The worldwide incidence and prevalence of systemic lupus erythematosus: a systematic review of epidemiological studies

Rees, Frances; Doherty, Michael; Grainge, Matthew J.; Lanyon, Peter; Zhang, Weiya

doi:10.1093/rheumatology/kex260

Cited by 591 publications

(463 citation statements)

References 83 publications

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“…Interestingly, males are also overrepresented in other immune-mediated neuropathies including the GuillainBarré syndrome (GBS) and multifocal motor neuropathy [9,[37][38][39][40]. The male predominance in these immunemediated neuropathies is unexplained and deviates from female predominance in many classic autoimmune disorders [41][42][43]. A male predominance has also been suggested for other forms of polyneuropathies, suggesting that males are more at risk to develop a polyneuropathy [44,45].…”

Section: Discussionmentioning

confidence: 99%

Incidence and Prevalence of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Systematic Review and Meta-Analysis

et al. 2019

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Background: Prevalence and incidence rates of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are required to determine the impact of CIDP on society. We aimed to estimate the prevalence and incidence of CIDP worldwide and to determine the effect of diagnostic criteria on prevalence and incidence. Method: A systematic review was conducted for all published incidence and prevalence studies on CIDP until May 18, 2017. Methodological quality was assessed using the Methodological Evaluation of Observational Research checklist. We performed a random effect meta-analysis to estimate pooled prevalence and incidence rates. Results: Of the 907 studies, 11 were included in the systematic review, 5 in the meta-analysis of incidence (818 cases; 220,513,514 person-years) and 9 in the meta-analysis of prevalence (3,160 cases; 160,765,325 population). These studies had a moderate quality. The pooled crude incidence rate was 0.33 per 100,000 person-years (95% CI 0.21–0.53; I² = 95.7%) and the pooled prevalence rate was 2.81 per 100,000 (95% CI 1.58–4.39; I² = 99.1%). Substantial heterogeneity in incidence and prevalence across studies seems to be partly explained by using different diagnostic criteria. Conclusion: These findings provide a starting point to estimate the social burden of CIDP and demonstrate the need to reach consensus on diagnostic criteria for CIDP.

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Section: Discussionmentioning

confidence: 99%

Incidence and Prevalence of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Systematic Review and Meta-Analysis

et al. 2019

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“…SLE affects women more often than men and it is commonly known as the disease of women of childbearing age. 1,2 In a study, to assess the differences between SLE clinics in men and women; men were more affected than women in terms of disability, hypertension, thrombosis, renal and haematological involvement. Women were more likely to have malar rash, photosensitivity, oral ulcer, alopecia, Raynaud phenomenia and arthralgia.…”

Section: Discussionmentioning

confidence: 99%

“…The aetiology of SLE is not fully understood, but both genetic predisposition and enviromental triggers are belived to be involved. 1 In a recent study, the overall age-adjusted incidence and prevalence per 100,000 persons were 5.5 and 72.8, respectively. 2 The incidence and prevalance of SLE is higher in females compared with males regardless of age or ethnic origin.…”

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confidence: 96%

Systemic Lupus Erythematosus and Secondary Antiphospholipid Syndrome Diagnosed After Pulmonary Thromboembolism in a Male Patient

ÖZİŞLER

2017

Turkiye Klinikleri J Cardiovasc Sci

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Cem ÖZİŞLERTurkiye Klinikleri J Cardiovasc Sci 2017;29(3):82-5 83 female predominance (female:male ratio, 5:1) was confirmed in APS patients, but this was greater in patients with associated SLE (7:1) than in the primary APS (3.5:1). 5 In this article, I present a male patient with SLE and secondary APS diagnosed after pulmonary thromboembolism. A written informed consent was obtained from the patient. CASE REPORTA 34-year-old male patient admitted to another hospital with a complaint of dyspnea and chest pain. The patient was diagnosed as pulmonary thromboembolism and the lower extremity deep venous thrombosis was detected as an embolism source and anticoagulant treatment was initiated to the patient. The patient was sent to our hospital for rheumatologic evaluation when the antinuclear antibody and anticardiolipin antibodies were detected positive.Approximately four months after the diagnosis of pulmonary thromboembolism, he referred to our rheumatology outpatient clinic. He had no other chronic illness in his medical history and was not using any treatment other than warfarin. There was not any feature in rheumatological questioning except mild arthralgia and short-term morning stiffness in hand joints. Except from mild tenderness in the hand joints, there was no feature in his physical examination. The laboratory tests results of the patient are summarized (Table 1).The patient was diagnosed with SLE according to the SLICC classification criteria because of ANA, anti-dsDNA and antiphospholipid antibodies positivity, hypocomplementemia and thrombocytopenia. 6 In addition, antiphospholipid syndrome was diagnosed according to the Sapporo classification criteria due to deep vein thrombosis and pulmonary thromboembolism, aCL IgG/IgM positivity (4 months ago, aCL IgG and IgM were positive, too).7 Anticoagulant treatment was supplemented with 400 mg/day of hydroxychloroquine and 6 mg/day of methylprednisolone. After 1 month, the patient's joint complaints and morning stiffness had improved, platelet counts, ESR and CRP levels were normal. If the patient continues to be in good clinical condition, our treatment plan is to discontinue methylprednisolone, continue with hydroxychloroquine and warfarin treatment. The treatment was planned according to the EULAR recommendations for the management of SLE. DISCUSSIONSLE is a chronic autoimmune disease with multisystem involvement that can cause life-threatening clinical conditions from time to time. SLE affects women more often than men and it is commonly known as the disease of women of childbearing age. 1,2 In a study, to assess the differences between SLE clinics in men and women; men were more affected than women in terms of disability, hypertension, thrombosis, renal and haematological involvement. Women were more likely to have malar rash, photosensitivity, oral ulcer, alopecia, Raynaud phenomenia and arthralgia. It is also stated that end-organ damage and related deaths such as neuropsychiatric, renal, cardiovascular, peripheral vascular disease and myocardial ...

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“…103,104 A second and complimentary model holds that selection pressures due to exposure to pathogens endemic to Africa may account for increased type I IFN production and responses in the AA population. [105][106][107][108] Other population level studies have shown that genetic variants across populations play a major role in shaping an individual's immune response, 109 including variability in cytokine responses to various stimuli. [105][106][107][108] Other population level studies have shown that genetic variants across populations play a major role in shaping an individual's immune response, 109 including variability in cytokine responses to various stimuli.…”

Section: What Drives Transitional B-cell Ifnβ Production?mentioning

confidence: 99%

Autoreactive B cells in SLE, villains or innocent bystanders?

Hamilton

Hsu

Mountz

2019

Immunological Reviews

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Autoreactive B-cell development in SLE (systemic lupus erythematosus) is often considered in terms of the extrinsic stimuli and factors that drive B cells into autoantibody production. This review focuses on the novel concept that autoreactive B cells are initially programmed at the transitional stage for heightened susceptibility for development into autoantibody secreting plasmablasts (Figure 1). During peripheral B-cell development in the spleen, transitional B-cells expressing elevated levels of endogenous intracellular interferon-β (IFNβ) exhibit enhanced survival and activation through the B-cell receptor (BCR), a feature associated with more active SLE, particularly in African American (AA) patients. 1 Following passage through the transitional stage, a second major defect is the failure of B cells to maintain the integrity of tolerogenic splenic marginal zone macrophages (MZM), which normally function to remove apoptotic cell debris in a non-inflammatory fashion through upregulation of indoleamine-pyrrole 2,3-dioxygenase (IDO). 2 This failure is amplified by the type I IFN-driven migratory properties of marginal zone-precursor (MZ-P) B cells as they lose their tethering to sphingosine-1-phosphate (S1P) and drift across the follicular exclusion barrier. 3-8 Here they act as potent antigen-carrying, co-stimulatory cells expressing inflammatory cytokine IL-6 and low levels of the antiinflammatory cytokine IL-10. 9 In addition, Ag transporting MZ-P B-cells Abstract The current concepts for development of autoreactive B cells in SLE (systemic lupus erythematosus) focus on extrinsic stimuli and factors that provoke B cells into tolerance loss. Traditionally, major tolerance loss pathways are thought to be regulated by factors outside the B cell including autoantigen engagement of the B-cell receptor (BCR) with simultaneous type I interferon (IFN) produced by dendritic cells, especially plasmacytoid dendritic cells (pDCs). Later, in autoreactive follicles, B-cells encounter T-follicular helper cells (Tfh) that produce interleukin (IL)-21, IL-4 and pathogenic cytokines, IL-17 and IFN gamma (IFNɣ). This review discusses these mechanisms and also highlights recent advances pointing to the peripheral transitional B-cell stage as a major juncture where transient autocrine IFNβ expression by developing B-cells imprints a heightened susceptibility to external factors favoring differentiation into autoantibody-producing plasmablasts. Recent studies highlight transitional B-cell heterogeneity as a determinant of intrinsic resistance or susceptibility to tolerance loss through the shaping of B-cell responsiveness to cytokines and other environment factors.

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The worldwide incidence and prevalence of systemic lupus erythematosus: a systematic review of epidemiological studies

Abstract: There are worldwide differences in the incidence and prevalence of SLE that vary with sex, age, ethnicity and time. Further study of genetic and environmental risk factors may explain the reasons for these differences. More epidemiological studies in Africa are warranted.

Cited by 591 publications

References 83 publications

Incidence and Prevalence of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Systematic Review and Meta-Analysis

Incidence and Prevalence of Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Systematic Review and Meta-Analysis

Systemic Lupus Erythematosus and Secondary Antiphospholipid Syndrome Diagnosed After Pulmonary Thromboembolism in a Male Patient

Autoreactive B cells in SLE, villains or innocent bystanders?

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