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| 2. |
- Bairkdar, Majd, et al.
(författare)
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Incidence and prevalence of systemic sclerosis globally : A comprehensive systematic review and meta-analysis
- 2021
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Ingår i: Rheumatology (United Kingdom). - : Oxford University Press (OUP). - 1462-0324 .- 1462-0332. ; 60:7, s. 3121-3133
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Forskningsöversikt (refereegranskat)abstract
- Objectives: We aimed to conduct a systematic review and meta-analysis on the incidence and prevalence of SSc covering the entire literature. Methods: This study followed the recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement of 2009. We conducted a systematic search in MEDLINE, Web of Science and Embase to identify articles reporting incidence and/or prevalence of SSc. Two authors conducted the search, reviewed articles for inclusion and extracted relevant data. We used random-effects models to estimate the pooled prevalence and incidence of SSc and performed subgroup analyses by sex, case definition and region to investigate heterogeneity. We explored the association between calendar period and reported estimates using meta-regression. Results: Among 6983 unique records identified, we included 61 studies of prevalence and 39 studies of incidence in the systematic review. The overall pooled prevalence of SSc was 17.6 (95% CI 15.1, 20.5) per 100 000 and the overall pooled incidence rate of SSc was 1.4 (95% CI 1.1, 1.9) per 100 000 person-years. We observed significant regional variations in reported estimates; studies conducted in North America reported considerably higher estimates than other regions. The pooled incidence and prevalence in women were five times higher than in men. More recent studies reported higher estimates than older ones. Conclusion: In this comprehensive review of the incidence and prevalence of SSc across the world, there was large heterogeneity among estimates, which should be taken into consideration when interpreting the results.
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| 3. |
- Edstorp, Jessica, et al.
(författare)
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Does a prior diagnosis of infectious disease confer an increased risk of latent autoimmune diabetes in adults?
- 2024
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Ingår i: Diabetes/Metabolism Research and Reviews. - 1520-7552. ; 40:3, s. e3758-
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Infections are proposed risk factors for type 1 diabetes in children. We examined whether a diagnosis of infectious disease also confers an increased risk of latent autoimmune diabetes in adults (LADA). Materials and methods: We used data from a population-based Swedish case-control study with incident cases of LADA (n = 597) and matched controls (n = 2386). The history of infectious disease was ascertained through national and regional patient registers. We estimated adjusted odds ratios (OR) with 95% confidence intervals for ≥1 respiratory (any/upper/lower), gastrointestinal, herpetic, other or any infectious disease episode, or separately, for 1 and ≥2 infectious disease episodes, within 0–1, 1–3, 3–5 and 5–10 years before LADA diagnosis/matching. Stratified analyses were performed on the basis of HLA risk genotypes and Glutamic acid decarboxylase antibodies (GADA) levels. Results: Individuals who developed LADA did not have a higher prevalence of infectious disease 1–10 years before diabetes diagnosis. For example, OR was estimated at 0.87 (0.66, 1.14) for any versus no respiratory infectious disease within 1–3 years. Similar results were seen for LADA with high-risk HLA genotypes (OR 0.95 [0.64, 1.42]) or high GADA levels (OR 1.10 [0.79, 1.55]), ≥2 episodes (OR 0.89 [0.56, 1.40]), and in infections treated using antibiotics (OR 1.03 [0.73, 1.45]). The only significant association was observed with lower respiratory disease the year preceding LADA diagnosis (OR 1.67 [1.06, 2.64]). Conclusions: Our findings do not support the idea that exposure to infections increases the risk of LADA. A higher prevalence of respiratory infection in the year before LADA diagnosis could reflect increased susceptibility to infections due to hyperglycemia.
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| 4. |
- Rossides, Marios
(författare)
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Epidemiological aspects of sarcoidosis : risk factors and long-term consequences
- 2021
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Sarcoidosis is a systemic inflammatory disease of unknown etiology in which granulomatous lesions form mostly in the lungs and the lymphatic system of patients. Although more than a century has passed since sarcoidosis was first described, our understanding of its etiology and clinical course is limited. That is because epidemiological studies on large and representative patient cohorts have been lacking. The scope of this thesis was to examine aspects of sarcoidosis epidemiology using a linkage of large, nationwide health and administrative databases from Sweden complemented by clinical data. Six individual studies are included in this thesis; the first two dealt with risk factors for sarcoidosis, namely familial and infectious disease, and the rest with long-term debilitating patient outcomes: mortality, infection, and heart failure. In Study I, a case-control-family study, we estimated familial relative risks and the heritability of sarcoidosis. We found that having first-degree relatives with sarcoidosis increased the risk of being diagnosed with the disease by more than threefold. 39% of the susceptibility to sarcoidosis in the Swedish population was estimated to be attributable to additive genetic effects; the rest was due to non-shared (among siblings) environmental factors. Study II was a case-control study in which we estimated relative risks of sarcoidosis associated with having a history of infectious disease diagnoses. We showed that infectious diseases (commonly upper respiratory and genitourinary) diagnosed before sarcoidosis diagnosis were associated with a small increased risk of sarcoidosis in the future, a relative risk that did not vary markedly by latency period between infectious disease ascertainment and sarcoidosis diagnosis. These small relative risks could be easily explained away in analyses designed to test the robustness of these associations in the presence of reverse causation bias. In Study III, a cohort study, we followed individuals with sarcoidosis and general population comparators for all-cause death. We showed that there was an overall 61% increased risk of death associated with sarcoidosis. Stratification by treatment status around the time of sarcoidosis diagnosis approximating disease severity revealed a 2.3-fold higher risk of all-cause mortality compared to the general population in those treated while no risk increase was observed for untreated patients with sarcoidosis. Similarly, in Study IV, we followed individuals for a first or recurrent serious (hospitalized) infections. We observed a 1.8-fold higher risk of serious infection in sarcoidosis compared to the general population, which was even higher during the first two years since diagnosis and in individuals who were treated with an immunosuppressant around sarcoidosis diagnosis likely due to more severe or progressive disease at the time. In Study V, a target trial emulation, we compared six-month risks of infectious disease in initiators of methotrexate compared to azathioprine, two second line treatments for sarcoidosis. Six months after treatment initiation, a 43% lower risk of infectious disease was observed in the methotrexate compared to the azathioprine group. Study VI was a cohort study in which we examined the relative risk of heart failure and its predictors in sarcoidosis. We found a 2.4-fold increased relative risk of heart failure associated with sarcoidosis that was higher during the first two years since sarcoidosis diagnosis and in individuals without a history of ischemic heart disease. Diabetes, atrial fibrillation, and other arrhythmias were the strongest clinical predictors of heart failure diagnosis in sarcoidosis. Overall, findings from studies on risk factors in this thesis suggest that familial disease and genetics are important in sarcoidosis, albeit a larger contribution to the etiology of sarcoidosis is likely due to environmental factors. Among environmental factors, clinically identifiable infectious diseases are unlikely to be strong risk factors for sarcoidosis diagnosis. Future molecular and epidemiological studies on environmental triggers of sarcoid inflammation and disease should consider the issue of reverse causality owing to long preclinical disease in some patients. Studies on long-term patient outcomes in this thesis showed that sarcoidosis is not a ‘benign’ disease. Therefore, our quest to identify effective interventions and groups of patients to target should continue. If applied early, these measures can help alleviate some of the risks related to infection and heart failure, and improve life expectancy, especially in patients with severe or chronic disease.
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| 5. |
- Rossides, Marios, et al.
(författare)
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Mortality and Functionality after Stroke in Patients with Systemic Lupus Erythematosus
- 2017
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Ingår i: Journal of Rheumatology. - Toronto, Canada : The Journal of Rheumatology Publishing Co. Ltd. - 0315-162X .- 1499-2752. ; 44:11, s. 1590-1596
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate mortality and functional impairment after stroke in systemic lupus erythematosus (SLE).METHODS: Using Swedish nationwide registers, we identified 423 individuals with SLE and 1652 people without SLE who developed a first-ever ischemic or hemorrhagic stroke (1998-2013) and followed them until all-cause death or for 1 year. HR for death after ischemic or hemorrhagic stroke and the risk ratio of functional impairment (dependence in either transferring, toileting, or dressing) 3 months after ischemic stroke were estimated.RESULTS: One year after stroke, 22% of patients with SLE versus 16% of those without SLE died. After ischemic stroke, patients with SLE had an increased risk of death (HR 1.85, 95% CI 1.39-2.45), which was attenuated after controlling for SLE-related comorbidities (HR 1.41, 95% CI 1.04-1.91). Functional impairment at 3 months was increased in SLE by almost 2-fold (risk ratio 1.73, 95% CI 1.16-2.57). After hemorrhagic stroke, patients with SLE had an HR of 2.30 (95% CI 1.38-3.82) for death, which was increased even during the first month.CONCLUSION: Compared to subjects without SLE, mortality after ischemic stroke increases after the first month in individuals with SLE, and functionality is worse at 3 months. SLE is associated with all-cause death after hemorrhagic stroke even during the first month. A shift of focus to patient functionality and prevention of hemorrhagic strokes is required.
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| 6. |
- Simard, Julia F., et al.
(författare)
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Evidence of under-reporting of early-onset preeclampsia using register data
- 2021
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Ingår i: Paediatric and Perinatal Epidemiology. - : Wiley. - 0269-5022 .- 1365-3016. ; 35:5, s. 596-600
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundEarly-onset preeclampsia, traditionally defined as presenting before 34 gestational weeks, is associated with even higher risks of perinatal death, placental abruption, and stroke, than late-onset preeclampsia.ObjectiveWe estimated the degree of misclassification in a high-risk population of lupus pregnancies and a general population comparator when gestational age at delivery defined preeclampsia phenotype compared to first preeclampsia diagnosis.MethodsPatients with lupus and general population comparators from Sweden with ≥1 singleton pregnancy in the Medical Birth Register with a documented ICD code for preeclampsia were included (2002-2016). We used gestational age at delivery (<34 versus ≥34 weeks) to phenotype preeclampsia early- versus late-onset and then reclassified based on first preeclampsia diagnosis date in the Patient Register. We cross-tabulated the two definitions and calculated sensitivity using the visit-based definition as the reference standard for general population and lupus pregnancies, overall and among nulliparous women.Results331 pregnancies were diagnosed with preeclampsia, of which 322 were in both registers. Of those, 58 were early-onset based on gestational age at delivery (n = 29 in lupus pregnancies). Overall, 9% of early-onset preeclampsia in lupus (sensitivity 91%, 95% confidence interval [CI] 75, 98) was misclassified as late-onset compared to 19% in the general population (sensitivity 81%, 95% CI 64, 92). We noted similar misclassification (4% vs 22%) among nulliparous women.ConclusionsIn the general population, early-onset preeclampsia was more likely misclassified as late-onset than in the high-risk lupus population. Relying on gestational age at delivery to phenotype preeclampsia, this way underestimates the occurrence of early-onset preeclampsia. This also suggests that the burden of early-onset preeclampsia as a public health concern may be under-reported, although this may be more applicable to milder preeclampsia where expectant management is employed. Research of biological and maternal predictors of early-onset preeclampsia may be dealing with differentially misclassified outcomes or samples.
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| 7. |
- Simard, Julia F., et al.
(författare)
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Maternal Hypertensive Disorders in Pregnant Women With Systemic Lupus Erythematosus and Future Cardiovascular Outcomes
- 2021
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Ingår i: Arthritis care & research. - : John Wiley & Sons. - 2151-464X .- 2151-4658. ; 73:4, s. 574-579
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Hypertensive disorders of pregnancy (HDPs) increase cardiovascular disease (CVD) risk. Pregnancy morbidities, including preeclampsia and CVD, are common in systemic lupus erythematosus (SLE). Possible connections are important to explore. In a population-based cohort, we investigated whether HDPs are associated with a higher risk of cardiovascular outcomes separately in women with SLE and those without SLE to examine the role of SLE.Methods: We identified first singleton births in the Medical Birth Register (1987-2012) among mothers with SLE and a large general population comparison group. Discharge diagnoses for HDPs, cardiovascular outcomes, and hypertension in the National Patient Register were identified using International Classification of Diseases codes. We estimated adjusted hazard ratios and 95% confidence intervals of the association between HDPs and outcomes in separate models in women with and without SLE. We then evaluated additive and multiplicative effect modification using relative excess risk due to interaction and Cox models jointly accounting for SLE and HDPs, respectively. Mediation analysis estimated the proportion of the association between SLE and outcome explained by HDPs.Results: HDPs were more common in pregnant women with SLE (20% versus 7%). In SLE, HDPs were associated with a 2-fold higher rate of cardiovascular outcomes and a 3-fold higher rate of incident hypertension. HDPs mediated 20% of the latter association. In women without SLE, HDPs were associated with higher incidence of hypertension later in life.Conclusion: In women with SLE and those without SLE, HDPs were associated with a 3-fold higher rate of hypertension. In SLE, women with HDPs developed cardiovascular outcomes twice as often as women without HDPs.
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| 8. |
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| 9. |
- Simard, Julia F., et al.
(författare)
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Preterm Delivery Phenotypes in Systemic Lupus Erythematosus Pregnancies
- 2019
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Ingår i: American Journal of Perinatology. - : THIEME MEDICAL PUBL INC. - 0735-1631 .- 1098-8785. ; 36:9, s. 964-968
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Women with systemic lupus erythematosus (SLE) are at a greater risk of preterm delivery, many of which may be medically indicated (iatrogenic). We investigated preterm delivery phenotypes in SLE and general population comparators and assessed the role of preeclampsia.Study Design: We used population-based Swedish Register data (2001-2013) and defined maternal SLE as >= 2 SLE-coded discharge diagnoses from the Patient Register with >= 1 coded by an appropriate specialist. Women from the general population were identified using the Total Population Register. Preterm delivery was defined as <37 weeks and separated into spontaneous and iatrogenic, as well as later versus extremely preterm (32 to <37 weeks vs. <32 weeks). Maternal comorbidity was assessed, and the proportion mediated by preeclampsia was calculated examining first, subsequent, and all pregnancies.Results: Preterm delivery was more common in SLE for the first (22 vs. 6%) and subsequent (15 vs. 4%) pregnancies among 781 SLE-exposed pregnancies and 11,271 non-SLE pregnancies. Of SLE-exposed first births, 27% delivered before 32 weeks, and 90% were iatrogenic (compared with 47% of non-SLE first births).Conclusion: Preterm delivery complicates a greater proportion of SLE pregnancies than general population pregnancies, and a considerable proportion of risk is mediated through preeclampsia.
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| 10. |
- Svenungsson, Elisabet, et al.
(författare)
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Complement deposition, C4d, on platelets is associated with vascular events in systemic lupus erythematosus
- 2020
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Ingår i: Rheumatology. - : Oxford University Press. - 1462-0324 .- 1462-0332. ; 59:11, s. 3264-3274
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Complement components, including C4d, can be found on activated platelets, a process associated with vascular disease in SLE. We investigated whether platelet C4d (PC4d) adds additional value to traditional and known lupus-associated risk factors when identifying SLE patients with vascular disease. Methods. This cross-sectional study included 308 well-characterized SLE patients and 308 matched general population controls. PC4d deposition was analysed using flow cytometry. Values >95% of controls were considered as PC4d positive (+). aPL were determined by Luminex, and the LA test was performed by DRVVT. History of vascular disease (composite and as separate outcomes) was defined at inclusion. Results. SLE patients had increased PC4d deposition as compared with population controls (50 vs 5%, P < 0.0001). PC4d+ positively associated with any vascular events, and separately with venous and cerebrovascular events, and also with all investigated aPL profiles. The association for any vascular event remained statistically significant after adjustment for traditional and SLE-associated risk factors (odds ratio: 2.3, 95% CI: 1.3, 4.3, P = 0.008). Compared with patients negative for both PC4d and LA, patients with double positivity were more likely to have vascular disease (odds ratio: 12.3, 95% CI: 5.4, 29.3; attributable proportion due to interaction 0.8, 95% CI: 0.4, 1.1) Conclusion. PC4d+ is associated with vascular events in SLE, independently of traditional and SLE-associated risk factors. Concurrent presence of PC4d and LA seem to interact to further increase the odds for vascular events. Prospective studies should examine whether the aPL/PC4d combination can improve prediction of vascular events in SLE and/or APS.
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