| 1. |
- Ahrén, Jonatan, et al.
(författare)
-
Multimorbidity disease clusters are associated with venous thromboembolism : an extended cross-sectional national study
-
Ingår i: Journal of Thrombosis and Thrombolysis. - 0929-5305.
-
Tidskriftsartikel (refereegranskat)abstract
- Multimorbidity, i.e., two or more non-communicable diseases (NCDs), is an escalating challenge for society. Venous thromboembolism (VTE) is a common cardiovascular disease and it is unknown which multimorbidity clusters associates with VTE. Our aim was to examine the association between different common disease clusters of multimorbidity and VTE. The study is an extended (1997–2015) cross-sectional Swedish study using the National Patient Register and the Multigeneration Register. A total of 2,694,442 Swedish-born individuals were included in the study. Multimorbidity was defined by 45 NCDs. A principal component analysis (PCA) identified multimorbidity disease clusters. Odds ratios (OR) for VTE were calculated for the different multimorbidity disease clusters. There were 16% (n = 440,742) of multimorbid individuals in the study population. Forty-four of the individual 45 NCDs were associated with VTE. The PCA analysis identified nine multimorbidity disease clusters, F1-F9. Seven of these multimorbidity clusters were associated with VTE. The adjusted OR for VTE in the multimorbid patients was for the first three clusters: F1 (cardiometabolic diseases) 3.44 (95%CI 3.24–3.65), F2 (mental disorders) 2.25 (95%CI 2.14–2.37) and F3 (digestive system diseases) 4.35 (95%CI 3.63–5.22). There was an association between multimorbidity severity and OR for VTE. For instance, the occurrence of at least five diseases was in F1 and F2 associated with ORs for VTE: 8.17 (95%CI 6.32–10.55) and 6.31 (95%CI 4.34–9.17), respectively. In this nationwide study we have shown a strong association between VTE and different multimorbidity disease clusters that might be useful for VTE prediction. Graphical abstract: (Figure presented.)
|
|
| 2. |
- Akrawi, Delshad Saleh, et al.
(författare)
-
Heritability of End-Stage Renal Disease : A Swedish Adoption Study
- 2018
-
Ingår i: Nephron. - : S. Karger AG. - 1660-8151 .- 2235-3186. ; 138:2, s. 157-165
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: The heritability of end-stage renal disease (ESRD) among adoptees has not been examined so far. By studying adoptees and their biological and adoptive parents, it is possible to differentiate between the genetic causes and environmental causes of familial aggregation. This nationwide study aimed to disentangle the genetic and shared environmental contribution to the familial transmission of ESRD. Methods: We performed a family study for Swedish-born adoptees (born between 1945 until 1995) and their biological and adoptive parents. The Swedish Multi-Generation Register was linked to the National Patient Registry for the period 1964–2012. ESRD was defined as patients in active uremic care, that is, chronic dialysis or kidney transplantation. OR for ESRD was determined for adoptees with an affected biological parent with ESRD compared with adoptees without a biological parent with ESRD. The OR for ESRD was also calculated in adoptees with an adoptive parent with ESRD compared with adoptees with an adoptive parent without ESRD. Moreover, heritability for ESRD was estimated with Falconer’s regression. Results: A total of 111 adoptees, 463 adoptive parents, and 397 biological parents were affected by ESRD. The OR for ESRD was 6.41 in adoptees (95% CI 2.96–13.89) of biological parents diagnosed with ESRD. The OR for ESRD was 2.40 in adoptees (95% CI 0.76–7.60) of adoptive parents diagnosed with ESRD. The heritability of ESRD was 59.5 ± 18.2%. Conclusion: The family history of ESRD in a biological parent is an important risk factor for ESRD. The high heritability indicates that genetic factors play an important role in understanding the etiology of ESRD.
|
|
| 3. |
- Akrawi, Delshad Saleh, et al.
(författare)
-
Heritability of glomerulonephritis : A Swedish adoption study
- 2019
-
Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 49:8
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Glomerulonephritis clusters in families. However, infections are common inducers of glomerulonephritis and may also cluster in families. Studies of adoptees and their biological and adoptive parents may disentangle genetic from environmental causes of familial clustering. This is the first adoption study aimed to estimate the genetic contribution to the familial transmission of glomerulonephritis. Materials and methods: We performed a family study for Swedish-born adoptees (born 1945–2000) and their biological and adoptive parents. The Swedish Multi-Generation Register was linked to the Hospital Inpatient Register for the period 1964–2012 and the Hospital Outpatient Register for 2001–2012. Odds ratio (OR) for glomerulonephritis was determined for adoptees with a biological parent with glomerulonephritis compared with adoptees without an affected biological parent. Similarly, the OR for glomerulonephritis was also determined in adoptees with an affected adoptive parent compared with adoptees without an affected adoptive parent. Heritability was estimated to be twice the observed tetrachoric correlation among adoptees and biological parents, under the assumption that only additive genetic factors contribute to the similarity between biological parents and adoptees. Results: The OR for glomerulonephritis was 4.08 in adoptees (95% confidence interval [CI] 1.79-9.27, P-value = 0.001) of biological parents diagnosed with glomerulonephritis. The OR for glomerulonephritis was 1.67 in adoptees (95% CI 0.53-5.26, P-value = 0.380) of adoptive parents diagnosed with glomerulonephritis. The heritability was 48%. Conclusion: Family history of glomerulonephritis in a biological parent is a risk factor for glomerulonephritis. The present study indicates that genetic factors play an important role in the aetiology of glomerulonephritis.
|
|
| 4. |
- Zöller, Bengt, et al.
(författare)
-
Association of Short-Term Mortality of Venous Thromboembolism with Family History of Venous Thromboembolism and Charlson Comorbidity Index
- 2019
-
Ingår i: Thrombosis and Haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 119:1, s. 48-55
-
Tidskriftsartikel (refereegranskat)abstract
- Studies on short-term prognosis of venous thromboembolism (VTE) that take family history of VTE and Charlson Comorbidity Index (CCI) into account are sparse. The aim was to investigate the importance of family history of VTE and CCI for short-term mortality after a first episode of VTE. Using Swedish medical databases, we conducted a 90-day nationwide cohort study of 41,700 Swedish born patients with a first-time VTE (July 2005-August 2012). Patients diagnosed with VTE and prescribed anticoagulant treatment were included. Mortality hazard ratios (HRs) with 95% confidence intervals (CIs) were determined with Cox regression. Patients with first-degree (sibling/parent) family history of VTE (n = 11,405, 27.4%) had significantly lower CCI than those without family history. Independent risk factors for 90-day mortality in the adjusted model were: female sex (HR = 1.19, 95% CI: 1.09-1.29), increasing age (HR = 1.02, 95% CI: 1.01-1.02 per year), pulmonary embolism (HR = 1.21, 95% CI: 1.11-1.32) or combined pulmonary embolism and deep venous thrombosis (HR = 1.60, 95% CI: 1.27-2.01) compared with deep venous thrombosis, CCI = 1 (HR = 2.93, 95% CI: 2.32-3.72), CCI = 2 (HR = 8.65, 95% CI: 7.16-10.46) or CCI = 3 (HR = 22.25, 95% CI: 18.73-26.44) compared with CCI = 0. Having one or two or more affected first-degree relatives with VTE was associated with lower mortality, HR = 0.83 (95% CI: 0.74-0.92) and HR = 0.65 (95% CI: 0.51-0.85), respectively. The mortality rate was 0.70% in patients with a CCI of zero. In receiver operating characteristic (ROC) analysis, the area under the ROC curve for CCI was 0.84 (0.83-0.95). Family history of VTE is associated with lower mortality while CCI is a strong predictor for short-term mortality in VTE. Co-morbidities are important for risk assessment of VTE.
|
|
| 5. |
- Zöller, Bengt, et al.
(författare)
-
Familial Mortality Risks in Patients with Ischemic Stroke : A Swedish Sibling Study
- 2022
-
Ingår i: Stroke. - 0039-2499. ; 53:5, s. 1615-1623
-
Tidskriftsartikel (refereegranskat)abstract
- Background: The influence of familial factors on the prognosis of ischemic stroke (IS) is unknown. This nationwide follow-up study evaluated familial mortality risks of IS among Swedish sibling pairs hospitalized for IS. Methods: We linked Swedish nationwide registers for the identification of 1380 Swedish born sibling pairs (2760 cases), where both siblings were hospitalized for first-time IS between 1991 and 2010. Median age was 62 years (range, 26-78 years). Sibling pairs with cancer were excluded. Familial hazard ratios (FHRs) for mortality after first IS hospitalization were determined with Cox regression. The influence of proband survival after IS was categorized as short sibling survival (<1, 2, 3, 4, or 5 years) or long sibling survival (≥1, 2, 3, 4, or 5 years) after IS. FHRs were adjusted for age at onset, sex, education, county, year of diagnosis, days of hospitalization, and comorbidities. Results: Short sibling survival (ie, <3 or <4 years) after IS was associated with an adjusted FHR of 1.29 (95% CI, 1.05-1.58) and 1.24 (95% CI, 1.02-1.51), respectively, for overall mortality after IS. Stratified analysis showed that short sibling survival (ie, <2 - <5 years) was stronger and significant only among younger individuals (<62 years) and males. Highest FHR for short sibling survival (ie, <4 years) was 1.42 (95% CI, 1.08-1.88) for younger individuals and 1.50 (95% CI, 1.21-1.87) for males. For young male subjects, FHR was 1.80 (95% CI, 1.33-2.46). In the adjusted model, mortality was also associated with sex, education, age at onset, year of diagnosis, days of hospitalization, coronary heart disease, diabetes, dementia, heart failure, obesity, alcoholism, and hyperlipidemia. Conclusions: Our results suggest that family history of short survival in siblings after IS is associated with mortality after IS for younger male subjects. Additional studies are needed to characterize possible genetic and nongenetic familial environmental causes of this association.
|
|
