Mediterranean Journal of Rheumatology最新文献

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that is characterised by a wide range of symptoms and a risk for irreversible organ damage, leading to increased morbidity and mortality. To improve long-term outcomes, innovative therapeutic goals have been explored, including attainment and maintenance of remission or low disease activity, with minimal use of glucocorticoids. Other goals encompass early diagnosis, potent yet less toxic therapies, appropriate glucocorticoid tapering, and better quality of life for the patients. Implementing a treat-to-target (T2T) approach involves treatment adjustments to achieve predefined objectives. Evidence from other chronic diseases, like hypertension and diabetes, supports the success of target-based approaches. In rheumatic diseases, the multitude of clinical features adds complexity to T2T strategies, but in rheumatoid arthritis, T2T has yielded improved outcomes. The application of T2T in SLE requires realistic therapeutic goals and practical tools for their measurement. International task forces have developed T2T recommendations for SLE, focusing on limiting disease activity, preventing organ damage, and minimising glucocorticoid use, while considering patients' quality of life. Advancements in defining clinically meaningful remission and low disease activity states, coupled with promising novel therapies, have spurred progress in the management of SLE.

Advances in knowledge of the microbiome and its relationship with the immune system have led to a better understanding of the pathogenesis of chronic inflammatory rheumatic diseases (CIRD). Indeed, the microbiome dysbiosis now occupies a particular place with implications for the determinism and clinical expression of CIRD, as well as the therapeutic response of affected patients. Several approaches exist to limit the impact of the microbiome during CIRD. This review aimed to present current strategies to prevent or reverse microbiome dysbiosis based on existing knowledge, in order to provide practical information to healthcare professionals treating patients suffering from CIRD.

Background: The cardiovascular disease (CVD) risk is elevated by 1.5 times among South Asians with rheumatological conditions like rheumatoid arthritis (RA) in the UK. However, there is a dearth of culturally sensitive educational interventions tailored to this population. We have culturally adapted an existing cognitive behavioural patient education intervention, originally designed for predominantly White populations, to address this gap.

Methods: The adaptation process followed the Ecological Validity Model, comprising four phases: stage-setting and expert consultations, preliminary content adaptation, iterative content adaptation with patient partners, and finalisation with patient partners and feedback. The Theoretical Domains Framework (TDF) was employed to evaluate the relevance, acceptability, and cultural adaptation of the existing intervention. Seven South Asian Patient Experts with RA were interviewed, and their input aided in developing new content for the culturally sensitive intervention.

Results: The intervention was successfully adapted to suit South Asians. Cultural adaptation involved reviewing elements of the existing intervention, including language tone, content, and metaphors. Moreover, by incorporating behaviour change techniques, the content was designed to enhance understanding of RA, CVD risk associated with RA, and promote a healthy lifestyle. The newly developed educational intervention addressed topics such as community resistance, perspectives on health and culture, societal pressure, and opportunities for change. Key messages were visually illustrated through pictorial diagrams in a twenty-five-minute online resource.

Conclusion: The first culturally adapted CVD intervention targeting South Asian individuals with RA, particularly those who are non-English-speaking, is now accessible free of charge at www.nras.org.uk/apnijung nationally and internationally.

Aim: The present study aims to investigate the prevalence, causes and outcomes of acute gastrointestinal (GI) bleeding in Rheumatoid arthritis (RA).

Methods: A systemic search was conducted from electronic databases (PubMed/Medline, Cochrane Library, and Google Scholar) from inception to 14^th November 2023. All statistical analyses were conducted in Review Manager 5.4.1. Studies meeting inclusion criteria were selected. A random-effect model was used when heterogeneity was seen to pool the studies, and the result was reported in prevalence and their corresponding 95% confidence interval (CI). Other outcomes were assessed using qualitative analysis.

Results: A total of eight studies (six observational studies and 2 trials were used to conduct this systematic review and meta-analysis. A total population of 138,041 patients was used. Pooled analysis showed a statistically significant risk of GI bleeding in RA patients receiving NSAIDs (prevalence = 2% (1%, 3%); P < 0.00001; I2 = 98%). Qualitatively, causes and outcomes were discussed.

Conclusion: Our study showed that 2% RA patients were subjected to GI bleeding, when they used NSAIDs. Other causes of GI bleeding were age-related factors, cardiovascular events, history of GI complications, and peptic ulcers. Outcome varied by the use of specific NSAIDs and the presence of comorbidities. Recent guidelines for the management of RA may mention GI bleeding as a potential complication, but the level of emphasis placed on this issue varies. Some guidelines provide comprehensive recommendations for its prevention and management, while others offer limited guidance.

Type I interferon (IFN) pathway dysregulation plays a crucial role in the pathogenesis of several systemic autoimmune rheumatic diseases (SARDs), including systemic lupus erythematosus (SLE), Sjögren's disease (SjD), systemic sclerosis (SSc), dermatomyositis (DM) and rheumatoid arthritis (RA). Genetic and epigenetic alterations have been involved in dysregulated type I IFN responses in systemic autoimmune disorders. Aberrant type I IFN production and secretion have been associated with distinct clinical phenotypes, disease activity, and severity as well as differentiated treatment responses among SARDs. In this review, we provide an overview of the role of type I IFNs in systemic autoimmune diseases including SLE, RA, SjD, SSc, and DM focusing on pathophysiological, clinical, and therapeutical aspects.

Glucocorticoids (GCs) are one of the most effective first-line treatments for systemic lupus erythematosus (SLE). However, GC burden is associated with damage. The initial GC dose and tapering schedule should be tailored to the severity of the clinical scenario. As lupus therapy should prompt remission while minimising damage, recent guidelines recommend a more accurate approach to the use of GCs, setting lower starting doses and rapid tapering schemes, and encouraging maintenance prednisolone doses <5 mg/day. Methylprednisolone pulses (MP) help to reduce the dose of oral GCs and improve the clinical response in both severe and non-severe manifestations, without significant side effects. Fixed-tapering GC scheme provides a useful strategy to reduce GCs exposure. Long-term antimalarial treatment and early initiation of immunosuppressive drugs improve clinical efficacy while reducing GC toxicity. Besides, withdrawal of GCs is an achievable goal in patients in prolonged remission on stable treatment, and recent studies have attempted to identify the most suitable candidates. In this article, we review the pharmacological basis, clinical evidence of efficacy, dose-related harms, and potential withdrawal of GCs. We also review guidelines recommendations and finally give a personal and practical approach to dealing with the use of GCs in SLE patients.

Systemic lupus erythematosus is the prototype multisystem autoimmune disorder characterised by a broad spectrum of organ involvement and a multitude of laboratory abnormalities. Clinical heterogeneity, unpredictable course and lack of pathognomonic clinical and serological features pose a considerable challenge in the diagnosis of SLE. The latter remains largely clinical, typically accompanied however by features of serologic autoimmunity, which are characteristic for the disease. Despite significant improvements in treatment strategies, an early diagnosis often continues to be an unmet need, as the median reported delay from symptom onset to SLE diagnosis is approximately 2 years. Classification criteria are usually used to support the diagnosis, yet with significant caveats. In this article, we provide an updated review of the clinical presentation of lupus and give clues for an accurate diagnosis.

Despite advances in the management of systemic lupus erythematosus (SLE), it remains a chronic disease with frequent flares, requiring constant medical care, laboratory exams, hospitalisations, and the use of immunosuppressive drugs and corticosteroids, increasing the morbidity and mortality of these patients. The past decade of research has brought to light multiple observations on the role of interferons (IFNs) in the pathogenesis of SLE, which paved the way for the development of potential novel therapies targeting the interferon pathway. Following two phase III trials, anifrolumab, a monoclonal antibody which binds to the type I IFN receptor, blocking the activity of type I IFNs, was approved for active SLE. This review summarises the latest research on the role and mechanisms of type I IFNs in SLE and the development and advances on new therapeutic drugs based on IFN inhibition for SLE.

Systemic lupus erythematosus (SLE) has a spectrum of phenotypes. Its management should target remission or low disease activity, prevention of relapses and organ damage, minimisation of drug-related harms, and optimisation of health-related quality of life. Advances in our understanding of the disease pathophysiology have expanded the treatment armamentarium with targeted biologics that demonstrate superiority over conventional drugs in controlling activity, reducing flares and glucocorticoid exposure, and improving patient-related outcomes. In view of this, there is a critical need for real-world evidence providing insight into the spectrum of activity, the treatment landscape, and unmet needs among SLE patients. Such information can support regulatory and reimbursement decision-making. The primary objective of the NYMERIA multicentre study is to generate real-world evidence on the activity state of SLE patients treated in routine care settings in Greece. The overarching aim is to capture the disease burden based on both clinical aspects and the patient perspective.

Lupus enteritis is a rare gastrointestinal complication of systemic lupus erythematosus (SLE) associated with significant morbidity and mortality. Rituximab, a monoclonal antibody targeting CD20-positive B cells, has shown promise in refractory SLE cases. We present a case of a 45-year-old female with SLE who developed lupus enteritis and experienced an unusually rapid and remarkable response to Rituximab. The patient presented with severe abdominal pain and distension. Within two days of Rituximab treatment, the patient's abdominal pain, distension, and associated complications resolved completely. This exceptional response challenges the typical timeline of Rituximab efficacy in SLE and highlights the need for further investigation into the factors influencing treatment response. Understanding the mechanisms underlying such rapid improvement may provide insights into SLE pathogenesis and guide therapeutic strategies for optimal outcomes.