Revista Colombiana de Reumatologia最新文献

Introduction/Objective

To evaluate the association between autoantibodies with clinical manifestations (extraglandular and glandular) and histopathological findings of minor salivary gland biopsy in primary Sjögren's syndrome.

Materials and methods

Observational, descriptive, and cross-sectional study. Forty-seven patients with primary Sjögren's syndrome according to the ACR/EULAR 2016 criteria were included. A face-to-face survey, a review of medical records, and the measurement of autoantibodies anti-Ro 52, anti-Ro 60, anti-La, antinuclear antibodies, rheumatoid factor IgA, IgG and IgM, and anti-alpha fodrin IgA and IgG were done. Characterization of the population and analysis of the association between clinical characteristics, autoantibodies, and histopathology were performed.

Results

Association of anti-alpha fodrin IgA and anti-Ro 52 Ab was found with pulmonary involvement (P = .014 and P = .031 respectively) and anti-La antibodies with haematological manifestations, specifically leukopenia (P = .011), lymphopenia (P = .023), and anaemia (P = .09). We found no association between the histopathological findings of the minor salivary gland biopsy and extraglandular manifestations.

Conclusions

The activation of B cells, reflected in the increased production of autoantibodies, is related to extraglandular manifestations in primary Sjögren's syndrome, which is observed more frequently in patients with earlier diagnosis.

Interstitial lung disease (ILD) is a common and potentially devastating complication of systemic sclerosis (SSc), a chronic autoimmune disorder characterized by fibrosis and vascular abnormalities. The association between SSc and ILD underscores the intricate interplay between immune dysregulation, vasculopathy, and tissue fibrosis. This review provides a comprehensive overview of the immunological, clinical, and radiological features of ILD in the context of SSc. It highlights the diverse spectrum of ILD patterns observed in SSc patients, ranging from non-specific interstitial pneumonia to usual interstitial pneumonia. The intricate pathogenic mechanisms linking SSc and ILD involve aberrant immune responses, endothelial dysfunction, profibrotic cytokine signaling, and genetic factors. Immunological alterations, diagnostic challenges, and prognostic implications are discussed, underscoring the need for multidisciplinary management strategies. By elucidating the complex relationship between SSc and ILD, this review aims to contribute to a deeper understanding of the underlying mechanisms and facilitate the development of interdisciplinary interventions for improved patient outcomes.

An increasing number of musculoskeletal clinical manifestations, the onset of diseases and rheumatological manifestations have been seen in the paediatric population surviving COVID-19, however, the medical literature on the subject is limited.

The objective is to explore the available evidence on musculoskeletal symptoms and autoimmune diseases in the paediatric population with post-COVID syndrome.

Scoping systematic review in PubMed and Scopus through search strategies. Observational and experimental studies are included in populations under 21 years of age with and without autoimmune diseases, without time limit in English and Spanish.

The 28 documents included: case reports (n = 6), cross-sectional studies (n = 5), prospective cohort studies (n = 5), retrospective cohort (n = 6), case series (n = 6), ambidirectional section (n = 1), randomized controlled trial (n = 1), and longitudinal section study (n = 1). The total study population was 56,738 patients. The most frequent symptoms presented in long COVID-19 are myalgias and arthralgias. The evidence showing a relationship between SARS-CoV-2 infection in the development of musculoskeletal symptoms and autoimmune diseases in the convalescent period is limited.

As a conclusion, myalgias and arthralgias are the most frequent symptoms in long COVID. patients with SARS-CoV-2 infection and a history of rheumatic disease who are undergoing immunomodulatory treatment do not have a dangerous risk of developing severe presentations and/or complications of the disease.

Recent advances in deciphering the genetic architecture of RA-ILD support the hypothesis of RA-ILD as a complex disease with a heterogeneous phenotype encompassing at least the usual interstitial pneumonia (UIP) and non-UIP high-resolution CT patterns. The results of genetic studies support the hypothesis of a common genetic background between idiopathic pulmonary fibrosis (IPF) and RA-ILD, and more specifically RA-UIP, a subset of the disease associated with a poor prognosis. Overall, these findings suggest the existence of shared pathogenic pathways between IPF and RA-ILD providing new opportunities for future intervention in RA-ILD, particularly with drugs that have been shown to be active in IPF.

Introduction

Connective tissue disease-related interstitial lung disease (CTD-ILD) accounts for 30% of all cases of ILD. Some patients progress and develop progressive pulmonary fibrosis, which has a prognosis comparable to interstitial pulmonary fibrosis. In this study, relevant evidence about epidemiology, risk factors, biomarkers, and treatment are reviewed.

Materials and methods

A systematic review of the literature was carried out. Original observational and descriptive articles were included. Articles not providing information about the CTD diagnosis were excluded. PUBMED, EMBASE, SCOPUS, and LILACS were all searched. The total number of articles obtained was 528; data were extracted from 61 original articles.

Results

On average, ILD in these patients progressed by 33.7% over time. Patients with progressive pulmonary fibrosis had a similar 3.7-year median survival as those with idiopathic pulmonary fibrosis. Mortality was markedly increased (hazards ratio 3.29; 95% CI 2.76–3.82). A progressive course was seen in 34% of scleroderma (SSc) related ILD cases. Six interferon-induced proteins and a proteomic profile of 12 biomarkers were used to predict progression and response to treatment. The INBUILD and SENSCIS studies that assessed the effectiveness of nintedanib effectiveness revealed a reduced decrease in forced vital capacity. Progression in rheumatoid arthritis (RA) related ILD ranges from 38% to 50%. Control of RA disease activity and use of antifibrotics benefit the lungs.

Conclusion

A significant proportion of patients with CTD-ILD have progressive lung disease, with the corresponding adverse mortality effects. The majority of the data regarding CTD-ILD are from cohorts of patients with RA-ILD and SSc-ILD, in which antifibrotics and concurrent immunosuppressive treatments have been effective. There is not enough information available on other autoimmune disorders to draw any firm conclusions regarding progression rates or treatment effects.

Introduction/Objective

The aim of this study was to investigate the frequency of fibromyalgia (FM) in axial spondyloarthritis (ax-SpA) patients using the current FM diagnostic criteria (2016 Revised Fibromyalgia Diagnostic Criteria). Additionally, we aimed to investigate the relationship between FM severity and disease activity, functional status, and quality of life (QoL).

Materials and methods

Disease activity, functional disability and QoL were evaluated. FM severity was measured with the fibromyalgia impact questionnaire (FIQ).

Results

One hundred and three patients with ax-SpA (55.3% female; mean age 44 ± 10.85 years) were included. FM was detected in 49.5% of the patients. While FM was detected in 71% of patients with a history of peripheral arthritis, FM was present in 59.2% of patients without (p = 0.009). FM-ax-SpA patients showed higher disease activity except for C-reactive protein; functional status and QoL were statistically worse in patients with FM-SpA. Significant positive correlations were found between FIQ and disease activity, functional disability and QoL (p < .001).

Conclusions

The most effective features associated with the presence of FM were detected as gender and a history of peripheral arthritis. Presence of FM may cause an overestimation of disease activity, FM severity correlates with disease activity.

Interstitial lung disease (ILD) is a serious extra-articular co-morbidity in rheumatoid arthritis (RA) patients and accounts for a substantial part of the increased mortality in RA. In this review, we describe how environmental and lifestyle factors interact with genetic variants in the HLA genetic locus in triggering RA-specific antibodies against post-translationally modified, mainly citrullinated proteins (ACPA), which are associated with an increased risk of ILD. The same environmental risk factors, i.e. exposure to noxious agents such as smoke to the lungs contribute additionally to the emergence of RA ILD as does long-lasting high disease activity and an additional ILD-specific genetic risk variant related to mucus formation (MUC5B). Options for prevention and therapy of RA ILD resulting from this so far incomplete knowledge of its pathophysiology are expanding. The most obvious option is to address modifiable environmental risk factors, such as smoking and exposure to other noxious agents affecting the lungs. The second option is to reduce the inflammatory activity of RA; here different anti-rheumatic therapies appear to have differential effects on ILD development. The third and novel option is to use anti-fibrotic therapy which may reduce the development of RA ILD but has not yet been shown to revert existing fibrosis. The main conclusion concerning the clinical handling of RA ILD is therefore an early awareness of the risk for RA ILD combined with active measures to reduce modifiable environmental/lifestyle factors and use optimal anti-rheumatic therapies for early and sustained reduction of disease activity. These actions should be combined with a preparedness to use anti-fibrotic therapy for patients at high risk for ILD despite previous risk reduction efforts.

Introduction/Objective

To review the epidemiology, general clinical aspects and diagnosis, impact on morbidity and mortality, and general treatment approaches for myositis-associated ILD.

Materials and methods

The relevant literature was reviewed.

Results

The clinical, radiographic, and histopathological features of interstitial lung disease (ILD) in idiopathic inflammatory myopathies (IIM) are similar to idiopathic ILD. Patients with a known diagnosis of myositis require prompt clinical evaluation including the determination of myositis-associated autoantibodies. Patients possessing autoantibodies associated with ILD or those with any pulmonary symptoms should undergo a pulmonary function test and high-resolution CT (HRCT) scanning of their lungs.

Conclusion

Despite the lack of placebo-controlled trials, systemic glucocorticoids are considered the mainstay of initial treatment of myositis-associated ILD. Glucocorticoid-sparing agents are often concomitantly administered, particularly in patients with severe disease. The first-line conventional immunosuppressive drugs include either mycophenolate mofetil or azathioprine. If these agents fail or if the pulmonary features are severe or rapidly progressive, then more aggressive immunosuppressive or immunomodulatory therapy including cyclophosphamide, tacrolimus or cyclosporine, rituximab, IVIg, or tofacitinib can be considered. Further investigations are required to assess the role of novel therapies in the treatment of myositis-associated ILD.

Rheumatoid arthritis associated interstitial lung disease (RA-ILD) has significant clinical impact on patients due to increased morbidity and mortality. Understanding the progression of ILD in patients with RA from when asymptomatic to clinical progression and the clinical, genetic, and novel markers associated with disease progression is an important step in altering the natural history of ILD in patients with RA. We review the natural history and epidemiology of RA-ILD, with a focus on Latin-American epidemiology in RA-ILD. Additionally, we discuss unique features of RA-ILD compared to other forms of ILD, early disease detection, and current concepts in treatment.

Introduction/Objective

Early diagnosis of rheumatoid arthritis (RA) can improve the prognosis of the disease by reducing joint destruction and achieving a better rate of remission. Musculoskeletal ultrasound (US) has become a potent tool to detect synovitis and erosions. However, until now, there has been a lack of consensus on the US scoring system to help in diagnosing RA early. The purpose of our study was to elaborate a US set suitable for classifying RA patients with inflammatory arthralgia or expressing synovitis and who did not satisfy ACR/EULAR criteria, called “USSRA” (UltraSound Set for Rheumatoid Arthritis).

Materials and methods

A multistep study was conducted. A preliminary set of joints, tendons, and erosions to include in the USSRA were identified through a deep literature screening. The final step of this study was the validation of the final set by international experts in US using a Delphi process.

Results

The preliminary set included 20 joints, 16 tendons, and 8 erosion sites for assessment. After the Delphi process, the changes were to add an assessment of two additional wrist joints and remove one. As for the tendons, two sites were removed from the final set. No changes were proposed for the section erosions. The elementary lesions and scoring system were clarified. The final USSRA forms include 18 joints, 12 tendons, and 8 sites of erosion.

Conclusion

The USSRA is a novel diagnostic tool proposed for detecting early RA in routine practice. The next step will be to assess the reliability of this set in a patient-based exercise.