| 1. |
- 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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| 2. |
- 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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| 3. |
- 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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| 4. |
- 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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