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Sökning: WFRF:(Fall Ole)

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1.
  • Bergh, Cecilia, 1972-, et al. (författare)
  • Severe infections and subsequent delayed cardiovascular disease
  • 2017
  • Ingår i: European Journal of Preventive Cardiology. - : Sage Publications. - 2047-4873 .- 2047-4881. ; 24:18, s. 1958-1966
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Severe infections in adulthood are associated with subsequent short-term cardiovascular disease. Whether hospital admission for sepsis or pneumonia is associated with persistent increased risk (over a year after infection) is less well established.Design: The design of this study was as a register-based cohort study.Methods: Some 236,739 men born between 1952-1956 were followed from conscription assessments in adolescence to 2010. All-cause cardiovascular disease ( n = 46,754), including coronary heart disease ( n = 10,279) and stroke ( n = 3438), was identified through national registers 1970-2010 (at ages 18-58 years).Results: Sepsis or pneumonia in adulthood (resulting in hospital admission) are associated with increased risk of cardiovascular disease in the years following infection. The risk is highest during the first year after the infection, with an adjusted hazard ratio (and 95% confidence intervals) of 6.33 (5.65-7.09) and a notably increased risk persisted with hazard ratios of 2.47 (2.04-3.00) for the second and 2.12 (1.71-2.62) for the third year after infection. The risk attenuated with time, but remained raised for at least five years after infection; 1.87 (1.47-2.38). The results are adjusted for characteristics in childhood, cardiovascular risk factors and medical history in adolescence. Similar statistically significant associations were found for coronary heart disease and stroke.Conclusions: Raised risks of cardiovascular disease following hospital admission for sepsis or pneumonia were increased for more than five years after the infection, but with the highest magnitude during the first three years following infection, suggesting a period of vulnerability when health professionals and patients should be aware of the heightened risk for cardiovascular disease.
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  • Ladfors, Lars, 1951, et al. (författare)
  • Is a speculum examination sufficient for excluding the diagnosis of ruptured fetal membranes?
  • 1997
  • Ingår i: Acta obstetricia et gynecologica Scandinavica. - 0001-6349. ; 76:8, s. 739-42
  • Tidskriftsartikel (refereegranskat)abstract
    • To determine the false negative rate of a sterile speculum examination for the diagnosis of rupture of the membranes in women not in labor and without visible amniotic fluid at speculum examination. Furthermore, possible risks to the mother and the baby after suspected rupture of the membranes were analyzed.
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6.
  • Ladfors, Lars, 1951, et al. (författare)
  • Risk factors for neonatal sepsis in offspring of women with prelabor rupture of the membranes at 34-42 weeks.
  • 1998
  • Ingår i: Journal of perinatal medicine. - 0300-5577. ; 26:2, s. 94-101
  • Tidskriftsartikel (refereegranskat)abstract
    • One thousand three hundred eighty-five women with PROM (prelabor rupture of the membranes) participated in a prospective randomized study. Women with PROM were randomized to induction the following morning after PROM (early induction group) or induction two days later (late induction group). If contractions started within 2 hours after admission these women were included in the short latency group. All neonatal infections were classified as verified sepsis (positive culture) or clinical sepsis. The aim of the study was to compare the perinatal infectious outcome between the groups with different expectant managements in women with PROM and to study the association between demographic, intrapartum and postpartum variables and neonatal sepsis. In the short latency group one neonate had a proven sepsis while four neonates with proven sepsis were found in the early induction group. No proven sepsis was detected in the late induction group. Univariate analyses showed a significant association between clinical sepsis and: induction of labor (OR = 2.94, 95% CI 1.30-6.68), established labor 24.1-32 hours after ROM (OR = 5.89, 95% CI 1.68-20.63), established labor > 32 hours after ROM (OR = 4.59, 95% CI 1.52-13.87), time from ROM to delivery > 32 hours (OR = 5.07, 95% CI 1.40-18.39), cesarean section (OR = 11.03, 95% CI 4.10-29.68), chorioamnionitis before or during delivery (OR = 27.14, 95% CI 2.38-309.16), endometritis (OR = 18.08, 95% CI 1.82-179.87), CRP over 20 mg/l in the umbilical cord (OR = 17.12, 95% CI 5.68-52.12) and Apgar score < 7 after 1, 5 or 10 minutes. In a stepwise logistic regression analysis a significant association was found between clinical sepsis and cesarean section (OR = 10.08, 95% CI = 3.26-31.20), time from ROM to delivery > 32 h (OR = 3.74, 95% CI 1.62-8.62), gestational age 34-36 weeks (OR = 3.16, 95% CI 1.11-8.96) and parous women (OR = 2.41, 95% CI 1.04-5.57). In conclusion, this study indicates that that there was no difference in the incidence of neonatal infections between those with early and late induction. Clinical neonatal sepsis was associated with time from PROM to delivery over 32 hours, cesarean section, parous women and gestational age between 34 and 36 weeks.
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7.
  • Montgomery, Scott, 1961-, et al. (författare)
  • Childhood exposures among mothers and Hodgkin's lymphoma in offspring
  • 2015
  • Ingår i: Cancer Epidemiology. - : Elsevier. - 1877-7821 .- 1877-783X. ; 39:6, s. 1006-1009
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Childhood exposures in mothers, signaled by number of older and younger siblings, have lifelong consequences for aspects of immune function. We hypothesized that these may influence young adult-onset Hodgkin's lymphoma (HL) risk in offspring.Materials and methods: Swedish registers identified 2028 cases of young adult onset HL (diagnosed between ages 15-39 years) up to 2012 among those born since 1958; and 18,374 matched controls. Conditional logistic regression was used to assess HL risk associated with number of older and younger siblings of mothers.Results: Having a mother with more than two older siblings is associated with lower HL risk, and the association is statistically significant for mothers with three or more siblings, compared with none. The adjusted odds ratios (and 95% confidence intervals) are 1.04 (0.93-1.16); 0.95 (0.81-1.10); and 0.81 (0.66-0.98) for one, two, and three or more older siblings, respectively. There is no association between number of mothers' younger siblings and HL risk.Conclusions: Exposures during the childhood of mothers may influence young onset adult HL risk in offspring, perhaps through vertical transmission of infectious agents, or through other long-term influences on maternal immune function.
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8.
  • Montgomery, Scott, 1961-, et al. (författare)
  • Mortality following a brain tumour diagnosis in patients with multiple sclerosis
  • 2013
  • Ingår i: BMJ Open. - London, United Kingdom : BMJ Publishing Group. - 2044-6055. ; 3:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: As brain tumours and their treatment may theoretically have a poorer prognosis in inflammatory central nervous system diseases such as multiple sclerosis (MS), all-cause mortality following a brain tumour diagnosis was compared between patients with and without MS. The potential role of age at tumour diagnosis was also examined.Setting: Hospital inpatients in Sweden with assessment of mortality in hospital or following discharge.Participants: Swedish national registers identified 20 543 patients with an MS diagnosis (1969–2005) and they were matched individually to produce a comparison cohort of 204 163 members of the general population without MS. Everyone with a primary brain tumour diagnosis was selected for this study: 111 with MS and 907 without MS.Primary and secondary outcome measures: 5-year mortality risk following brain tumour diagnosis and age at brain tumour diagnosis.Results: A non-statistically significant lower mortality risk among patients with MS (lower for those with tumours of high-grade and uncertain-grade malignancy and no notable difference for low-grade tumours) produced an unadjusted HR (and 95% CI) of 0.75 (0.56 to 1.02). After adjustment for age at diagnosis, grade of malignancy, sex, region of residence and socioeconomic index, the HR is 0.91 (0.67–1.24). The change in estimate was largely due to adjustment for age at brain tumour diagnosis, as patients with MS were on average 4.7 years younger at brain tumour diagnosis than those in the comparison cohort (p<0.001).Conclusions: Younger age at tumour diagnosis may contribute to mortality reduction in those with highgrade and uncertain-grade brain tumours. Survival following a brain tumour is not worse in patients with MS; even after age at brain tumour diagnosis and grade of malignancy are taken into account.
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9.
  • Shen, Qing, et al. (författare)
  • Psychiatric disorders and subsequent risk of cardiovascular disease : a longitudinal matched cohort study across three countries
  • 2023
  • Ingår i: eClinicalMedicine. - : Elsevier. - 2589-5370. ; 61
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Several psychiatric disorders have been associated with increased risk of cardiovascular disease (CVD), however, the role of familial factors and the main disease trajectories remain unknown.METHODS: In this longitudinal cohort study, we identified a cohort of 900,240 patients newly diagnosed with psychiatric disorders during January 1, 1987 and December 31, 2016, their 1,002,888 unaffected full siblings, and 1:10 age- and sex-matched reference population from nationwide medical records in Sweden, who had no prior diagnosis of CVD at enrolment. We used flexible parametric models to determine the time-varying association between first-onset psychiatric disorders and incident CVD and CVD death, comparing rates of CVD among patients with psychiatric disorders to the rates of unaffected siblings and matched reference population. We also used disease trajectory analysis to identify main disease trajectories linking psychiatric disorders to CVD. Identified associations and disease trajectories of the Swedish cohort were validated in a similar cohort from nationwide medical records in Denmark (N = 875,634 patients, same criteria during January 1, 1969 and December 31, 2016) and in Estonian cohorts from the Estonian Biobank (N = 30,656 patients, same criteria during January 1, 2006 and December 31, 2020), respectively.FINDINGS: During up to 30 years of follow-up of the Swedish cohort, the crude incidence rate of CVD was 9.7, 7.4 and 7.0 per 1000 person-years among patients with psychiatric disorders, their unaffected siblings, and the matched reference population. Compared with their siblings, patients with psychiatric disorders experienced higher rates of CVD during the first year after diagnosis (hazard ratio [HR], 1.88; 95% confidence interval [CI], 1.79-1.98) and thereafter (1.37; 95% CI, 1.34-1.39). Similar rate increases were noted when comparing with the matched reference population. These results were replicated in the Danish cohort. We identified several disease trajectories linking psychiatric disorders to CVD in the Swedish cohort, with or without mediating medical conditions, including a direct link between psychiatric disorders and hypertensive disorder, ischemic heart disease, venous thromboembolism, angina pectoris, and stroke. These trajectories were validated in the Estonian Biobank cohort.INTERPRETATION: Independent of familial factors, patients with psychiatric disorders are at an elevated risk of subsequent CVD, particularly during first year after diagnosis. Increased surveillance and treatment of CVDs and CVD risk factors should be considered as an integral part of clinical management, in order to reduce risk of CVD among patients with psychiatric disorders.
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