Patricia H. Owens

Prior medical conditions and medication use and risk of non-Hodgkin lymphoma in connecticut United States women

AbstractObjective: To further investigate the role of prior medical conditions and medication use in the etiology of non-Hodgkin lymphoma (NHL), we analyzed the data from a population-based case–control study of NHL in Connecticut women. Methods: A total of 601 histologically confirmed incident cases of NHL and 717 population-based controls were included in this study. In-person interviews were administered using standardized, structured questionnaires to collect information on medical conditions and medication use. Results: An increased risk was found among women who had a history of autoimmune disorders (such as rheumatoid arthritis, lupus erythematosus, Sjogrens syndrome, and multiple sclerosis), anemia, eczema, or psoriasis. An increased risk was also observed among women who had used steroidal anti-inflammatory drugs and tranquilizers. A reduced risk was found for women who had scarlet fever or who had used estrogen replacement therapy, aspirin, medications for non-insulin dependent diabetes, HMG-CoA reductase inhibitors, or beta-adrenergic blocking agents. Risk associated with past medical history appeared to vary based on NHL subtypes, but the results were based on small number of exposed subjects. Conclusion: A relationship between certain prior medical conditions and medication use and risk of NHL was observed in this study. Further studies are warranted to confirm our findings.

African-American/White differences in breast carcinoma: p53 alterations and other tumor characteristics.

Despite mounting evidence that breast tumors in African‐American (AA) women are more aggressive compared with breast tumors in white (W) women, little is known regarding racial/ethnic differences in genetic alterations that may be of prognostic importance.

A brief intervention reduces hazardous and harmful drinking in emergency department patients.

STUDY OBJECTIVE Brief interventions have been shown to reduce alcohol use and improve outcomes in hazardous and harmful drinkers, but evidence to support their use in emergency department (ED) patients is limited. The use of research assessments in studies of brief interventions may contribute to uncertainty about their effectiveness. Therefore we seek to determine (1) if an emergency practitioner-performed Brief Negotiation Interview or a Brief Negotiation Interview with a booster reduces alcohol consumption compared with standard care; and (2) the impact of research assessments on drinking outcomes using a standard care-no-assessment group. METHODS We randomized 889 adult ED patients with hazardous and harmful drinking. A total of 740 received an emergency practitioner-performed Brief Negotiation Interview (n=297), a Brief Negotiation Interview with a 1-month follow-up telephone booster (Brief Negotiation Interview with booster) (n=295), or standard care (n=148). We also included a standard care with no assessments (n=149) group to examine the effect of assessments on drinking outcomes. Primary outcomes analyzed with mixed-models procedures included past 7-day alcohol consumption and 28-day binge episodes at 6 and 12 months, collected by interactive voice response. Secondary outcomes included negative health behaviors and consequences collected by telephone surveys. RESULTS The reduction in mean number of drinks in the past 7 days from baseline to 6 and 12 months was significantly greater in the Brief Negotiation Interview with booster (from 20.4 [95% confidence interval {CI} 18.8 to 22.0] to 11.6 [95% CI 9.7 to 13.5] to 13.0 [95% CI 10.5 to 15.5]) and Brief Negotiation Interview (from 19.8 [95% CI 18.3 to 21.4] to 12.7 [95% CI 10.8 to 14.6] to 14.3 [95% CI 11.9 to 16.8]) than in standard care (from 20.9 [95% CI 18.7 to 23.2] to 14.2 [95% CI 11.2 to 17.1] to 17.6 [95% CI 14.1 to 21.2]). The reduction in 28-day binge episodes was also greater in the Brief Negotiation Interview with booster (from 7.5 [95% CI 6.8 to 8.2] to 4.4 [95% CI 3.6 to 5.2] to 4.7 [95% CI 3.9 to 5.6]) and Brief Negotiation Interview (from 7.2 [95% CI 6.5 to 7.9] to 4.8 [95% CI 4.0 to 5.6] to 5.1 [95% CI 4.2 to 5.9]) than in standard care (from 7.2 [95% CI 6.2 to 8.2] to 5.7 [95% CI 4.5 to 6.9] to 5.8 [95% CI 4.6 to 7.0]). The Brief Negotiation Interview with booster offered no significant benefit over the Brief Negotiation Interview alone. There were no differences in drinking outcomes between the standard care and standard care-no assessment groups. The reductions in rates of driving after drinking more than 3 drinks from baseline to 12 months were greater in the Brief Negotiation Interview (38% to 29%) and Brief Negotiation Interview with booster (39% to 31%) groups than in the standard care group (43% to 42%). CONCLUSION Emergency practitioner-performed brief interventions can reduce alcohol consumption and episodes of driving after drinking in hazardous and harmful drinkers. These results support the use of brief interventions in ED settings.

Emergency Department–Initiated Buprenorphine/Naloxone Treatment for Opioid Dependence: A Randomized Clinical Trial

IMPORTANCE Opioid-dependent patients often use the emergency department (ED) for medical care. OBJECTIVE To test the efficacy of 3 interventions for opioid dependence: (1) screening and referral to treatment (referral); (2) screening, brief intervention, and facilitated referral to community-based treatment services (brief intervention); and (3) screening, brief intervention, ED-initiated treatment with buprenorphine/naloxone, and referral to primary care for 10-week follow-up (buprenorphine). DESIGN, SETTING, AND PARTICIPANTS A randomized clinical trial involving 329 opioid-dependent patients who were treated at an urban teaching hospital ED from April 7, 2009, through June 25, 2013. INTERVENTIONS After screening, 104 patients were randomized to the referral group, 111 to the brief intervention group, and 114 to the buprenorphine treatment group. MAIN OUTCOMES AND MEASURES Enrollment in and receiving addiction treatment 30 days after randomization was the primary outcome. Self-reported days of illicit opioid use, urine testing for illicit opioids, human immunodeficiency virus (HIV) risk, and use of addiction treatment services were the secondary outcomes. RESULTS Seventy-eight percent of patients in the buprenorphine group (89 of 114 [95% CI, 70%-85%]) vs 37% in the referral group (38 of 102 [95% CI, 28%-47%]) and 45% in the brief intervention group (50 of 111 [95% CI, 36%-54%]) were engaged in addiction treatment on the 30th day after randomization (P < .001). The buprenorphine group reduced the number of days of illicit opioid use per week from 5.4 days (95% CI, 5.1-5.7) to 0.9 days (95% CI, 0.5-1.3) vs a reduction from 5.4 days (95% CI, 5.1-5.7) to 2.3 days (95% CI, 1.7-3.0) in the referral group and from 5.6 days (95% CI, 5.3-5.9) to 2.4 days (95% CI, 1.8-3.0) in the brief intervention group (P < .001 for both time and intervention effects; P = .02 for the interaction effect). The rates of urine samples that tested negative for opioids did not differ statistically across groups, with 53.8% (95% CI, 42%-65%) in the referral group, 42.9% (95% CI, 31%-55%) in the brief intervention group, and 57.6% (95% CI, 47%-68%) in the buprenorphine group (P = .17). There were no statistically significant differences in HIV risk across groups (P = .66). Eleven percent of patients in the buprenorphine group (95% CI, 6%-19%) used inpatient addiction treatment services, whereas 37% in the referral group (95% CI, 27%-48%) and 35% in the brief intervention group (95% CI, 25%-37%) used inpatient addiction treatment services (P < .001). CONCLUSIONS AND RELEVANCE Among opioid-dependent patients, ED-initiated buprenorphine treatment vs brief intervention and referral significantly increased engagement in addiction treatment, reduced self-reported illicit opioid use, and decreased use of inpatient addiction treatment services but did not significantly decrease the rates of urine samples that tested positive for opioids or of HIV risk. These findings require replication in other centers before widespread adoption. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00913770.

Lactation and breast cancer risk: a case-control study in Connecticut.

In this report, we examined the relationship between lactation and breast cancer risk, in a case–control study of breast cancer, conducted in Connecticut between 1994 and 1998. Included were 608 incident breast cancer cases and 609 age frequency matched controls, aged 30–80 years old. Cases and controls were interviewed by trained study interviewers, using a standardized, structured questionnaire, to obtain information on lactation and other major risk factors. Parous women who reported ever lactation had a borderline significantly reduced risk of breast cancer (OR=0.83, 95% CI, 0.63–1.09). An OR of 0.53 (95% CI, 0.27–1.04) was observed in those having breastfed more than 3 children compared to those who never lactated. Women having breastfed their first child for more than 13 months had an OR of 0.47 (95% CI, 0.23–0.94) compared to those who never breastfed. Lifetime duration of lactation also showed a risk reduction while none of the ORs were statistically significant. Further stratification by menopausal status showed a risk reduction related to lactation for both pre- and postmenopausal women, while the relationship is less consistent for the latter. These results support an inverse association between breastfeeding and breast cancer risk.

Can mammography screening explain the race difference in stage at diagnosis of breast cancer

Background. A race difference in the stage at diagnosis of breast cancer is well established: African American women are less likely than white women to be diagnosed at a localized stage. The purpose of this study was to determine the extent to which the observed race (black/white) difference in stage at diagnosis of breast cancer could be accounted for by race differences in the mammography screening history.

Cigarette smoking and risk of non-Hodgkin lymphoma subtypes among women

Previous studies of the relationship between cigarette smoking and non-Hodgkin lymphoma (NHL) have yielded conflicting results, perhaps because most studies have evaluated the risk for all NHL subtypes combined. Data from a population-based case–control study conducted among women in Connecticut were used to evaluate the impact of cigarette smoking on the risk of NHL by histologic type, tumour grade, and immunologic type. A total of 601 histologically confirmed, incident cases of NHL and 718 population-based controls provided in-person interviews. A standardised, structured questionnaire was used to collect information on each subjects current smoking status, age at initiation, duration and intensity of smoking, and cumulative lifetime exposure to smoking. Our data suggest that cigarette smoking does not alter the risk of all NHL subtypes combined. However, increased risk of follicular lymphoma appears to be associated with increased intensity and duration of smoking, and cumulative lifetime exposure to smoking. Compared with nonsmokers, women with a cumulative lifetime exposure of 16–33 pack-years and 34 pack-years or greater experience 50% increased risk (OR=1.5, 95% CI 0.9–2.5) and 80% increased risk (OR=1.8, 95% CI 1.1–3.2), respectively, of follicular lymphoma (P for linear trend=0.05). Our study findings are consistent with several previous epidemiologic studies suggesting that cigarette smoking increases the risk of follicular lymphoma. This research highlights the importance of distinguishing between NHL subtypes in future research on the aetiology of NHL.

Alcohol use and risk of non-Hodgkin's lymphoma among Connecticut women (United States).

Objective: Incidence rates of non-Hodgkins lymphoma (NHL) have risen dramatically over the past several decades; however, the etiology of NHL remains largely unknown. Previous studies of the relationship between alcohol consumption and NHL have yielded conflicting results. Data from a population-based case–control study among women in Connecticut were analyzed to determine the potential impact of alcohol consumption on risk of NHL. Methods: The study included 601 histologically confirmed, incident cases of NHL and 718 population-based controls. In-person interviews were administered using standardized, structured questionnaires to collect data on history of consumption for beer, wine, and liquor. Results: When compared to non-drinkers, women who reported consumption of at least 12 drinks per year of any type of alcohol experienced slightly reduced risk of NHL (OR: 0.82; 95% CI: 0.65–1.04). Further stratification by alcohol type revealed that the inverse association was mainly limited to wine consumption (OR: 0.75; 95% CI: 0.59–0.96), with no clear association for beer or liquor consumption. Risk of NHL was further reduced with increasing duration of wine consumption (p for linear trend = 0.02). Consumption of wine for greater than 40 years was associated with approximately 40% reduction in risk (OR: 0.63; 95% CI: 0.44–0.91). Conclusion: Our results are consistent with several recent epidemiologic studies that have also suggested an inverse association between wine consumption and risk of NHL. The reduction in risk of NHL associated with increased duration of wine consumption warrants further investigation in other populations.

Glutathione S-transferase M1 and T1 genetic polymorphisms, alcohol consumption and breast cancer risk.

Alcohol consumption has been inconsistently associated with breast cancer risk. Recent studies suggest that genetic polymorphisms of glutathione S-transferases (GSTs) may modify this relation. To determine if breast cancer risk is associated with GSTM1 and GSTT1 genetic polymorphisms, and to evaluate the effect modification between GST genotypes and alcohol consumption in the risk of breast cancer, we conducted a case–control study in the state of Connecticut in the period 1998 and 2001. Cases were histologically confirmed, incident breast cancer patients in New Haven County, CT. Controls were randomly selected from women histologically confirmed to be without breast cancer. The study results show that, while GSTM1 genotypes were not associated with breast cancer risk, GSTT1-null genotype was associated with a significant 90% increased risk for postmenopausal women (OR=1.9, 95% CI 1.2–3.0). Analysis by GST genotypes and alcohol consumption shows that GSTM1A ever-drinking women had a 2.5-fold (OR=2.5, 95% CI 1.1–5.5) increased risk of breast cancer compared to the GSTM1A never-drinkers, and the risk increases with duration and daily amount of alcohol consumption. Postmenopausal women with GSTT1-null genotype, who consumed a lifetime of >250 kg of spirit-equivalents, had an almost seven-fold increased risk (OR=6.8, 95% CI 1.4–33.9), and drinking commencing at younger ages appears to carry a higher risk. An OR of 8.2 (95% CI 1.2–57.4) was observed for those with GSTM1A, and GSTT1-null genotypes who had consumed a lifetime of >250 kg of spirit-equivalents. In conclusion, alcohol consumption may increase breast cancer risk among those who carry susceptible GST genotypes.

Cigarette smoking, glutathione-S-transferase M1 and T1 genetic polymorphisms, and breast cancer risk (United States)

Objective: It has been suggested that functional polymorphisms in genes encoding tobacco carcinogen-metabolizing enzymes may modify the relationship between tobacco smoking and breast cancer risk. We sought to determine if there is a gene–environment interaction between GSTM1 (GSTM1A and GSTM1B), and GSTT1 genotypes and cigarette smoking in the risk of breast cancer. Methods: Cases and controls were recruited in a case–control study conducted in Connecticut from 1994 to 1998. Cases were histologically confirmed, incident breast cancer patients, and controls were randomly selected from women histologically confirmed to be without breast cancer. A total of 338 cases and 345 controls were genotyped for GSTM1 and GSTT1. Results: None of the GSTM1 genotypes, either alone or in combination with cigarette smoking, was associated with breast cancer risk. There was, however, a significantly increased risk of breast cancer among postmenopausal women with a GSTT1 null genotype (OR = 1.9, 95% CI 1.2–2.9). There were also indications of increased risk of breast cancer associated with cigarette smoking for postmenopausal women with GSTT1-null genotype, especially for those who commenced smoking before age 18 (OR = 2.9, 95% CI 1.0–8.8). Conclusion: Women with a GSTT1-null genotype may have an increased breast cancer risk, especially postmenopausal women who started smoking at younger ages.