Smoking is Associated with Increased Risk of Major Bleeding: A Prospective Cohort Study

2018 ◽  
Vol 119 (01) ◽  
pp. 039-047
Author(s):  
Anne Langsted ◽  
Børge Nordestgaard

Background Tobacco smoking represents the most preventable cause of several fatal and disabling diseases worldwide. Several ingredients in tobacco have been suspected to cause changes in the arterial wall leading to instability of blood vessels. The association of smoking with major bleeding is largely unexplored. We tested the hypothesis that smoking and high tobacco consumption are associated with increased risk of bleeding. Materials and Methods This is a prospective cohort study with a mean follow-up of 5.9 years including 99,359 individuals from the Copenhagen General Population Study, with a questionnaire including self-reported smoking status and information on smoking intensity in cigarettes per day and pack-years. In this study, 17,555 were current smokers, 40,182 former smokers and 41,622 were never smokers. Results Multivariable adjusted hazard ratios for current smokers versus never smokers were 1.49 (95% confidence interval [CI]: 1.38–1.61) for any major bleeding, 1.71 (1.37–2.13) for intracranial bleeding, 1.35 (1.14–1.60) for airway bleeding, 2.20 (1.84–2.62) for gastrointestinal bleeding and 1.39 (1.26–1.55) for urinary bleeding. Increased smoking intensity was also associated with increased risk of any major bleeding, where > 40 pack-years in current and former smokers compared with never smokers had a multivariable adjusted hazard ratio of 1.59 (95% CI: 1.45–1.73) (p for trend across four groups: < 0.001). Also, current smokers smoking > 20 cigarettes per day compared with former and never smokers had a corresponding hazard ratio of 1.67 (1.51–1.85) (p for trend across four groups: < 0.001). Conclusion Current smokers have an increased risk of any major bleeding as well as of intracranial, airway, gastrointestinal and urinary bleeding. Also, increased smoking intensity was associated with increased risk of major bleeding.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 33.1-34 ◽  
Author(s):  
D. Simon ◽  
K. Tascilar ◽  
A. Kleyer ◽  
S. Bayat ◽  
E. Kampylafka ◽  
...  

Background:We have previously reported that the presence of musculoskeletal pain in psoriasis patients is associated with a higher risk of developing psoriatic arthritis (PsA) (1). Furthermore, a subset of psoriasis patients shows evidence for structural entheseal lesions (SEL) in their hand joints (2), sometimes also referred as “Deep Koebner Phenomenon”, which are highly specific for psoriatic disease and virtually absent in healthy controls, rheumatoid arthritis and hand osteoarthritis patients (2-4). However, it remains unclear whether SEL alone or in combination with musculoskeletal pain are associated with the development of PsA.Objectives:To test whether the presence of SEL in psoriasis patients increases the risk for progression to PsA and how this is related to the presence of musculoskeletal pain.Methods:Psoriasis patients without evidence of PsA were enrolled in a prospective cohort study between 2011 and 2018. All patients underwent baseline assessment of SEL in their 2ndand 3rdMCP joints by high-resolution peripheral quantitative computed tomography (HR-pQCT). The risk of PsA development associated with SEL and arthralgia was explored using survival analyses and multivariable Cox regression models.Results:114 psoriasis patients (72 men/42 women) with a mean (SD) follow-up duration of 28.2 (17.7) months were included, 24 of whom developed PsA (9.7 /100 patient-years, 95%CI 6.2 to 14.5) during the observation period. Patients with SEL (N=41) were at higher risk of developing PsA compared to patients without such lesions (21.4/100 patient-years, 95%CI 12.5 to 34.3, HR 5.10, 95%CI 1.53 to 16.99, p=0.008) (Kaplan Meier plot A). Furthermore, while patients without arthralgia and without SEL had a very low progression rate to PsA (1/29; 3.4%), patients with arthralgia but no SEL showed higher progression (5/33; 15.2%), which was in line with previous observations (1) (Kaplan Meier plot B). Presence of SEL further enhanced the risk for progression to PsA both in the absence (6/16; 37.5%) and presence (6/14; 42.8%) of arthralgia with the highest progression rate in those subjects with both arthralgia and SEL (p<0.001 by log rank test for trend) (Kaplan Meier plot B).Conclusion:Presence of SEL is associated with an increased risk of developing PsA in patients with psoriasis. If used together with pain, SEL allow defining subsets of psoriasis patients with very low and very high risk to develop PsA.References:[1]Faustini F et al. Ann Rheum Dis. 2016;75:2068-2074[2]Simon D et al. Ann Rheum Dis. 2016;75:660-6[3]Finzel S et al. Ann Rheum Dis. 2011;70:122-7[4]Finzel S et al. Arthritis Rheum. 2011;63:1231-6Disclosure of Interests:David Simon Grant/research support from: Else Kröner-Memorial Scholarship, Novartis, Consultant of: Novartis, Lilly, Koray Tascilar: None declared, Arnd Kleyer Consultant of: Lilly, Gilead, Novartis,Abbvie, Speakers bureau: Novartis, Lilly, Sara Bayat Speakers bureau: Novartis, Eleni Kampylafka Speakers bureau: Novartis, BMS, Janssen, Axel Hueber Grant/research support from: Novartis, Lilly, Pfizer, Consultant of: Abbvie, BMS, Celgene, Gilead, GSK, Lilly, Novartis, Speakers bureau: GSK, Lilly, Novartis, Jürgen Rech Consultant of: BMS, Celgene, Novartis, Roche, Chugai, Speakers bureau: AbbVie, Biogen, BMS, Celgene, MSD, Novartis, Roche, Chugai, Pfizer, Lilly, Louis Schuster: None declared, Klaus Engel: None declared, Michael Sticherling Grant/research support from: Novartis, Consultant of: Advisory boards Abbvie, Celgene, Janssen Cilag, Lilly, Pfizer, MSD, Novartis, Amgen, Leo, Sanofi, UCB, Speakers bureau: Abbvie, Celgene, Janssen Cilag, Leo, MSD, Novartis, Pfizer, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB


2020 ◽  
Vol 179 (11) ◽  
pp. 1711-1719
Author(s):  
Alessandro Andreucci ◽  
Paul Campbell ◽  
Lisa K Mundy ◽  
Susan M Sawyer ◽  
Silja Kosola ◽  
...  

Abstract Adults with sleep problems are at higher risk for onset of musculoskeletal pain, but the evidence is less clear for children. This prospective cohort study investigated whether children with sleep problems are at higher risk for onset of musculoskeletal pain and explored whether sex is a modifier of this association. In a prospective cohort study of Australian schoolchildren (n = 1239, mean age 9 years), the associations between sleep problems at baseline and new onset of both musculoskeletal pain and persistent musculoskeletal pain (pain lasting > 3 months) 1 year later were investigated using logistic regression. The potential modifying effect of sex was also assessed. One-year incidence proportion for musculoskeletal pain onset is 43% and 7% for persistent musculoskeletal pain. Sleep problems were associated with musculoskeletal pain onset and persistent musculoskeletal pain onset in boys, odds ratio 2.80 (95% CI 1.39, 5.62) and OR 3.70 (1.30, 10.54), respectively, but not girls OR 0.58 (0.28, 1.19) and OR 1.43 (0.41, 4.95), respectively. Conclusions: Rates of musculoskeletal pain are high in children. Boys with sleep problems are at greater risk of onset of musculoskeletal pain, but girls do not appear to have higher risk. Consideration of sleep health may help prevent persistent musculoskeletal pain in children. What is Known:• Sleep problems are associated with the onset of musculoskeletal pain in adults.• It is not clear if the association between sleep problems and the onset of musculoskeletal pain is present also in children and if sex plays a role in this association. What is New:• This is the first large population-based study that has prospectively investigated the relationship between sleep problems and onset of musculoskeletal pain in school-aged children.• Children, especially boys with sleep problems, were at increased risk for the development of persistent musculoskeletal pain.


Author(s):  
Jessica G Abell ◽  
Camille Lassale ◽  
G David Batty ◽  
Paola Zaninotto

Abstract Background Falls in later life that require admission to hospital have well-established consequences for future disability and health. The likelihood and severity of a fall will result from the presence of one or more risk factors. The aim of this study is to examine risk factors identified for their ability to prevent falls and to assess whether they are associated with hospital admission after a fall. Methods Analyses of data from the English Longitudinal Study of Aging (ELSA), a prospective cohort study. In a sample of 3783 men and women older than 60 years old, a range of potential risk factors measured at Wave 4 (demographic, social environment, physical, and mental functioning) were examined as predictors of fall-related hospitalizations, identified using International Classification of Diseases, 10th Revision (ICD-10) code from linked hospital records in the United Kingdom. Subdistribution hazard models were used to account for competing risk of death. Results Several risk factors identified by previous work were confirmed. Suffering from urinary incontinence (subdistribution hazard ratio = 1.49; 95% CI: 1.14, 1.95) and osteoporosis (subdistribution hazard ratio = 1.48; 95% CI: 1.05, 2.07), which are not commonly considered at an early stage of screening, were found to be associated with hospital admission after a fall. Both low and moderate levels of physical activity were also found to somewhat increase the risk of hospital admission after a fall. Conclusions Several predictors of having a fall, severe enough to require hospital admission, have been confirmed. In particular, urinary incontinence should be considered at an earlier point in the assessment of risk.


2020 ◽  
Author(s):  
Evangelia Elenis ◽  
Anna-Karin Wikström ◽  
Marija Simic

Abstract Background: Preterm birth (occurring before 37 completed weeks of gestation) affects 15 million infants annually, 7.5% of which die due to related complications. The detection and early diagnosis are therefore paramount in order to prevent the development of prematurity and its consequences. So far, focus has been laid on the association between reduced intrauterine fetal growth during late gestation and prematurity. The aim of the current study was to investigate the association between accelerated fetal growth in early pregnancy and the risk of preterm birth. Methods: This prospective cohort study included 69 617 singleton pregnancies without congenital malformations and with available biometric measurements during the first and second trimester. Estimation of fetal growth was based on measurements of biparietal diameter (BPD) at first and second trimester scan. We investigated the association between accelerated fetal growth and preterm birth prior to 37 weeks of gestation. The outcome was further stratified into very preterm birth (before 32 weeks of gestation) or moderate preterm birth (between 32 and 37 weeks of gestation) and medically induced or spontaneous preterm birth and was further explored. Results: The odds of prematurity were increased among fetuses with accelerated BPD growth (> 90th centile) estimated between first and second ultrasound scan, even after adjustment for possible confounders (aOR 1.36; 95% CI 1.20-1.54). The findings remained significant what regards moderate preterm births but not earlier births. Regarding medically induced preterm birth, the odds were found to be elevated in the group of fetuses with accelerated growth in early pregnancy (aOR 1.34; 95% CI 1.11-1.63). On the contrary, fetuses with delayed fetal growth exhibited lower risk for both overall and spontaneous preterm birth.Conclusions: Fetuses with accelerated BPD growth in early pregnancy, detected by ultrasound examination during the second trimester, exhibited increased risk of being born preterm. The findings of the current study suggest that fetal growth in early pregnancy should be taken into account when assessing the likelihood for preterm birth.


BMJ ◽  
2018 ◽  
pp. k3547 ◽  
Author(s):  
Julie C Antvorskov ◽  
Thorhallur I Halldorsson ◽  
Knud Josefsen ◽  
Jannet Svensson ◽  
Charlotta Granström ◽  
...  

Abstract Objective To examine the association between prenatal gluten exposure and offspring risk of type 1 diabetes in humans. Design National prospective cohort study. Setting National health information registries in Denmark. Participants Pregnant Danish women enrolled into the Danish National Birth Cohort, between January 1996 and October 2002, Main outcome measures Maternal gluten intake, based on maternal consumption of gluten containing foods, was reported in a 360 item food frequency questionnaire at week 25 of pregnancy. Information on type 1 diabetes occurrence in the participants’ children, from 1 January 1996 to 31 May 2016, were obtained through registry linkage to the Danish Registry of Childhood and Adolescent Diabetes. Results The study comprised 101 042 pregnancies in 91 745 women, of whom 70 188 filled out the food frequency questionnaire. After correcting for multiple pregnancies, pregnancies ending in abortions, stillbirths, lack of information regarding the pregnancy, and pregnancies with implausibly high or low energy intake, 67 565 pregnancies (63 529 women) were included. The average gluten intake was 13.0 g/day, ranging from less than 7 g/day to more than 20 g/day. The incidence of type 1 diabetes among children in the cohort was 0.37% (n=247) with a mean follow-up period of 15.6 years (standard deviation 1.4). Risk of type 1 diabetes in offspring increased proportionally with maternal gluten intake during pregnancy (adjusted hazard ratio 1.31 (95% confidence interval 1.001 to 1.72) per 10 g/day increase of gluten). Women with the highest gluten intake versus those with the lowest gluten intake (≥20 v <7 g/day) had double the risk of type 1 diabetes development in their offspring (adjusted hazard ratio 2.00 (95% confidence interval 1.02 to 4.00)). Conclusions High gluten intake by mothers during pregnancy could increase the risk of their children developing type 1 diabetes. However, confirmation of these findings are warranted, preferably in an intervention setting.


Author(s):  
H. Miao ◽  
K. Chen ◽  
X. Yan ◽  
F. Chen

Background: This study aimed to investigate the association between sugar in beverage and dementia, Alzheimer Disease (AD) dementia and stroke. Methods: This prospective cohort study were based on the US community-based Framingham Heart Study (FHS). Sugar in beverage was assessed between 1991 and 1995 (5th exam). Surveillance for incident events including dementia and stroke commenced at examination 9 through 2014 and continued for 15-20 years. Results: At baseline, a total of 1865 (63%) subjects consumed no sugar in beverage, whereas 525 (18%) subjects consumed it in 1-7 servings/week and 593 (29%) in over 7 servings/week. Over an average follow-up of 19 years in 1384 participants, there were 275 dementia events of which 73 were AD dementia. And 103 of 1831 participants occurred stroke during the follow-up nearly 16 years. After multivariate adjustments, individuals with the highest intakes of sugar in beverage had a higher risk of all dementia, AD dementia and stroke relative to individuals with no intakes, with HRs of 2.80(95%CI 2.24-3.50) for all dementia, 2.55(95%CI 1.55-4.18) for AD dementia, and 2.11(95%CI 1.48-3.00) for stroke. And the same results were shown in the subgroup for individuals with median intakes of sugar in beverage. Conclusion: Higher consumption of sugar in beverage was associated with an increased risk of all dementia, AD dementia and stroke.


Sign in / Sign up

Export Citation Format

Share Document