Preventive asthma medication discontinuation among children enrolled in fee-for-service Medicaid.

OBJECTIVE: Local-area studies demonstrate that preventive asthma medication discontinuation among Medicaid and Children's-Health-Insurance-Program (CHIP) enrolled children leads to adverse outcomes. We assessed time-to-discontinuation for preventive asthma medication and its risk factors among fee-for-service Medicaid/CHIP child beneficiaries. METHODS: National-Health-Interview-Survey participants (1997-2005) with ≥1 Medicaid- or CHIP-paid claims when 2-17 years old (n = 4262) were linked to Medicaid-Analytic-eXtract claims (1999-2008). Multivariate Cox proportional-hazards models to assess time-to-discontinuation (i.e. failing to refill prescriptions <30 d after previous supplies ran out) included demographic factors and medication regimen (inhaled corticosteroids [ICS], long-acting ß2-agonists, leukotriene modifiers, mast cell stabilizers, and monoclonal antibodies). RESULTS: Sixty-three percent discontinued preventive asthma medications by 90 d after the first prescription. Adolescents and toddlers had slightly higher hazards of discontinuation (adjusted hazard ratios [aHR], 1.13; 95% CI, 1.05-1.23; and 1.12; 1.03-1.21, respectively) versus 5-11-year-olds, as did Hispanics (aHR, 1.24; 1.13-1.35) and non-Hispanic blacks (aHR, 1.17; 1.07-1.28) versus non-Hispanic whites, children in households with one adult and ≥3 children (aHR, 1.17; 1.05-1.30) versus multiple adults and ≤2 children, and children with caregivers' educational-attainment ≤12th grade (aHR, 1.11; 1.02-1.20) versus caregivers with some college. Compared to regimens including both ICS and leukotriene modifiers, discontinuation was greater for those on ICS without leukotriene modifiers or on other preventive asthma medications (aHR, 1.67; 1.56-1.80; and 2.23; 1.78-2.80, respectively). CONCLUSION: More than 60% of children enrolled in fee-for-service Medicaid/CHIP discontinued preventive asthma medications by 90 d. Risk was increased for minorities and children from disadvantaged households. Understanding these factors may inform future pediatric asthma guidelines.

Breast cancer molecular subtypes and survival in a hospital-based sample in Puerto Rico.

Information on the impact of hormone receptor status subtypes in breast cancer (BC) prognosis is still limited for Hispanics. We aimed to evaluate the association of BC molecular subtypes and other clinical factors with survival in a hospital-based female population of BC cases in Puerto Rico. We analyzed 663 cases of invasive BC diagnosed between 2002 and 2005. Information on HER-2/neu (HER-2) overexpression, estrogen (ER), and progesterone (PR) receptor status and clinical characteristics were retrieved from hospitals cancer registries and record review. Survival probabilities by covariates of interest were described using the Kaplan-Meier estimators. Cox proportional hazards models were employed to assess factors associated with risk of BC death. Overall, 17.3% of BC cases were triple-negative (TN), 61.8% were Luminal-A, 13.3% were Luminal-B, and 7.5% were HER-2 overexpressed. In the multivariate Cox model, among patients with localized stage, women with TN BC had higher risk of death (adjusted hazard ratio [HR]: 2.57, 95% confidence interval [CI]: 1.29-5.12) as compared to those with Luminal-A status, after adjusting for age at diagnosis. In addition, among women with regional/distant stage at diagnosis, those with TN BC (HR: 5.48, 95% CI: 2.63-11.47) and those HER-2+, including HER-2 overexpressed and Luminal-B, (HR: 2.73, 95% CI:1.30-5.75) had a higher mortality. This is the most comprehensive epidemiological study to date on the impact of hormone receptor expression subtypes in BC survival in Puerto Rico. Consistent to results in other populations, the TN subtype and HER-2+ tumors were associated with decreased survival.

Socioeconomic status and hepatocellular carcinoma in the United States.

BACKGROUND: Hepatocellular carcinoma (HCC) has a poor prognosis and, unlike most cancers, HCC incidence and mortality rates are increasing in the United States. While risk is known to vary among different racial and ethnic groups, less is known about the variability of risk within these groups by neighborhood socioeconomic status (SES). METHODS: HCC cases diagnosed in the Surveillance, Epidemiology and End Results (SEER) 11 cancer registries between 1996 and 2007, and the population of the SEER 11 catchment areas was studied. Analyses were conducted to compare census tract area family poverty, educational attainment, and unemployment by race and ethnicity. A multiple linear regression model, weighted by the number of cases and the number of individuals in each census tract, with adjustment for registry, was used to calculate mean differences in area-level attributes between HCC cases and the population. RESULTS: HCC cases in most racial/ethnic groups had lower mean neighborhood-level measures of SES than their referent population. An exception was seen among Hispanics. Comparing white cases with cases of other racial groups and to Hispanics, white cases lived in neighborhoods with less family poverty, fewer high-school dropouts, and lower unemployment. Compared with white cases, Asian and Pacific Islander and Hispanic cases lived in neighborhoods with a higher percentage of foreign-born population. CONCLUSIONS: Low neighborhood-level SES and immigrant status may be associated with greater risk of HCC within specific racial and ethnic groups. IMPACT: These findings could help to focus control resources for HCC toward the most affected communities.

Mood disorders and risk of lung cancer in the EAGLE case-control study and in the U.S. Veterans Affairs inpatient cohort.

BACKGROUND: Mood disorders may affect lung cancer risk. We evaluated this hypothesis in two large studies. METHODOLOGY/PRINCIPAL FINDINGS: We examined 1,939 lung cancer cases and 2,102 controls from the Environment And Genetics in Lung cancer Etiology (EAGLE) case-control study conducted in Italy (2002-2005), and 82,945 inpatients with a lung cancer diagnosis and 3,586,299 person-years without a lung cancer diagnosis in the U.S. Veterans Affairs Inpatient Cohort (VA study), composed of veterans with a VA hospital admission (1969-1996). In EAGLE, we calculated odds ratios (ORs) and 95% confidence intervals (CI), with extensive adjustment for tobacco smoking and multiple lifestyle factors. In the VA study, we estimated lung cancer relative risks (RRs) and 95% CIs with time-dependent Poisson regression, adjusting for attained age, calendar year, hospital visits, time within the study, and related previous medical diagnoses. In EAGLE, we found decreased lung cancer risk in subjects with a personal history of mood disorders (OR: 0.59, 95% CI: 0.44-0.79, based on 121 lung cancer incident cases and 192 controls) and family history of mood disorders (OR: 0.62, 95% CI: 0.50-0.77, based on 223 lung cancer cases and 345 controls). The VA study analyses yielded similar results (RR: 0.74, 95% CI: 0.71-0.77, based on 2,304 incident lung cancer cases and 177,267 non-cancer person-years) in men with discharge diagnoses for mood disorders. History of mood disorders was associated with nicotine dependence, alcohol and substance use and psychometric scales of depressive and anxiety symptoms in controls for these studies. CONCLUSIONS/SIGNIFICANCE: The consistent finding of a relationship between mood disorders and lung cancer risk across two large studies calls for further research into the complex interplay of risk factors associated with these two widespread and debilitating diseases. Although we adjusted for smoking effects in EAGLE, residual confounding of the results by smoking cannot be ruled out.

Estrogen-dependent alterations in D2/D3-induced G protein activation in cocaine-sensitized female rats.

Estrogen potentiates behavioral sensitization to cocaine in the female rat by mechanisms that remain undetermined. In this study, functional receptor autoradiography was used to investigate estrogen modulation of D2/D3 receptor-induced G protein activation in components of the reward pathway of female rats treated acutely and repeatedly with cocaine. Rats were ovariectomized and given an empty (OVX group) or estradiol benzoate-filled (OVX-EB group) implant. After a week, animals received a daily saline or cocaine injection (15 mg/kg, i.p.) for 5 days, and again on day 13. Animals were killed, and brains were removed and cryosectioned. D2/D3-stimulated [35S]guanosine 5'-(gamma-thio) triphosphate (GTPgammaS) binding was assessed in the cingulate cortex area 2 (Cg2), striatum (STR), nucleus accumbens (NAc) and ventral tegmental area (VTA). OVX-EB rats showed more [35S]GTPgammaS binding in the Cg2 and lower binding in the VTA than OVX rats; in the VTA this effect was reversed by a single cocaine injection. Repeated cocaine administration had opposite effects in OVX and OVX-EB rats. [35S]GTPgammaS binding was decreased in the Cg2, NAc and STR of OVX-EB rats, and increased in OVX rats. The present results support the hypothesis that cocaine-induced changes in D2/D3 receptor activation are regulated by estrogen. These data suggest that changes in D2/D3 receptor function represent one mechanism by which estrogen regulates behavioral sensitization to cocaine.