23 research outputs found

    Predictive risk factors before the onset of familial rheumatoid arthritis: the Tatarstan cohort study

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    BackgroundA familial history of rheumatoid arthritis (RA) predisposes an individual to develop RA. This study aimed at investigating factors associated with this conversion from the Tatarstan cohort.MethodsA total of 144 individuals, referred to as pre-RA and at risk for familial RA, were selected 2 years (range: 2–21 years) before conversion to RA and compared to non-converted 328 first-degree relatives (FDR) from RA as assessed after ≥2 years follow-up, and 355 healthy controls were also selected (HC). Preclinical parameters and socio-demographic/individual/HLA genetic factors were analyzed when data were available at the time of enrollment.ResultsAs compared to FDR and HC groups, pre-RA individuals were characterized before conversion to RA by the presence of arthralgia, severe morning symptoms, a lower educational level, and rural location. An association with the HLA-DRB1 SE risk factor was also retrieved with symmetrical arthralgia and passive smoking. On the contrary, alcohol consumption and childlessness in women were protective and associated with the HLA-DRB1*07:01 locus.ConclusionBefore RA onset, a combination of individual and genetic factors characterized those who are at risk of progressing to RA among those with familial RA relatives

    Prevalence and Incidence of Upper Respiratory Tract Infection Events Are Elevated Prior to the Development of Rheumatoid Arthritis in First-Degree Relatives

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    Introduction: The aim of this study was to characterize infection events in a longitudinal cohort of first-degree relatives (FDR) of probands with rheumatoid arthritis (RA) and explore their associations with RA development. To this end, newly diagnosed RA patients (n = 283), unaffected related FDR and age-matched healthy women were ascertained from the Caucasian triple women prospective Tatarstan cohort.Methods: In this cohort initiated in 1997, 26/283 (9.2%) FDR developed RA (incidence: 9.1 cases/1,000/year). At baseline and during the follow-up, information regarding infectious events (prevalence) and their incidence and duration per year were collected from all individuals.Results: Results reveal in the unaffected FDR developing RA subgroup: (i) a higher prevalence and/or incidence at baseline of upper respiratory infections (URI), otitis, tonsillitis, herpes reactivation, and skin infections; (ii) Mycoplasma sp detection was increased during pregnancy; (iii) a peak of infections started in the 3 years preceding RA onset, and thereafter decreased following RA diagnosis and treatment initiation with disease-modifying anti-rheumatic drugs (DMARDs) when considering URI, and acute tonsillitis; (iv) herpes virus reactivation, at baseline, was associated with a higher report of morning stiffness and arthralgia while independent from rheumatoid factors and anti-citrullinated peptide (CCP)2 Ab positivity; and (v) infection events represent an independent environmental factor associated with RA development.Conclusion: In conclusion, an annual increase of respiratory tract infections was found at the pre-clinical stage of RA. This could be due to alterations in the immune system that result in susceptibility to infection, controlled by DMARDs, or that the infectious events predispose to RA

    Microbial and Environmental Factors in Autoimmune and Inflammatory Diseases

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    In recent years there has been a substantial increase in the number of diseases with the inflammatory component such as such as allergy, asthma, rheumatoid arthritis, inflammatory bowl disease (IBD, which includes ulcerative colitis and Crohn's disease), chronic sinusitis, and many other conditions. The majority of these diseases are multifactorial, with the contribution of genetic and environmental factors. Among the latter, the role of certain microorganisms and viruses in triggering or sustaining the inflammatory process is most controversial. In rheumatoid arthritis, for example, the following bacteria and viruses have been implicated in triggering the disease: Mycoplasma spp., Proteus mirabilis, Escherichia coli, Staphylococcus spp., Bordetella spp., Acinetobacter spp., the parvoviruses, Epstein-Barr virus, and retroviruses. The list of putative microbial triggers of rheumatoid arthritis is still growing, and it becomes essentially impossible to make a causation link between certain infectious agents and the disease. In the light of these disappointing results there are calls for even larger studies with the use of more advanced and large-scale technologies. The primary function of the immune system is the maintenance of body homeostasis and protection against any threats to it via several lines of elaborate and complex immune defense. Given even higher complexity that involves the microbiota and the corresponding host-microbe interaction, the conditions for this equilibrium become even more challenging. In the absence of a defined pathogen, for example, the spectrum of microorganisms involved in triggering inappropriate immune responses may include polymicrobial communities or the cumulative effect of several microbial/viral factors. Under the normal circumstances there is a fine-tuned balance between commensal microbiota and the host’s immune responses. However, when this balance is compromised, for example in IBD, a massive immune response is launched against commensal microbiota resulting in chronic inflammation. Besides the microbial/viral factors, the balance of the immune system can be compromised by other causes. Given, for example, the close and inclusive interaction of the immune, nervous and endocrine systems, the list of these provoking factors can expand even more. For instance, it has been demonstrated that even mild sleep deprivation may increase the production of interleukin-6 and C-reactive protein. Understanding the complex role of microbial and environmental factors in inflammatory and autoimmune diseases, therefore, is the main subject of this topic
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