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The Association Between Schizophrenia and Rheumatoid Arthritis: A Nationwide Population-Based Swedish Study on Intraindividual and Familial Risks

Artikel i vetenskaplig tidskrift
Författare C. Sellgren
T. Frisell
P. Lichtenstein
Mikael Landén
J. Askling
Publicerad i Schizophrenia Bulletin
Volym 40
Nummer/häfte 6
Sidor 1552-1559
ISSN 0586-7614
Publiceringsår 2014
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 1552-1559
Språk en
Länkar dx.doi.org/10.1093/schbul/sbu054
Ämnesord epidemiology, population register, major histocompatibility complex, schizophrenia, rheumatoid, GENOME-WIDE ASSOCIATION, AUTOIMMUNE-DISEASES, BIPOLAR DISORDER, DETERMINANTS, IMMUNE, SUSCEPTIBILITY, MICROGLIA, PSYCHOSES, RELATIVES, PROTEINS, Psychiatry, HRMANN J, 1995, BRAIN RESEARCH REVIEWS, V20, P269
Ämneskategorier Neurovetenskaper

Sammanfattning

Numerous studies have reported a reduced risk of rheumatoid arthritis (RA) in schizophrenia. The mechanisms are unknown, but recent genome-wide association studies of schizophrenia have shown strong associations with markers spanning the major histocompatibility complex region, indicating a possible role for adaptive immunity also in schizophrenia. In this population-based cohort study, we assess the associations between RA and schizophrenia and the extent to which any observed associations are specific to RA/schizophrenia. We then extend the assessments per RA subtype and to risks in first-degree relatives. The study population included every individual identified in the Swedish Population Register born in Sweden between 1932 and 1989. The risk for RA in schizophrenia was significantly decreased (hazard ratio [HR] = 0.69, 95% CI = 0.59-0.80), but similar reductions were noted for osteoarthritis (a noninflammatory joint disorder) and ankylosing spondylitis (a non-RA inflammatory disorder). Comparable associations were seen in schizoaffective subjects while no significant associations were observed in bipolar disorder. Overall, first-degree relatives of schizophrenia patients were not at reduced risk of RA, but the risk for seronegative RA was significantly decreased in children and siblings of schizophrenia probands (HR = 0.13, 95% CI = 0.02-0.95 and HR = 0.67, 95% CI = 049-0.92, respectively). In conclusion, our intraindividual analyses suggest that differential misclassification bias is an important factor for the observed inverse association and emphasize the need of optimized care-provision for nonpsychiatric symptoms in schizophrenia patients. Our familial analyses indicted the possibility of an inverse coinheritance of schizophrenia and seronegative RA.

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