| 31. |
- Ugge, Henrik, 1987-, et al.
(författare)
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Asthma and allergy in adolescence and risk of prostate cancer
- 2017
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Ingår i: Scandinavian journal of urology. - : Taylor & Francis. - 2168-1805 .- 2168-1813. ; 51:Suppl. 220, s. 20-20
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Introduction: The role of inflammation in prostate cancer has been widely discussed [1]. Exploring the association between immunological or inflammatory conditions, that reflect immune response profile, and prostate cancer risk may provide clues to the type of inflammatory processes involved in the etiology of prostate cancer. Asthma and allergic conditions have been suggested to reduce the risk of prostate cancer, but data from large studies are currently scarce and results are conflicting [2,3].Objectives: To test if asthma, hay fever, or any allergic condition present in adolescence is associated with a decreased risk of prostate cancer later in life.Methods: This study is based on a cohort of 243,309 men born in Sweden between 1952 and 1956 who underwent mandatory conscription assessments for military service around ages 18-19 years. At this time, a thorough assessment of the men’s health was performed, and conditions such as asthma, hay fever, and allergies were recorded. The cohort was followed for incident prostate cancer through linkage with the Swedish cancer- and population registers. Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between the selected conditions and prostate cancer incidence.Results: A total of 1,654 men were diagnosed with prostate cancer during a maximum of 40.3 years of follow-up (median 36.7 years). At the time of conscription assessment, there were 11,754 men with hay fever, 4,943 with an asthma-diagnosis and 16,112 with any allergic condition. We observed no difference in prostate cancer risk for men with asthma (HR: 0.91, 95% CI: 0.63-1.3), hay fever (HR: 1.03, 95% CI: 0.82-1.28) or any allergic condition (HR: 0.98, 95% CI: 0.8-1.19) compared with men without these diagnoses. Small numbers precluded separate analyses of men with advanced or lethal prostate cancer (n¼6 andn¼3, respectively).Conclusion: Our results do not support the hypothesis that presence of asthma or allergic conditions in late adolescence reduces the risk of prostate cancer later in life. If inflammatory processes are involved in the pathogenesis of prostate cancer, the immune response profiles likely differ from those reflected in clinical diagnoses of asthma or allergic conditions. The possibility that different risk patterns may be observed among older men with advanced or lethal prostate cancer, however, cannot be excluded.
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| 32. |
- Vingeliene, Snieguole, 1985-, et al.
(författare)
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Atopic dermatitis, systemic inflammation and subsequent dementia risk
- 2023
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Ingår i: JEADV Clinical Practice. - : John Wiley & Sons. - 2768-6566. ; 2:4, s. 839-848
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Tidskriftsartikel (refereegranskat)abstract
- Background: Atopic dermatitis is a chronic inflammatory skin disease and inflammation has been implicated in development of other chronic diseases, but few studies have examined the relationship with dementia.Objectives: This study examines associations of atopic dermatitis (AD) and systemic inflammation in adolescence measured using erythrocyte sedimenta-tion rate (ESR), as well as AD diagnosed in adulthood, with dementia risk.Methods: We used three Swedish register‐based cohorts. Cohort I (N= 795,680) comprised men, born in 1951–1968, who participated in themilitary conscription examinations with physician‐assessed AD and ESR; Cohort II (N= 1,757,600) included men and women, born in 1951–1968; and Cohort III (N= 3,988,783) included all individuals in Sweden, born in 1930–1968. We used Cox regression, estimating hazard ratios (HR), with thefollow‐up from 50 years of age to dementia diagnosis, date of emigration, death, or 31 December 2018, which ever occurred first. Further, we used asibling comparison design to adjust for unmeasured confounders shared among siblings.Results: Cohort I: 1466 dementia events were accrued during follow‐up of 7.8 years, with a crude rate of 21.6 [95% confidence interval (CI): 20.6, 22.8] per 100,000 person‐years. Cohort II: 3549 dementia events were accrued duringfollow‐up of 7.4 years, with a crude rate of 23.7 (95% CI: 22.9, 24.5) per 100,000 person‐years. Cohort III: 120,303 dementia events were accrued during follow‐up of 23.7 years, with a crude rate of 180.3 (95% CI: 179.3, 181.3) per 100,000 person‐years. In multivariable analysis using Cohort I, there was no association between AD and dementia [HR 0.68 (95% CI 0.32, 1.43)], norwith moderate [HR 0.71 (95% CI: 0.46, 1.10)] or high [HR 1.23 (95% CI: 0.87, 1.75)] ESR. AD was not associated with dementia risk in Cohort II [HR 1.28(0.97, 1.71)] or Cohort III [HR 1.01 (0.92, 1.11)].Conclusions: AD was not associated with dementia risk, neither was systemic inflammation measured by ESR in adolescence.
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| 33. |
- Wernroth, Lisa, et al.
(författare)
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Development of gut microbiota during the first 2 years of life
- 2022
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Ingår i: Scientific Reports. - : Nature Portfolio. - 2045-2322. ; 12:1
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Tidskriftsartikel (refereegranskat)abstract
- Although development of microbiota in childhood has been linked to chronic immune-related conditions, early childhood determinants of microbiota development have not been fully elucidated. We used 16S rRNA sequencing to analyse faecal and saliva samples from 83 children at four time-points during their first 2 years of life and from their mothers. Our findings confirm that gut microbiota in infants have low diversity and highlight that some properties are shared with the oral microbiota, although inter-individual differences are present. A considerable convergence in gut microbiota composition was noted across the first 2 years of life, towards a more diverse adult-like microbiota. Mode of delivery accounted for some of the inter-individual variation in early childhood, but with a pronounced attenuation over time. Our study extends previous research with further characterization of the major shift in gut microbiota composition during the first 2 years of life.
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| 34. |
- Wernroth, Lisa, et al.
(författare)
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Early Childhood Antibiotic Treatment for Otitis Media and Other Respiratory Tract Infections Is Associated With Risk of Type 1 Diabetes : A Nationwide Register-Based Study With Sibling Analysis
- 2020
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Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 43:5, s. 991-999
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The effect of early life antibiotic treatment on the risk of type 1 diabetes is debated. This study assessed this question, applying a register-based design in children up to age 10 years including a large sibling-control analysis.RESEARCH DESIGN AND METHODS: = 797,318) born in Sweden between 1 July 2005 and 30 September 2013 were included and monitored to 31 December 2014. Cox proportional hazards models, adjusted for parental and perinatal characteristics, were applied, and stratified models were used to account for unmeasured confounders shared by siblings.RESULTS: for interaction = 0.016). The association was driven by exposure to antibiotics primarily used for acute otitis media and respiratory tract infections. Further, we found an association of antibiotic prescriptions in pregnancy (22.5%) with type 1 diabetes (adjusted HR 1.15 [95% CI 1.00-1.32]). In general, sibling analysis supported these results, albeit often with statistically nonsignificant associations.CONCLUSIONS: Dispensed prescription of antibiotics, mainly for acute otitis media and respiratory tract infections, in the 1st year of life is associated with an increased risk of type 1 diabetes before age 10, most prominently in children delivered by cesarean section.
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| 35. |
- Wernroth, M. -L, et al.
(författare)
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Childhood bereavement and risk of type 1 diabetes : a Swedish population-based register study
- 2021
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Ingår i: Diabetologia. - : Springer. - 0012-186X .- 1432-0428. ; 64:Suppl. 1, s. 140-140
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background and aims: Loss of a first-degree family member in childhood constitutes a major psychological stressor, and is associated both with subsequent psychiatric and somatic morbidity. The potential influence on type 1 diabetes risk has however not yet been fully elucidated. In this study we therefore aimed to investigate the impact of childhood bereavement on type 1 diabetes risk.Materials and methods: We conducted a population-based study in Sweden, encompassing 2,321,318 children born in Sweden January 1 1990 to December 31 2012. The follow up ended December 31 2013, at death of the child, type 1 diabetes diagnosis, emigration or when the child turned 19 years. All children were followed from the age of one, with exposure defined as death of a mother, father, or sibling. Type 1 diabetes diagnoses were extracted from the National Patient Register. We applied Cox proportional hazards models with attained age as time scale and loss of family member as a time varying variable, adjusting for potential confounders including parental type 1 diabetes, parental country of birth, and region of residence. We further categorized child age at bereavement as pre-school (1-6 years), school age (7-12 years) and teenage (13-18 years).Results: During follow-up (median 10.8 years), 50,253 (2.2%) children experienced loss of a family member. Median age at loss was 9.6 years, and 32% of all deaths were categorized as traumatic (accident, suicide, violence, or other sudden unnatural deaths). In total 10,965 children were diagnosed with type 1 diabetes during follow-up and median age at diagnosis was 8.5 years. We observed no overall association between childhood bereavement and type 1 diabetes risk (crude HR 1.00, 95% CI 0.86-1.18, adjusted HR 0.96, 95% CI 0.82 -1.13). The risk was not influenced by sex of the child, cause of death of family member, or familial relationship to the deceased. However, we noted an association when the exposure occurred during the teenage years (adjusted HR 1.67, 95% CI 1.15-2.43).Conclusion: Overall, childhood bereavement was not associated with the risk of type 1 diabetes, but the impact of childhood loss on type 1 diabetes may be modified by age at bereavement.
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| 36. |
- Wernroth, Mona-Lisa, et al.
(författare)
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Dog Exposure During the First Year of Life and Type 1 Diabetes in Childhood
- 2017
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Ingår i: JAMA pediatrics. - : AMER MEDICAL ASSOC. - 2168-6203 .- 2168-6211. ; 171:7, s. 663-669
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Tidskriftsartikel (refereegranskat)abstract
- IMPORTANCE The association between early exposure to animals and type 1 diabetes in childhood is not clear. OBJECTIVE To determine whether exposure to dogs during the first year of life is associated with the development of type 1 diabetes in childhood. DESIGN, SETTING, AND PARTICIPANTS A nationwide cohort study utilizing high-quality Swedish national demographic and health registers was conducted. A total of 840 593 children born in Sweden from January 1, 2001, to December 31, 2010, were evaluated. Type 1 diabetes was identified using diagnosis codes from hospitals and dispensed prescriptions of insulin. Cox proportional hazards regression models were used to assess the association between exposure to dogs and risk of type 1 diabetes in childhood. The possible association was further investigated by performing dose-response and breed group-specific analyses. The cohort was followed up until September 30, 2012. Data analysis was conducted from October 15, 2015, to February 8, 2017. EXPOSURES Having a parent who was registered as a dog owner during the child's first year of life. MAIN OUTCOMES AND MEASURES Childhood-onset type 1 diabetes. RESULTS Of the 840 593 children reviewed, 408 272 (48.6%) were girls; mean (SD) age at diagnosis of type 1 diabetes was 5.1 (2.6) years. Dog exposure was identified in 102 035 children (12.1%). Follow-up started at age 1 year, and the children were followed up for as long as 10.7 years (median, 5.5 years). During follow-up, 1999 children developed type 1 diabetes. No association was found between exposure to dogs (adjusted hazard ratio [HR], 1.00; 95% CI, 0.86-1.16) and type 1 diabetes in childhood. The size of the dog (adjusted HR per 10-cm increase in height, 0.96; 95% CI, 0.86-1.06) or number of dogs in the household (1 dog: adjusted HR, 1.07; 95% CI, 0.91-1.26; 2 dogs: 0.79; 95% CI, 0.54-1.15; >= 3 dogs: 0.50; 95% CI, 0.23-1.12; compared with nonexposed children) also was not associated with type 1 diabetes risk. An analysis of children whose parent had type 1 diabetes (210 events) yielded an adjusted HR of 0.71 (95% CI, 0.43-1.17) for dog exposure. CONCLUSIONS AND RELEVANCE In a nationwide study, no evidence supporting an association of register-derived measures of dog exposure with childhood type 1 diabetes was identified.
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| 37. |
- Xu, Yin, 1991-, et al.
(författare)
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Validity of Routinely Collected Swedish Data in the International Enhanced Recovery After Surgery (ERAS) Database
- 2021
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Ingår i: World Journal of Surgery. - : Springer. - 0364-2313 .- 1432-2323. ; 45:6, s. 1622-1629
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: This study aims to assess patient coverage, validity and data quality in the Swedish part of the International Enhanced Recovery After Surgery (ERAS) Interactive Audit System (EIAS).METHOD: All Swedish ERAS centers that recorded colorectal surgery data in EIAS between January 1, 2017, and December 31, 2017, were included (N = 12). Information registered in EIAS was compared with data from electronic medical records at each hospital to assess the overall coverage of EIAS. Twenty random-selected patients from each of the contributing centers were assessed for accuracy for a set of clinically relevant variables. All patients admitted to the contributing centers were included for the assessment of rate of missing on a selection of key clinical variables.RESULTS: Eight hospitals provided complete information for the evaluation, while four hospitals only allowed assessment of coverage and missing data. The eight hospitals had an overall coverage of 98.8% in EIAS (n = 1301) and the four 86.7% (n = 811). The average agreement for the assessed postoperative outcome variables was 96.5%. The accuracy was excellent for 'length of hospital stay,' 'reoperation,' and 'any complications,' but lower for other types of complications. Only a few variables had more than 5% missing data, and missingness was associated with hospital type and size.CONCLUSION: This validation of the Swedish part of the international ERAS database suggests high patient coverage in EIAS and high agreement and limited missingness in clinically relevant variables. This validation approach or a modified version can be used for continued validation of the International ERAS database.
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| 38. |
- Akre [Fall], Katja, 1971-, et al.
(författare)
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Aspirin and risk for gastric cancer : a population-based case-control study in Sweden
- 2001
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Ingår i: British Journal of Cancer. - Edinburgh, United Kingdom : Churchill Livingstone. - 0007-0920 .- 1532-1827. ; 84:7, s. 965-8
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Tidskriftsartikel (refereegranskat)abstract
- While aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) are associated with gastric mucosal damage, they might reduce the risk for gastric cancer. In a population-based case-control study in 5 Swedish counties, we interviewed 567 incident cases of gastric cancer and 1165 controls about their use of pain relievers. The cases were uniformly classified to subsite (cardia/non-cardia) and histological type and information collected on other known risk factors for gastric cancer. Helicobacter pylori serology was tested in a subset of 542 individuals. Users of aspirin had a moderately reduced risk of gastric cancer compared to never users; odds ratio (OR) adjusted for age, gender and socioeconomic status was 0.7 (95% CI = 0.6-1.0). Gastric cancer risk fell with increasing frequency of aspirin use (P for trend = 0.02). The risk reduction was apparent for both cardia and non-cardia tumours but was uncertain for the diffuse histologic type. No clear association was observed between gastric cancer risk and non-aspirin NSAIDs or other studied pain relievers. Our finding lends support to the hypothesis that use of aspirin reduces the risk for gastric cancer.
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| 39. |
- Akre [Fall], Katja, 1971-, et al.
(författare)
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Risk for gastric cancer after antibiotic prophylaxis in patients undergoing hip replacement
- 2000
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Ingår i: Cancer Research. - Birmingham, USA : American Asoociation for Cancer Research. - 0008-5472 .- 1538-7445. ; 60, s. 6376-
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Tidskriftsartikel (refereegranskat)abstract
- Despite strong evidence of an association between Helicobacter pylori and gastric cancer, the benefit of eradicating H. pylori infection is unknown. Our aim was to test the hypothesis that exposure to high doses of antibiotics reduces risk for gastric cancer via possible eradication of H. pylori We conducted a nationwide case-control study nested in a cohort of 39,154 patients who underwent hip replacement surgery between 1965 and 1983. Such patients frequently receive prophylactic antibiotic treatment. During follow-up through 1989, we identified 189 incident cases of gastric cancer. For each case, three controls were selected from the cohort. Exposure data were abstracted from hospital records. Blood samples from a separate cohort undergoing hip replacement surgery were analyzed for anti-H. pylori IgG before and after surgery. Both long-term antibiotic treatment before surgery [odds ratio (OR), 0.3; 95% confidence interval (CI), 0.1-0.7] and prophylactic antibiotic treatment (OR, 0.7; 95% CI, 0.5-1.1) conferred a reduction in gastric cancer risk. The reduction appeared stronger after 5 years (OR, 0.6; 95% CI, 0.3-1.2) than during shorter follow-up after hip replacement (OR, 0.8; 95% CI, 0.4-1.7). There was an apparent decrease in risk with increasing body weight-adjusted doses of antibiotics (P = 0.13). However, the rate of H. pylori antibody disappearance was not strikingly higher in the cohort of patients undergoing hip replacement than in a control cohort. Our findings provide indirect support for the hypothesis that treatment with antibiotics at a relatively advanced age reduces the risk of gastric cancer.
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| 40. |
- Arora, Manish, et al.
(författare)
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An exploration of shared genetic risk factors between periodontal disease and cancers : a prospective co-twin study
- 2010
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Ingår i: American Journal of Epidemiology. - Cary, USA : Oxford University Press. - 0002-9262 .- 1476-6256. ; 171:2, s. 253-9
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Tidskriftsartikel (refereegranskat)abstract
- Biologic mechanisms underlying associations of periodontal disease with cancers remain unknown. The authors propose that both conditions share common genetic risk factors. They analyzed associations between baseline periodontal disease, measured by questionnaire-recorded tooth mobility, and incident cancers, identified by linkage with national registries, between 1963 and 2004 in 15,333 Swedish twins. The authors used co-twin analyses to control for familial factors and undertook analyses restricted to monozygotic twins to further control for confounding by genetic factors. They observed 4,361 cancer cases over 548,913 person-years. After adjustment for covariates, baseline periodontal disease was associated with increased risk of several cancers ranging from 15% for total cancer (proportional hazard ratio (HR) = 1.15, 95% confidence interval (CI): 1.01, 1.32) to 120% for corpus uterine cancer (HR = 2.20, 95% CI: 1.16, 4.18). Periodontal disease was also associated with increased risk of colorectal (HR = 1.62, 95% CI: 1.13, 2.33), pancreatic (HR = 2.06, 95% CI: 1.14, 3.75), and prostate (HR = 1.47, 95% CI: 1.04, 2.07) cancers. In co-twin analyses, dizygotic twins with baseline periodontal disease showed a 50% increase in total cancer risk (HR = 1.50, 95% CI: 1.04, 2.17), but in monozygotic twins this association was markedly attenuated (HR = 1.07, 95% CI: 0.63, 1.81). Similar patterns emerged for digestive tract cancers, suggesting that shared genetic risk factors may partially explain associations between periodontal disease and cancers.
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