Background/Purpose:   Lyme arthritis (LA) usually responds to antibiotic therapy, though immune-mediated synovitis may persist after antibiotic treatment, usually confined to a previously infected joint, without systemic symptoms. In contrast, systemic autoimmune arthritides following Lyme disease have not been described. We report here a cohort of 30 patients who developed new-onset rheumatoid arthritis (RA), psoriatic arthritis or peripheral spondyloarthropathy (PsA/SpA), after antibiotic treatment for Lyme disease.

Methods:   We reviewed records of all adult patients referred to our Lyme arthritis (LA) clinic over a 13-year period in whom we diagnosed systemic autoimmune arthritis occurring within 2 years of Lyme disease, the interval in which LA may develop after erythema migrans (EM). For comparison, 43 patients enrolled in our LA cohort over a 2-year period were analyzed. IgG antibodies to Borrelia burgdorferi and to 3 Lyme-associated autoantigens, endothelial cell growth factor (ECGF), apolipoproteinB-100, and matrix metalloproteinase-10, were measured.

Results:   We identified 30 patients who developed new-onset systemic arthritis a median of 4 months after Lyme disease; 60% were seen in the past 3 years. Fifteen had RA, 13 had PsA, and 2 had peripheral SpA.  The majority (80%) had prior early Lyme disease, usually EM; all had been treated appropriately with antibiotics. In contrast, only 2 of 43 LA patients had prior EM (P<0.0001), and no patient received antibiotics prior to arthritis onset. All 15 RA patients had symmetrical polyarthritis; 6 had RF or anti-CCP antibodies. The 15 PsA/SpA patients often had axial arthritis, dactylitis, or enthesitis. Of the PsA patients, 9 had skin psoriasis prior to Lyme disease, whereas 4 developed new-onset skin psoriasis and arthritis after the infection. In contrast, the LA patients had monoarticular or oligoarticular arthritis, usually of knees, without SpA features or RA autoantibodies. Most systemic autoimmune patients had positive tests for B. burgdorferi IgG antibodies by ELISA, but had much lower titers than LA patients (P<0.0001). Moreover they had lower frequencies and levels of Lyme-associated autoantibodies, particularly anti-ECGF (P≤0.02).   Prior to our evaluation, the patients often received additional antibiotics for presumed Lyme arthritis without benefit. We prescribed anti-inflammatory therapies, usually DMARDs, resulting in improvement.

Conclusion:   Although systemic autoimmune arthritis may follow Lyme disease by chance, onset within months suggests that B. burgdorferi infection may be a pro-inflammatory trigger. Thus, when inflammatory arthritis develops in the context of Lyme disease, clinicians need to distinguish among three possibilities: patients who have active infection in joints, those who have post-infectious Lyme arthritis, and those who have developed another form of arthritis. Onset of polyarthritis after antibiotic-treated EM, prior psoriasis, or low-titer B. burgdorferi antibodies may be distinguishing features. As Lyme disease is now epidemic in parts of the U.S., awareness of this arthritis spectrum is essential in preventing delays in appropriate diagnosis and treatment.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/autoimmune-arthritides-rheumatoid-arthritis-psoriatic-arthritis-or-peripheral-spondyloarthropathy-following-lyme-disease/