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MO YIN MOK, W.K. EDDIE IP, CHAK SING LAU, YI LO, WILFRED H.S. WONG, and YU LUNG LAU

ABSTRACT.

Objective. To test the hypothesis that low serum mannose-binding lectin (MBL) levels, as a result of the single-nucleotide polymorphisms in the promoter region (–221 X/Y) and exon 1 (codon 54 A/B) of the MBL2 gene, predispose to infection in Chinese patients with systemic lupus erythematosus (SLE).

Methods. Two hundred forty-five patients with SLE were prospectively followed for the development of major infective episodes that required hospitalization and antibiotic treatment during 1992-2005. MBL genotypes were determined by polymerase chain reaction and serum MBL levels were measured by ELISA.

Results. In total, 254 major infections developed in 130 patients. Serum MBL levels were shown to correlate inversely with the number of bacterial infections (r = –0.13, p = 0.03). The distribution of MBL genotypes was similar in patients with and without major infection (p = 0.84). Patients with major infection also had more major lupus exacerbations that required daily prednisolone dose ≥ 15 mg. Logistic regression showed that log MBL level (odds ratio 0.516, 95% confidence interval 0.305–0.873; p = 0.01) and major lupus exacerbation (OR 1.382, 95% CI 1.154–1.654; p < 0.001) were independent risk factors to major bacterial infection after adjustment for age and disease duration. Multiple regression analysis showed an increase in risk of bacterial infection by 34.2% for every decrease in serum MBL level by one log, and by 22.8% for each increase in number of major lupus exacerbations.

Conclusion. Low serum MBL level predisposes Chinese patients with SLE to more major infections, in particular bacterial ones. (J Rheumatol 2007;34:1270-6)

Key Indexing Terms:

COMPLEMENT DEFICIENCY
HOSPITALIZATION
IMMUNOCOMPROMISED HOST
IMMUNOSUPPRESSANT
INFECTION

From the Departments of Medicine and Pediatrics and Adolescent Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong.

Supported by a University Department of Medicine Grant, University Department of Medicine, Queen Mary Hospital, Hong Kong and Shun Tak District Min Yuen Tong Fund.

M.Y. Mok, MD, Rheumatologist, Department of Medicine, Queen Mary Hospital; W.K.E. Ip, PhD, Research Fellow, Laboratory of Developmental Immunology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; C.S. Lau, MD, Professor in Medicine; Y. Lo, Research Assistant, Division of Rheumatology, Department of Medicine; W. Wong, MMedSc, Senior Statistician; Y.L. Lau, MD, Chair, Professor, Department of Pediatrics and Adolescent Medicine, Queen Mary Hospital.

Address reprint requests to Dr. M.Y. Mok, Division of Rheumatology, Queen Mary Hospital, Pokfulam Road, Hong Kong. E-mail: mymok@netvigator.com

Accepted for publication February 7, 2007.