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Research
Evidence of a distinct group of Black African patients with systemic lupus erythematosus
  1. Elopy N Sibanda1,2,
  2. Margo Chase-Topping3,
  3. Lorraine T Pfavayi1,
  4. Mark E J Woolhouse2,4,
  5. Francisca Mutapi2,5
  1. 1 Asthma, Allergy and Immunology Clinic, Twin Palms Medical Centre, Harare, Zimbabwe
  2. 2 TIBA Partnership, NIHR Global Health Research Unit Tackling Infections to Benefit Africa (TIBA), University of Edinburgh, Edinburgh, UK
  3. 3 Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, UK
  4. 4 Usher Institute of Population Health Sciences and Informatics and Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, UK
  5. 5 Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, Ashworth Laboratories, University of Edinburgh, Edinburgh, UK
  1. Correspondence to Professor Francisca Mutapi; f.mutapi{at}ed.ac.uk

Abstract

Background The autoimmune disease systemic lupus erythematosus (SLE) occurs more frequently in patients of African descent with high morbidity and mortality. Current SLE diagnostic criteria including antinuclear antibody (ANA) reactivity are derived largely from non-African populations. This study characterises ANA reactivity patterns and relates them to SLE clinical presentation in Black African patients.

Methods Sera from Black participants (61 patients with SLE and 100 controls) aged 1–81 years were analysed for reactivity against the antigens: uridine 1-ribonuclear protein, Smith uridine-1-5 ribonuclear protein antigen, soluble substance-A, recombinant Ro-52, soluble substance-B, Scl-70, cytoplasmic histidyl-tRNA synthetase antigen, proliferating cell nuclear antigen (PCNA), nucleosomes, ribonuclear P-protein, antimitochondrial antibody M2 (AMA-M2), histones, double-stranded DNA (dsDNA), centromere protein B and polymyositis–sclerosis overlap antigen.

Findings A significantly higher proportion (97%) of the 61 patients with SLE had detectable autoantibody reactivity compared with 15% of the 100 controls (p<0.001). The highest frequencies of autoantibody reactivity in patients with SLE were against the dsDNA antigen (41%) and PCNA (54%). Anti-PCNA and anti-dsDNA reactivity were mutually exclusive (p<0.001) giving rise to two distinct groups of Black African patients with SLE. The first group (n=25) had reactivity profiles consistent with international standard SLE definitions, including anti-dsDNA reactivity, and was 13 times more likely to present with joint symptoms. The larger, second group (n=34), characterised by anti-PCNA and anti-AMA-M2 reactivity, was nine times more likely to present with only cutaneous symptoms.

Interpretation Our study demonstrates a need to extend autoantibody panels to include anti-PCNA in the diagnostic process of Black African patients and further refine the predictive values of the reactivity to different antigens to differentiate SLE syndromes in African populations.

  • elisa
  • serology
  • screening
  • public health

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

https://doi.org/10.1136/bmjgh-2017-000697

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    Footnotes

    • Handling editor Seye Abimbola

    • Contributors ENS, FM and MEJW conceived the idea and informed data entry, data cleaning and data analyses. ENS conducted the clinical examinations. ENS and TLP conducted the laboratory work. MC-T conducted the statistical analyses. FM wrote the first draft of the manuscript and all co-authors contributed to the revisions of the manuscript.

    • Funding The study received funding from the OAK Foundation (FM, ENS,LTP), The Wellcome Trust (grant no. 108061/Z/15/Z (to FM) and Welcome Trust (Centre for Infection, Immunity and Evolution at the University of Edinburgh (MC-T, MEJW, FM)) . This research is also commissioned by the National Institute of Health Research, using Official Development Assistance (ODA) funding 16/136/33.

    • Disclaimer The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute of Health Research or the Department of Health (ES, MEJW, FM).

    • Competing interests None declared.

    • Ethics approval Medical Research Council of Zimbabwe.

    • Provenance and peer review Not commissioned; externally peer reviewed.