Undetectable mannose binding lectin and corticosteroids increase serious infection risk in rheumatoid arthritis

Carroll, G.J., Makin, K., Garnsey, M., Bulsara, M., Carroll, B.V., Curtin, S.M., Allan, E.M., McLean-Tooke, A., Bundell, C., Kemp, M.L., Deshpande, P., Ihdayhid, D., Coleman, S., Easter, T., Triplett, J., Disteldorf, T., Marsden, C.H. and Lucas, M. (2017) Undetectable mannose binding lectin and corticosteroids increase serious infection risk in rheumatoid arthritis. The Journal of Allergy and Clinical Immunology: In Practice, 5 (6). pp. 1609-1616.

Abstract

Background: Infection is the leading cause of death in rheumatoid arthritis (RA). Corticosteroid (CS) use is a known and important risk factor for serious infections (SIs). Mannose binding lectin (MBL) is a genetically determined component of the innate immune system implicated in neonatal infections.

Objective: Our aim was to determine whether MBL deficiency is a risk factor for SIs in RA and to compare it with CS use and also synthetic and biologic disease-modifying antirheumatic drug (DMARD) therapy.

Methods: Data on 228 patients with RA were collected for up to 7 years (median = 5.9 years). Serum MBL concentrations were determined in all patients receiving synthetic (n = 96) or biologic (n = 132) DMARD therapy.

Results: High rates of SIs were observed in RA irrespective of treatment (17%). Similar rates of SIs were observed in synthetic and biologic DMARD users. The rates of single and multiple SIs were similar, irrespective of the use of a biologic agent. Undetectable MBL (<56 ng/mL) concentrations and maintenance prednisolone at 10 mg per day or higher were associated with an increased risk for an SI, with incident risk ratio of 4.67 (P = .001) and 4.70 (P < .001), respectively.

Conclusions: Undetectable MBL and prednisolone confer a high risk for an SI. The use of biologic DMARDs did not confer substantial SI risk in this observational study. MBL deficiency is hitherto an unrecognized risk factor for an SI in RA.

Item Type:	Journal Article
Murdoch Affiliation(s):	Institute for Immunology and Infectious Diseases
Publisher:	Elsevier
Copyright:	© 2017 The Authors
URI:	http://researchrepository.murdoch.edu.au/id/eprint/37460

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