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STOP-JIA

Antibiotic Exposure, Infection and the Development of Pediatric Psoriasis

By: Kenneth Schikler, MD | April 7, 2016 | What Caught Our Eye

After Daniel Horton and his collaborators reported on the results of their nested case-controlled study regarding antibiotic exposure and JIA in Pediatrics (2015 vol 136 issue 2), the same group of data-miners did a similar, nested case-control study from UK’s Health Improvement Network data on children aged 1-15 years with newly diagnosed psoriasis, excluding those children with “juvenile arthritis”, immunodeficiency, or inflammatory bowel disease. Unlike the findings of their previous reports, which demonstrated an association between antibiotic exposure and newly-diagnosed JIA rather than between infections and JIA, in this study they found that infections are associated with pediatric psoriasis, and that antibiotic exposure “did not appear to contribute substantially to that risk”.

In the JIA paper, Horton et al. did not break out systemic JIA as a subtype; the JAMA Dermatology paper did not mention whether the newly diagnosed children with psoriasis had testing for either HLA-B27 or HLA-C*06. Both Systemic JIA and psoriasis are considered autoinflammatory diseases rather than autoimmune diseases. However, Michael Ombrello’s paper in the Proceedings of the National Academy of Science (112:1590-15975) describes their finding of HLA DRB1*ll and variants with a glutamate 68 as a strong risk factor for SJIA. Peter Nigrovic describes in the same issue the “bi-phasic hypothesis” in which an innate autoinflammatory process may then allow for a slip in immune tolerance and the evolution of an autoimmune component to the disease process.

If I meander back to psoriasis, in Rheumatology (2016, 55:221-229), Queiro and colleagues review of the relationship of HLA-B27 and psoriatic disease, the proclivity of HLA-B27 to be more strongly associated with a shorter interval between the onset of skin disease and the onset of psoriatic joint disease as compared to psoriasis patients who are HLA-C*06 + and HLA-B27 – . Finally, back to the initial question about the microbiome and early antibiotic exposure and “JIA”. Without differentiation of subtype (Systemic or HLA-B27+ enthesitis-related), might there be more to understand?  What could be gleaned from data-mining? Is it possible to follow up on the pediatric psoriasis population, track for emergence of psoriatic arthritis, and assess their MHC status?  Retrospectively, could the subtypes of the JIA population Horton had in his paper be determined? I would be interested to learn whether there are distinctions to be found among the autoinflammatory (or Bi-phasic) or the HLA-B-27 + groups of arthritis syndromes and infection, antibiotic exposure and, eventually the microbiome.