2.85) was similar. There was a dose-response relationship between the numbers of MetS components and the risk of incidence stroke. Persons with either elevated blood pressure or elevated fasting glucose in the clusters to form a MetS had the highest risk for incident stroke (hazard ratio, 2.74-4.16 comparing to the reference group) than MetS without these 2 components (hazard ratio,

Is age-related macular degeneration associated with stroke among elderly americans?

OBJECTIVE: To investigate whether age-related macular degeneration (AMD) is associated with the development of ischemic and hemorrhagic stroke among elderly Americans. DESIGN: Population-based cohort study. PARTICIPANTS: The five percent random sample of 2000-2003 Medicare enrollees was obtained. The cohort (n=1,519,086) consisted of enrollees who were aged 65 or older at the first two-year (January 1, 2000 to December 31, 2001). METHODS: Baseline demographic variables and chronic conditions (AMD and type, history of myocardial infarction (MI), stroke, hypertension, and diabetes) were defined based on the occurrence of relevant ICD-9 codes in relevant diagnosis fields of the baseline Medicare Data. We excluded 215,900 persons who had a diagnosis of MI or stroke during baseline period to form a cohort of 1,303,186 individuals who were free of major cardio-cerebral vascular disease (CVD) at baseline. MAIN OUTCOME MEASURES: In two years of follow-up (January 1, 2002 to December 31, 2003), a total of 89,501 incident stroke cases were identified, including 80,018 ischemic, 7048 hemorrhagic, and 2,435 stroke cases of both types. RESULTS: Baseline mean age was 75 years (Standard Divination=7.7), with 60% women and 88% whites. The prevalence of AMD was 10.6%, with 19.7% being neovascular AMD and 80.3% being non-neovascular AMD. Baseline age, gender, race, hypertension, and diabetes adjusted 2-year incident odds ratios and 95% confidence internal of stroke associated with AMD were 1.31 (1.26, 1.36) for neovascular AMD, 1.18 (1.15, 1.21) for non-neovascular AMD, and 1.21 (1.18, 1.23) for either neovascular or non-neovascular AMD. CONCLUSION: The findings are suggestive of an association between AMD, especially neovascular AMD, and incident stroke, independent of demographic factors and co-morbidity. These findings, if confirmed by other studies that control for smoking and other lifestyle covariables not measured in this study, suggest the possibility of shared common antecedents between stroke and AMD.

Age-related macular degeneration is associated with incident myocardial infarction among elderly Americans.

OBJECTIVE: To investigate whether age-related macular degeneration (AMD) is associated with the development of myocardial infarction (MI) among elderly Americans. DESIGN: Population-based cross-sectional and cohort study. PARTICIPANTS: Five percent random sample of 2000 to 2003 Medicare enrollees. METHODS: The cross-sectional study included the first 2-year (2000 and 2001) enrollees who were aged > or =65 years (n = 1,519,086). The cohort study included only baseline MI-free enrollees (n = 1445677). MAIN OUTCOME MEASURES: Chronic conditions (AMD and type, history of MI, hypertension, and diabetes) were defined based on any occurrence of relevant International Classification of Diseases 9 codes in relevant diagnosis fields of the baseline Medicare claim files. A total of 56611 incident MI cases were identified from the follow-up data (2002 and 2003). RESULTS: Baseline mean age was 76 years, with 60% women and 88% whites. The prevalence of neovascular AMD was 2.2% (2.3% in women vs. 1.7% in men and 2.3% in whites vs. 1.2% in blacks; P<0.01 for both gender and race differences). The prevalence of nonneovascular AMD was 8.8% (9.9% in women vs. 7.3% in men and 9.5% in whites vs. 4.3% in blacks; P<0.01 for both gender and race differences). Baseline age-, gender-, and race-adjusted prevalences of hypertension, diabetes, and history of MI were 75%, 33%, and 5.00%, respectively, in the neovascular AMD group. In contrast, they were 73%, 27%, and 4.68% in the nonneovascular AMD group, and 65%, 25%, and 4.54% in the non-AMD group (P<0.01 for comparing the prevalence in neovascular and nonneovascular AMD vs. non-AMD groups). Prospectively, baseline age-, gender-, race-, hypertension-, and diabetes-adjusted 2-year incident odds ratios and 95% confidence intervals of MI associated with AMD are 1.19 (1.16-1.22) for all persons with AMD, 1.26 (1.20-1.33) for neovascular AMD, and 1.18 (1.14-1.21) for nonneovascular AMD. CONCLUSIONS: AMD is associated with older age, female gender, being white, and having a history of MI, hypertension, and diabetes. Furthermore, presence of AMD, especially neovascular AMD, is prospectively associated with a higher risk of incident MI. These findings, if confirmed by other studies that control for smoking and other lifestyle covariables, suggest the possibility of shared common antecedents between MI and AMD.

GIS approaches for the estimation of residential-level ambient PM concentrations.

Spatial estimations are increasingly used to estimate geocoded ambient particulate matter (PM) concentrations in epidemiologic studies because measures of daily PM concentrations are unavailable in most U.S. locations. This study was conducted to a) assess the feasibility of large-scale kriging estimations of daily residential-level ambient PM concentrations, b) perform and compare cross-validations of different kriging models, c) contrast three popular kriging approaches, and d) calculate SE of the kriging estimations. We used PM data for PM with aerodynamic diameter

Association of criteria pollutants with plasma hemostatic/inflammatory markers: a population-based study.

To elucidate the health effects of air pollution, the short-term association of criteria pollutants (particles <10 microm in diameter [PM(10)], O(3), CO, NO(2), and SO(2)) with hemostatic and inflammatory markers were examined using a population-based sample of 10,208 middle-age males and females of the biracial cohort of Atherosclerosis Risk in Communities (ARIC) study. For each participant, we calculated the following pollutant exposures 1-3 days prior to the randomly allocated cohort examination date: PM(10), CO, NO(2), and SO(2) as 24-h averages, and O(3) as an 8-h average of the hourly measures. The hemostatic/inflammatory factors included fibrinogen, factor VIII-C, von Willebrand factor (vWF), albumin, and white blood cell count (WBC). Linear regression models were used to adjust for cardiovascular disease (CVD) risk factors, demographic and socioeconomic variables, and relevant meteorological variables. One standard deviation (SD) increment of PM(10) (12.8 microg/m(3)) was significantly (P < 0.05) associated with 3.93% higher of vWF among diabetics and 0.006 g/dl lower of serum albumin among persons with a history of CVD. One SD increment of CO (0.60 p.p.m.) was significantly (P < 0.01) associated with 0.018 g/dl lower of serum albumin. Significant curvilinear associations, indicative of threshold effects, for PM(10) with factor VIII-C, O(3) with fibrinogen and vWF, and SO(2) with factor VIII-C, WBC, and serum albumin were found. This population-based study suggest that the hemostasis/inmflammation markers analyzed, which are linked to higher risk of CHD, are associated adversely with environmentally relevant ambient pollutants, with the strongest associations in the upper range of the pollutant distributions, and in persons with a positive history of diabetes and CHD.

Lung function and long-term exposure to air pollutants in middle-aged American adults.

The authors examined the association of long-term exposure to ozone (03) and ambient particulate matter <10 microm in diameter (PM10) with pulmonary function by using cross-sectional data of 10,240 middle-aged adults who participated in the Atherosclerosis Risk in Communities study. Air-pollution data came from the US Environmental Protection Agency's Aerometric Information Retrieval System. After an adjustment for important covariates, the inverse associations with forced vital capacity or forced expiratory volume in 1 second were observed separately for 03 and PM10). These associations were stronger among smokers than among the nonsmokers; among users of respiratory medications than among nonusers; and among participants currently experiencing respiratory symptoms than among those without symptoms. However, an additional adjustment for the study center eliminated the PM10 association. Moreover, center-specific associations between PM10 and pulmonary function were not significant, possibly as a result of the homogeneity of within-center exposures.

Association of higher levels of ambient criteria pollutants with impaired cardiac autonomic control: a population-based study.

An association between air pollution and increased cardiovascular disease (CVD) mortality has been reported, but underlying mechanisms are unknown. The authors examined short-term associations between ambient pollutants (particulate matter less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide) and cardiac autonomic control using data from the fourth cohort examination (1996-1998) of the population-based Atherosclerosis Risk in Communities Study. For each participant, the authors calculated PM10 and gaseous pollutant exposures as 24-hour averages and ozone exposure as an 8-hour average 1 day prior to the randomly allocated examination date. They calculated 5-minute heart rate variability indices and used logarithmically transformed data on high-frequency (0.15-0.40 Hz) and low-frequency (0.04-0.15 Hz) power, standard deviation of normal R-R intervals, and mean heart rate. Linear regression was used to adjust for CVD risk factors and demographic, socioeconomic, and meteorologic variables. Regression coefficients for a one-standard-deviation increase in PM10 (11.5 microg/m3) were -0.06 ms2 (standard error (SE), 0.018), -1.03 ms (SE, 0.31), and 0.32 beats/minute (SE, 0.158) for log-transformed high-frequency power, standard deviation of normal R-R intervals, and heart rate, respectively. Similar results were found for gaseous pollutants. These cross-sectional findings suggest that higher ambient pollutant concentrations are associated with lower cardiac autonomic control, especially among persons with existing CVD, and highlight a putative mechanism through which air pollution is associated with CVD.