Undetectable mannose binding lectin is associated with HRCT proven bronchiectasis in rheumatoid arthritis (RA).


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 04 07 2018
accepted: 26 03 2019
entrez: 11 4 2019
pubmed: 11 4 2019
medline: 31 12 2019
Statut: epublish

Résumé

The aim of this study was to ascertain whether mannose binding lectin deficiency is implicated in coexistent rheumatoid arthritis and bronchiectasis and to determine whether undetectable mannose binding lectin confers poorer long-term survival in coexistent rheumatoid arthritis and bronchiectasis or in rheumatoid arthritis in general. A retrospective audit was conducted in a rheumatoid arthritis cohort in which mannose binding lectin had been measured by enzyme linked immunosorbent assay from 2007-11. Rheumatoid arthritis patients with physician diagnosed HRCT proven bronchiectasis were recruited during this time and compared to those with uncomplicated rheumatoid arthritis. Survival from disease onset was recorded in October 2018. Kaplan-Meier survival estimates were performed to assess mortality over time in the two groups. Log rank tests were used for equality of survivor functions. The two groups were demographically comparable. A higher frequency of undetectable mannose binding lectin was observed in coexistent rheumatoid arthritis and bronchiectasis (37.5%) compared to uncomplicated rheumatoid arthritis, (8.9%, P = 0.005). Undetectable mannose binding lectin correlated with a strong trend toward poor survival in rheumatoid arthritis overall (P = 0.057). Cox regression analysis however, showed no difference in the hazard ratio for survival between the two groups when corrected for age, gender, prednisolone use ever, rheumatoid factor status and the full range of MBL concentrations. In summary, undetectable mannose binding lectin is associated with coexistent rheumatoid arthritis and bronchiectasis and correlates with poor survival in rheumatoid arthritis overall. These findings further implicate immunodeficiency in the genesis of bronchiectasis in rheumatoid arthritis.

Identifiants

pubmed: 30970022
doi: 10.1371/journal.pone.0215051
pii: PONE-D-18-19867
pmc: PMC6457565
doi:

Substances chimiques

Antibodies 0
MBL2 protein, human 0
Mannose-Binding Lectin 0
Peptides, Cyclic 0
cyclic citrullinated peptide 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0215051

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Krista Makin (K)

Fiona Stanley Hospital, Perth, Western Australia, Australia.

Tracie Easter (T)

Department of Clinical Immunology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia.

Monica Kemp (M)

Department of Clinical Immunology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia.

Peter Kendall (P)

Fremantle Hospital, Fremantle, Western Australia, Australia.

Max Bulsara (M)

University of Notre Dame, Fremantle, Western Australia, Australia.

Sophie Coleman (S)

University of Notre Dame, Fremantle, Western Australia, Australia.

Graeme J Carroll (GJ)

Fiona Stanley Hospital, Perth, Western Australia, Australia.
Fremantle Hospital, Fremantle, Western Australia, Australia.
University of Notre Dame, Fremantle, Western Australia, Australia.

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Classifications MeSH