Our objective was to investigate whether a dietary pattern derived using inflammatory biomarkers is associated with rheumatoid arthritis (RA) risk. We prospectively followed 79,988 women in the Nurses’ Health Study (NHS, 1984–2014) and 93,572 women in the NHSII (1991–2013); incident RA was confirmed by medical records.
The objective of this article was to establish the clinical course of interstitial lung disease (ILD) in scleroderma related to the presence of anti-PM/Scl antibody compared with anti-Scl-70 in a Spanish cohort. Furthermore, no study has thoroughly investigated the outcome of pulmonary function test in the first group of patients.
Giant cell arteritis (GCA) is an autoimmune disorder which primarily affects large vessels, whilst inflammatory bowel diseases (IBD) mainly target the gut. Co-existence of the two maladies has been reported sporadically in the literature; therefore the purpose of this study was to assess the authenticity of such an association in a large, cross-sectional study.
The relationship between serum cytokine levels and degree of psychosis in patients with schizophrenia
Autoantibodies to the dense fine speckled 70 (DFS70) antigen are common among antinuclear antibodies (ANA) positive healthy individuals (HI). We assessed the prevalence of anti-DFS70 antibodies in patients with and without ANA-associated rheumatic diseases (AARDs) by two methods: chemiluminescent immunoassay (CIA) and an indirect immunofluorescence (IIF) assay based on immunoadsorption for DFS70.
The current paradigm in disease etiopathogenesis implicates the interplay of genetic and environmental factors. Multiple genes have been linked to susceptibility of patients to develop T1DM, including the human leukocyte antigen (HLA) loci HLA-DRB1 and DQB1.
Autoimmune disease are brought about by the inability of our immune system to identify self-antigens due to intrinsic loss of tolerance. Autoimmune diseases can be classified into either systematic or organspecific diseases. The central dogma in autoimmune diseases is their etiopathogenesis. Large strides in understanding the complex processes that drive disease emergence have been made in the past decades, however ongoing investigation is warranted. The current paradigm in disease etiology points towards the complex interplay between environmental triggers and epigenetic deregulations in genetically susceptible
hosts. A variety of environmental factors have been proposed including viral infections, exposure to smoke, hormones, stress,
drugs, pollutants and dietary factors among others.
In rheumatoid arthritis (RA), immunological triggers at mucosal sites, such as the gut microbiota, may promote autoimmunity that affects joints.
Antibodies that recognize the phosphatidylserine/prothrombin complex (antiphosphatidylserine/prothrombin antibodies; aPS/PT) might reveal enhanced thrombotic risk in patients with systemic lupus erythematosus. Little is known about their association with pregnancy complications in the antiphospholipid syndrome (APS).
Idiopathic inflammatorymyopathies are heterogeneous in their pathophysiologic features and prognosis. The emergence ofmyositis-specific autoantibodies suggests that subgroups of patients exist.