scholarly journals Racial Disparities in Delivery Gestational Age among Twin Pregnancies

2017 ◽  
Vol 34 (11) ◽  
pp. 1065-1071
Author(s):  
Catherine Vladutiu ◽  
Tracy Manuck ◽  
Jacqueline Grant

Objective This study aims to estimate the association between maternal race and delivery gestational age among women with twin gestations. Study Design Secondary analysis of a prospective, randomized control trial of 17-α hydroxyprogesterone caproate versus placebo for preterm birth (PTB) prevention in twin gestations. Non-Hispanic (NH) black and whites were included. Demographic and antenatal characteristics were compared. The primary outcome was delivery gestational age. Secondary outcomes included a composite of major neonatal morbidity. Kaplan–Meier curves estimated survival probabilities for delivery gestational age by race. Cox proportional hazards models estimated hazard ratios (HR) and 95% confidence intervals (CI). Results A total of 535 women with twin gestations were included; 150 were NH black. NH blacks delivered earlier than NH whites (33.6 ± 4.8 weeks vs. 35.1 ± 3.5 weeks, p < 0.001). Differences in delivery gestational age between NH blacks and whites were consistent across gestation. In adjusted analyses, NH black race (HR: 1.24, 95% CI: 1.02–1.51), prior PTB (HR: 1.59, 95% CI: 1.15–2.19), and cerclage (HR: 3.90, 95% CI: 2.00–7.60) were associated with an increased risk of earlier delivery. Major neonatal morbidity was higher for NH blacks compared with NH whites (12.7 vs. 7.0%, p = 0.036). Conclusion NH blacks with twin gestations have an increased risk of early delivery and neonatal morbidity compared with NH whites.

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1177
Author(s):  
In Young Choi ◽  
Sohyun Chun ◽  
Dong Wook Shin ◽  
Kyungdo Han ◽  
Keun Hye Jeon ◽  
...  

Objective: To our knowledge, no studies have yet looked at how the risk of developing breast cancer (BC) varies with changes in metabolic syndrome (MetS) status. This study aimed to investigate the association between changes in MetS and subsequent BC occurrence. Research Design and Methods: We enrolled 930,055 postmenopausal women aged 40–74 years who participated in a biennial National Health Screening Program in 2009–2010 and 2011–2012. Participants were categorized into four groups according to change in MetS status during the two-year interval screening: sustained non-MetS, transition to MetS, transition to non-MetS, and sustained MetS. We calculated multivariable-adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for BC incidence using the Cox proportional hazards models. Results: At baseline, MetS was associated with a significantly increased risk of BC (aHR 1.11, 95% CI 1.06–1.17) and so were all of its components. The risk of BC increased as the number of the components increased (aHR 1.46, 95% CI 1.26–1.61 for women with all five components). Compared to the sustained non-MetS group, the aHR (95% CI) for BC was 1.11 (1.04–1.19) in the transition to MetS group, 1.05 (0.96–1.14) in the transition to non-MetS group, and 1.18 (1.12–1.25) in the sustained MetS group. Conclusions: Significantly increased BC risk was observed in the sustained MetS and transition to MetS groups. These findings are clinically meaningful in that efforts to recover from MetS may lead to reduced risk of BC.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Kochav ◽  
R.C Chen ◽  
J.M.D Dizon ◽  
J.A.R Reiffel

Abstract Background Theoretical concern exists regarding AV block (AVB) with class I antiarrhythmics (AADs) when bundle branch block (BBB) is present. Whether this is substantiated in real-world populations is unknown. Purpose To determine the relationship between type of AAD and incidence of AVB in patients with preexisting BBB. Methods We retrospectively studied all patients with BBB who received class I and III AADs between 1997–2019 to compare incidence of AVB. We defined index time as first exposure to either drug class and excluded patients with prior AVB or exposed to both classes. Time-at-risk window ended at first outcome occurrence or when patients were no longer observed in the database. We estimated hazard ratios for incident AVB using Cox proportional hazards models with propensity score stratification, adjusting for over 32,000 covariates from the electronic health record. Kaplan-Meier methods were used to determine treatment effects over time. Results Of 40,120 individuals with BBB, 148 were exposed to a class I AAD and 2401 to a class III AAD. Over nearly 4,200 person-years of follow up, there were 22 and 620 outcome events in the class I and class III cohorts, respectively (Figure). In adjusted analyses, AVB risk was markedly lower in patients exposed to class I AADs compared with class III (HR 0.48 [95% CI 0.30–0.75]). Conclusion Among patients with BBB, exposure to class III AADs was strongly associated with greater risk of incident AVB. This likely reflects differences in natural history of patients receiving class I vs class III AADs rather than adverse class III effects, however, the lack of worse outcomes acutely with class I AADs suggests that they may be safer in BBB than suspected. Funding Acknowledgement Type of funding source: None


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Adam H de Havenon ◽  
Ka-Ho Wong ◽  
Eva Mistry ◽  
Mohammad Anadani ◽  
Shadi Yaghi ◽  
...  

Background: Increased blood pressure variability (BPV) has been associated with stroke risk, but never specifically in patients with diabetes. Methods: This is a secondary analysis of the Action to Control Cardiovascular Risk in Diabetes Follow-On Study (ACCORDION), the long term follow-up extension of ACCORD. Visit-to-visit BPV was analyzed using all BP readings during the first 36 months. The primary outcome was incident ischemic or hemorrhagic stroke after 36 months. Differences in mean BPV was tested with Student’s t-test. We fit Cox proportional hazards models to estimate the adjusted risk of stroke across lowest vs. highest quintile of BPV and report hazard ratios along with 95% confidence intervals (CI). Results: Our analysis included 9,241 patients, with a mean (SD) age of 62.7 (6.6) years and 61.7% were male. Mean (SD) follow-up was 5.7 (2.4) years and number of BP readings per patient was 12.0 (4.3). Systolic, but not diastolic, BPV was higher in patients who developed stroke (Table 1). The highest quintile of SBP SD was associated with increased risk of incident stroke, independent of mean blood pressure or other potential confounders. (Table 2, Figure 1). There was no interaction between SBP SD and treatment arm assignment, although the interaction for glucose approached significance (Table 2). Conclusion: Higher systolic BPV was associated with incident stroke in a large cohort of diabetic patients. Future trials of stroke prevention may benefit from interventions targeting BPV reduction.


2020 ◽  
Author(s):  
Yingting Zuo ◽  
Anxin Wang ◽  
Shuohua Chen ◽  
Xue Tian ◽  
Shouling Wu ◽  
...  

Abstract Background The relationship between estimated glomerular filtration rate (eGFR) trajectories and myocardial infarction (MI) remains unclear in people with diabetes or prediabetes. We aimed to identify common eGFR trajectories in people with diabetes or prediabetes and to examine their association with MI risk. Methods The data of this analysis was derived from the Kailuan study, which was a prospective community-based cohort study. The eGFR trajectories of 24,723 participants from year 2006 to 2012 were generated by latent mixture modeling. Incident cases of MI occurred during 2012 to 2017, confirmed by review of medical records. Cox proportional hazards models were used to calculate hazard ratios (HR) and their 95% confidence intervals (CIs) for the subsequent risk of MI of different eGFR trajectories. Results We identified 5 distinct eGFR trajectories, and named them as low-stable (9.4%), moderate-stable (31.4%), moderate-increasing (29.5%), high-decreasing (13.9%) and high-stable (15.8%) according to their range and pattern. During a mean follow-up of 4.61 years, there were a total of 235 incident MI. Although, the high-decreasing group had similar eGFR levels with the moderate-stable group at last exposure period, the risk was much higher (adjusted HR, 3.43; 95%CI, 1.56–7.54 versus adjusted HR, 2.82; 95%CI, 1.34–5.95). Notably, the moderate-increasing group had reached to the normal range, still had a significantly increased risk (adjusted HR, 2.55; 95%CI, 1.21–5.39). Conclusions eGFR trajectories were associated with MI risk in people with diabetes or prediabetes. Emphasis should be placed on early and long-term detection and control of eGFR decreases to further reduce MI risk.


Author(s):  
Thomas J Littlejohns ◽  
Shabina Hayat ◽  
Robert Luben ◽  
Carol Brayne ◽  
Megan Conroy ◽  
...  

Abstract Visual impairment has emerged as a potential modifiable risk factor for dementia. However, there are a lack of large studies with objective measures of vison and with more than ten years of follow-up. We investigated whether visual impairment is associated with an increased risk of incident dementia in UK Biobank and EPIC-Norfolk. In both cohorts, visual acuity was measured using a “logarithm of the minimum angle of resolution” (LogMAR) chart and categorised as no (≤0.30 LogMAR), mild (&gt;0.3 - ≤0.50 LogMAR), and moderate to severe (&gt;0.50 LogMAR) impairment. Dementia was ascertained through linkage to electronic medical records. After restricting to those aged ≥60 years, without prevalent dementia and with eye measures available, the analytic samples consisted of 62,206 UK Biobank and 7,337 EPIC-Norfolk participants, respectively. In UK Biobank and EPIC-Norfolk. respectively, 1,113 and 517 participants developed dementia over 11 and 15 years of follow-up. Using multivariable cox proportional-hazards models, the hazard ratios for mild and moderate to severe visual impairment were 1.26 (95% Confidence Interval [CI] 0.92-1.72) and 2.16 (95% CI 1.37-3.40), in UK Biobank, and 1.05 (95% CI 0.72-1.53) and 1.93 (95% CI 1.05-3.56) in EPIC-Norfolk, compared to no visual impairment. When excluding participants censored within 5 years of follow-up or with prevalent poor or fair self-reported health, the direction of the associations remained similar for moderate impairment but were not statistically significant. Our findings suggest visual impairment might be a promising target for dementia prevention, however the possibility of reverse causation cannot be excluded.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 5528-5528
Author(s):  
Sean Thomas McSweeney ◽  
Anna Prizment ◽  
Nathan Pankratz ◽  
Corinne E Joshu ◽  
Elizabeth A. Platz ◽  
...  

5528 Background: Genes involved in APUC may affect prognosis in PC. We tested the association of four SNPs involved in the APUC pathway: hydroxy-delta-5-steroid dehydrogenase, 3 beta-and steroid delta-isomerase 1 ( HSD3B1), 5α reductase enzyme ( SRD5A), and solute carrier organic ion ( SLCO2B1) with all-cause and PC mortality 596 in the Atherosclerosis Risk in Communities (ARIC) study. Methods: Between 1987 & 2015 596 men were diagnosed with PC. Median age at diagnosis was 70 (range 53-86) years; 21% of all PC patients were African American. After diagnosis, follow-up was median 8.4 years (max 26.7 years) until PrC death (N = 60), death from any cause (N = 253), or end of 2015. SNPs were genotyped using the Affymetrix Genome-Wide Human SNP Array 6.0 and imputed to the 1000 Genomes Phase 3 reference panel. To examine survival, we used Kaplan-Meier curves and Cox proportional hazards regression. Hazard ratios (HR) and 95% confidence intervals (CI) were adjusted for age, field center, stage and grade at diagnosis. We also controlled for confounding by ancestry by adjusting for genetic principal components. The analyses were conducted in all PrCa patients and in Whites PrCa patients only. Polymorphisms tested included rs1047303 (A = > C, also called 1245C); rs523349 (C = > G); and rs1789693 (A = > T) and rs12422149 (G = > A), located in the aforementioned genes. Results: The A allele for SLCO2B1 rs1789693 (A = > T) was significantly associated with an increased risk of PC mortality (versus T): multivariable-adjusted HRs (95%CI) were (2.06, 1.14-3.74; p = 0.02) and all-cause mortality (1.29, 1.00-1.66; p = 0.05) among Whites. The associations were similar when Whites and African-Americans were combined and when accounting for ancestry. The C allele for HSD3B1 rs1047303 (C = > A) was not statistically significantly associated with either PC or all-cause mortality in the whole cohort (which included localized disease), although HRs were increased for men diagnosed with stage 4 disease (n = 35) in both additive and dominant models. For carriers of the C allele (gain of function) versus AA, HRs were 5.32 (1.16-24.33; p = 0.03) and 6.13 (1.51-24.86; p = 0.01) for PC and all-cause mortality, respectively. All associations with SRDA2 (rs12422149) and SLCO2B1 (rs12422149) were not significant. Conclusions: The gain of function allele in HSD3B1 rs1047303 (1245C) was associated with increased PC and all-cause mortality in men diagnosed with metastatic PC, paralleling prior findings. Associations with SLCO2B1 SNP rs1789693 require validation in larger studies.


Author(s):  
Merethe S. Hansen ◽  
Idlir Licaj ◽  
Tonje Braaten ◽  
Eiliv Lund ◽  
Inger Torhild Gram

Abstract Background We examined the association between active and passive smoking and lung cancer risk and the population attributable fraction (PAF) of lung cancer due to active smoking, in the Norwegian Women and Cancer Study, a nationally representative prospective cohort study. Methods We followed 142,508 women, aged 31–70 years, who completed a baseline questionnaire between 1991 and 2007, through linkages to national registries through December 2015. We used Cox proportional hazards models, to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). We calculated PAF to indicate what proportion of lung cancer cases could have been prevented in the absence of smoking. Results During the more than 2.3 million person-years of observation, we ascertained 1507 lung cancer cases. Compared with never smokers, current (HR 13.88, 95% CI 10.18–18.91) smokers had significantly increased risk of lung cancer. Female never smokers exposed to passive smoking had a 1.3-fold (HR 1.34, 95% CI 0.89–2.01) non- significantly increased risk of lung cancer, compared with never smokers. The PAF of lung cancer was 85.3% (95% CI 80.0–89.2). Conclusion More than 8 in 10 lung cancer cases could have been avoided in Norway, if the women did not smoke.


2021 ◽  
Author(s):  
Somaya Albhaisi ◽  
Rehan Qayyum

Abstract BACKGROUND & AIMS: Interpreting levels of liver enzymes is often challenging because they may be influenced by metabolic processes beyond the liver. Given their pathophysiologic roles in inflammation and oxidative stress, higher levels of these enzymes may be associated with increased risk of mortality. However, studies have found inconsistent results. Thus, we examined the association of liver enzymes levels with cancer mortality in the general U.S. adult population. METHODS: We used the US National Health and Nutrition Examination Survey from 1999 to 2016. Kaplan-Meier survival curve comparisons were examined across quartiles of liver enzymes. Cox proportional hazards models were built to examine the relationship between cancer mortality and liver enzymes quartiles without and with adjustment for potential confounding factors. RESULTS: During the 338,882 person-years follow-up, 1059 participants had cancer-related deaths. There was a nonlinear U-shaped relationship between serum alanine and aspartate aminotransferase (ALT and AST) levels and cancer mortality. There was no relationship between cancer mortality and gamma glutamyltransferase (GGT), however, each 10 IU/L increase in GGT after median was associated with 1% higher mortality risk (HR=1.01; 95% CI=1.00, 1.02; P=0.001). Only subjects with high levels of alkaline phosphatase (ALP) had higher cancer mortality (HR=1.63; 95CI=1.30, 2.05; P<0.001 and HR=1.52; 95%CI=1.20, 1.94; P=0.001 respectively).CONCLUSIONS: Only the lowest and highest serum ALT and AST levels are associated with increased cancer mortality. For ALP, the relationship is present at higher levels. The association with GGT was not robust to different analyses. The mechanisms underlying the observed relationships need further exploration.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Annina Ropponen ◽  
Mo Wang ◽  
Jurgita Narusyte ◽  
Sanna Kärkkäinen ◽  
Victoria Blom ◽  
...  

Abstract Background The associations between a sickness absence spell duration and patient care have been rarely studied. An assumption is that associations would differ by spell duration and by the patient care type, inpatient- or specialized outpatient, due to severity of diseases and/or conditions. We aimed to investigate sickness absence spells in various spell durations as a predictor for subsequent inpatient- and specialized outpatient care separately, and to study if familial confounding plays a role in these associations. Methods We followed a population-based sample of Swedish twins born 1925–90 with national registers from 2001 for first incident sickness absence spell (days to calculate spell duration categorized into ≤30 days, 31–90 days, 91–180 days and ≥ 181 days), or no sickness absence, and for inpatient- and specialized outpatient care until 2013 (n = 24,975). Cox proportional hazards models were applied for hazard ratios (HR) with 95% confidence intervals (CI) while accounting for covariates and familial confounding. Results First incident sickness absence spell across all duration categories was associated with an increased risk of inpatient- (age- and sex adjusted HR 1.28 to 6.05) or specialized outpatient care (HR 1.17–2.50), both in comparison to those without any sickness absence or the shortest sickness absence spell category (1–30 days). The associations remained statistically significant while controlling for covariates or familial confounding. Conclusions First incident sickness absence spell increases the risk of inpatient care or specialized outpatient care regardless of the duration of the sickness absence spell. Hence, incident sickness absence spells should be noted and targeted to actions at workplaces as well as in primary and occupational health care.


Neurology ◽  
2017 ◽  
Vol 88 (19) ◽  
pp. 1849-1855 ◽  
Author(s):  
Chaoran Ma ◽  
Milena Pavlova ◽  
Yesong Liu ◽  
Ying Liu ◽  
Chunmei Huangfu ◽  
...  

Objective:To examine whether probable REM sleep behavior disorder (pRBD) was associated with increased risk of developing stroke in a community-based cohort.Methods:The study included 12,003 participants (mean age 54.0 years) of the Kailuan Study, free of stroke, cancer, Parkinson disease, dementia, and head injury at baseline (2012). We determined pRBD using a validated REM sleep behavior disorder (RBD) questionnaire in 2012. Incident stroke cases were confirmed by review of medical records. We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of stroke according to pRBD status, adjusting for several sleep measures (i.e., insomnia, daytime sleepiness, sleep duration, snoring, and use of hypnotics) and other potential confounders.Results:During 3 years of follow-up, we documented 159 incident stroke cases. Relative to participants without pRBD at the baseline, those with pRBD had a 157% higher risk (95% CI 59%–313%) of developing stroke. Presence of pRBD was associated with increased risk of both stroke types—the adjusted HR was 1.93 (95% CI 1.07–3.46) for ischemic stroke and 6.61 (95% CI 2.27–19.27) for hemorrhagic stroke.Conclusions:Presence of pRBD was associated with a higher risk of developing stroke, including both ischemic and hemorrhagic types. Future studies with clinically confirmed RBD and a longer follow-up would be appropriate to further investigate this association.


Sign in / Sign up

Export Citation Format

Share Document