impact factor, citescore
logo
 

Brief Papers

 

Autoantibodies in post-treatment Lyme disease and association with clinical symptoms


1, 2, 3, 4, 5, 6, 7, 8

 

  1. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  2. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  3. Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  4. Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  5. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  6. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  7. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
  8. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. jmill237@jhmi.edu

CER17009
Brief Papers

Free to view
(click on article PDF icon to read the article)

PMID: 38607687 [PubMed]

Received: 21/07/2023
Accepted : 31/10/2023
In Press: 05/04/2024

Abstract

OBJECTIVES:
Autoantibodies have been described in the post-infectious state, specifically after Lyme disease and COVID-19. We aimed to describe the prevalence and potential clinical utility of several commercially available autoantibodies after these infections.
METHODS:
Euroimmun panels (myositis, scleroderma and ANA5) were assayed using sera from patients with Lyme disease with return to health (RTH) (n=70), post-treatment Lyme disease (n=58), COVID-19 RTH (n=47) and post-acute symptoms of COVID-19 (n=22). The post-Lyme questionnaire of symptoms (PLQS) was used to determine symptom burden after Lyme disease.
RESULTS:
There was no statistically significant difference in autoantibody prevalence across the four groups (p=0.746). A total of 21 different antibodies were found in the Lyme cohorts and 8 different antibodies in the COVID-19 cohorts. The prevalence of scleroderma-associated antibodies was higher after Lyme disease than COVID-19 (12.5% vs. 2.9%, p=0.026). There was no statistically significant difference in symptom burden based on antibody status.
CONCLUSIONS:
Several autoantibodies were found after Borrelia burgdorferi and SARS-CoV2 infection, although the prevalence was similar in those with persistent symptoms and those who returned to health. While our data show no difference in autoantibody prevalence across the four post-infectious states, we do not imply that autoantibodies are irrelevant in this setting. Rather, this study highlights the need for novel antibody discovery in larger cohorts of well-defined patient populations.

DOI: https://doi.org/10.55563/clinexprheumatol/qcupkk

Rheumatology Article

Rheumatology Addendum