RESUMEN
OBJECTIVE: To evaluate impact of the Maryland Multipayor Patient-centered Medical Home Program (MMPP) on: (1) quality, utilization, and costs of care; (2) beneficiaries' experiences and satisfaction with care; and (3) perceptions of providers. DESIGN: 4-year quasiexperimental design with a difference-in-differences analytic approach to compare changes in outcomes between MMPP practices and propensity score-matched comparisons; pre-post design for patient-reported outcomes among MMPP beneficiaries. SUBJECTS: Beneficiaries (Medicaid-insured and privately insured) and providers in 52 MMPP practices and 104 matched comparisons in Maryland. INTERVENTION: Participating practices received unconditional financial support and coaching to facilitate functioning as medical homes, membership in a learning collaborative to promote education and dissemination of best practices, and performance-based payments. MEASURES: Sixteen quality, 20 utilization, and 13 cost measures from administrative data; patient-reported outcomes on care delivery, trust in provider, access to care, and chronic illness management; and provider perceptions of team operation, team culture, satisfaction with care provided, and patient-centered medical home transformation. RESULTS: The MMPP had mixed impact on site-level quality and utilization measures. Participation was significantly associated with lower inpatient and outpatient payments in the first year among privately insured beneficiaries, and for the entire duration among Medicaid beneficiaries. There was indication that MMPP practices shifted responsibility for certain administrative tasks from clinicians to medical assistants or care managers. The program had limited effect on measures of patient satisfaction (although response rates were low) and on provider perceptions. CONCLUSIONS: The MMPP demonstrated mixed results of its impact and indicated differential program effects for privately insured and Medicaid beneficiaries.
Asunto(s)
Actitud del Personal de Salud , Aceptación de la Atención de Salud/estadística & datos numéricos , Satisfacción del Paciente , Atención Dirigida al Paciente/organización & administración , Calidad de la Atención de Salud/organización & administración , Adulto , Femenino , Gastos en Salud , Humanos , Cobertura del Seguro/estadística & datos numéricos , Seguro de Salud/estadística & datos numéricos , Masculino , Maryland , Medicaid/estadística & datos numéricos , Manejo de Atención al Paciente/organización & administración , Atención Dirigida al Paciente/economía , Atención Dirigida al Paciente/normas , Indicadores de Calidad de la Atención de Salud , Calidad de la Atención de Salud/economía , Estados UnidosRESUMEN
Although exposure to estrogen may directly influence or modify the association between cigarette smoking and lung cancer risk, results from epidemiologic studies examining the association between reproductive and hormonal factors and risk of lung cancer among women have been inconsistent. Between 1998 and 2008, 430 women diagnosed with nonsmall cell lung cancer, 316 hospital controls and 295 population controls were recruited into the multi-center Maryland Lung Cancer Study. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) according to reproductive and hormonal exposures adjusting for age, smoking, passive smoking, education and household income. Results were similar for hospital and population based controls, so the control groups were combined. Reduced risks of lung cancer were observed among women with greater parity (≥ 5 vs. 1-2 births: OR = 0.50, 95% CI = 0.32, 0.78, p-trend = 0.002) and later ages at last birth (≥ 30 vs. <25 years old: OR = 0.68, 95% CI = 0.48, 0.98, p-trend = 0.04). After mutual adjustment parity, but not age at last birth, remained significantly inversely associated with risk (p-trend = 0.01). No associations were found for nonsmall cell lung cancer risk with age at menarche, age at first birth, menopausal status, oral contraceptive use or menopausal hormone use, including use of oral estrogens. Compatible with findings from recent epidemiologic studies, we observed a reduction in the risk of nonsmall cell lung cancer with increasing number of births. Other reproductive and hormonal exposures, including menopausal hormone therapy use, were not associated with risk.
Asunto(s)
Adenocarcinoma/epidemiología , Carcinoma de Pulmón de Células no Pequeñas/epidemiología , Terapia de Reemplazo de Hormonas , Neoplasias Pulmonares/epidemiología , Historia Reproductiva , Adenocarcinoma/etiología , Anciano , Carcinoma de Pulmón de Células no Pequeñas/etiología , Estudios de Casos y Controles , Anticonceptivos Orales , Femenino , Humanos , Neoplasias Pulmonares/etiología , Persona de Mediana Edad , Paridad , Pronóstico , Factores de Riesgo , FumarRESUMEN
Cell cycle checkpoints play critical roles in the maintenance of genomic integrity and inactivation of checkpoint genes are frequently perturbed in most cancers. In a case-control study of 299 non-small cell lung cancer cases and 550 controls in Baltimore, we investigated the association between gamma-radiation-induced G(2)/M arrest in cultured blood lymphocytes and lung cancer risk, and examined genotype-phenotype correlations between genetic polymorphisms of 20 genes involving in DNA repair and cell cycle control and gamma-radiation-induced G(2)/M arrest. The study was specifically designed to examine race and gender differences in risk factors. Our data indicated that a less efficient DNA damage-induced G(2)/M checkpoint was associated with an increased risk of lung cancer in African American women with an adjusted odds ratio (OR) of 2.63 (95% CI = 1.01-7.26); there were no statistically significant associations for Caucasians, or African American men. When the African American women were categorized into quartiles, a significant reverse trend of decreased G(2)/M checkpoint function and increased lung cancer risk was present, with lowest-vs.-highest quartile OR of 13.72 (95% CI = 2.30-81.92, p(trend) < 0.01). Genotype-phenotype correlation analysis indicated that polymorphisms in ATM, CDC25C, CDKN1A, BRCA2, ERCC6, TP53, and TP53BP1 genes were significantly associated with the gamma-radiation-induced G(2)/M arrest phenotype. This study provides evidence that a less efficient G(2)/M checkpoint is significantly associated with lung cancer risk in African American women. The data also suggested that the function of G(2)/M checkpoint is modulated by genetic polymorphisms in genes involved in DNA repair and cell cycle control.
Asunto(s)
División Celular , Fase G2 , Genes cdc/fisiología , Neoplasias Pulmonares/etiología , Anciano , Estudios de Casos y Controles , Reparación del ADN , Femenino , Genotipo , Humanos , Neoplasias Pulmonares/patología , Masculino , Persona de Mediana Edad , Fenotipo , Polimorfismo de Nucleótido Simple , Factores de RiesgoRESUMEN
Cell cycle checkpoints play critical roles in the maintenance of genomic integrity. The inactivation of checkpoint genes by genetic and epigenetic mechanisms is frequent in all cancer types, as a less-efficient cell cycle control can lead to genetic instability and tumorigenesis. In an on-going case-control study consisting of 216 patients with non-small cell lung cancer, 226 population-based controls, and 114 hospital-based controls, we investigated the relationship of gamma-radiation-induced G2-M arrest and lung cancer risk. Peripheral blood lymphocytes were cultured for 90 hours, exposed to 1.0 Gy gamma-radiation, and harvested at 3 hours after gamma-radiation treatment. gamma-Radiation-induced G2-M arrest was measured as the percentage of mitotic cells in untreated cultures minus the percentage of mitotic cells in gamma-radiation-treated cultures from the same subject. The mean percentage of gamma-radiation-induced G2-M arrest was significantly lower in cases than in population controls (1.18 versus 1.44, P < 0.01) and hospital controls (1.18 versus 1.40, P = 0.01). When dichotomized at the 50th percentile value in combined controls (population and hospital controls), a lower level of gamma-radiation-induced G2-M arrest was associated with an increased risk of lung cancer among African Americans after adjusting for baseline mitotic index, age, gender, and pack-years of smoking [adjusted odd ratio (OR), 2.25; 95% confidence interval (95% CI), 0.97-5.20]. A significant trend of an increased risk of lung cancer with a decreased level of G2-M arrest was observed (P(trend) = 0.02) among African Americans, with a lowest-versus-highest quartile adjusted OR of 3.74 (95% CI, 0.98-14.3). This trend was most apparent among African American females (P(trend) < 0.01), with a lowest-versus-highest quartile adjusted OR of 11.75 (95% CI, 1.47-94.04). The results suggest that a less-efficient DNA damage-induced G2-M checkpoint is associated with an increased risk of lung cancer among African Americans. Interestingly, we observed a stronger association of DNA damage-induced G2-M arrest and lung cancer among African Americans when compared with Caucasians. If replicated, these results may provide clues to the exceedingly high lung cancer incidence experienced by African Americans.
Asunto(s)
Población Negra , Carcinoma de Pulmón de Células no Pequeñas/patología , División Celular/efectos de la radiación , Fase G2/efectos de la radiación , Neoplasias Pulmonares/patología , Negro o Afroamericano , Anciano , Carcinoma de Pulmón de Células no Pequeñas/sangre , Carcinoma de Pulmón de Células no Pequeñas/genética , Estudios de Casos y Controles , División Celular/genética , Relación Dosis-Respuesta en la Radiación , Femenino , Fase G2/genética , Rayos gamma , Humanos , Neoplasias Pulmonares/sangre , Neoplasias Pulmonares/genética , Linfocitos/citología , Linfocitos/efectos de la radiación , Masculino , Persona de Mediana Edad , Factores de RiesgoRESUMEN
Environmental exposure to carcinogens and individual susceptibility play significant roles in cancer risk. Suboptimal DNA repair capability, measured by quantifying mutagen-induced chromosome breaks, might explain variable host susceptibility to environmental carcinogens. In an ongoing lung cancer case-control study, we compared individual sensitivity to bleomycin-induced chromosome breaks in 152 non-small cell lung cancer patients with 94 population controls and 85 hospital controls with no history of cancer. Mutagen sensitivity was measured by mean number of chromatid breaks per cell in cultured peripheral blood lymphocytes treated with bleomycin. Non-parametric tests and chi(2) tests were used to determine the statistical significance of the crude case-control comparisons, followed by logistic regression to adjust for important covariates. The mean number of bleomycin-induced breaks per cell was 1.01 for the cases compared with 0.86 for hospital controls (P < 0.01) and 0.89 for population controls (P < 0.01). The mean number of breaks per cell was 1.01 for those >65 years old and 0.81 for those < or = 65 years old (P < 0.01) among population controls. Defining bleomycin sensitive as >0.84 break/cell (the median level in population controls), 67% of the cases were bleomycin sensitive compared with 49% of the hospital controls [adjusted odds ratio (OR) = 2.69, 95% confidence interval (CI) = 1.44, 5.04], and 51% of the population controls (adjusted OR = 2.18, 95% CI = 1.13, 4.21). Our data indicate that the increased number of bleomycin-induced chromosome breaks was significantly associated with an increased risk of lung cancer in the first 331 subjects.