Potential role of the lectin pathway of complement in the pathogenesis and disease manifestations of systemic sclerosis: a case-control and cohort study

Table 2 Analysis of MBL2 geno- and phenotypes in SSc cases and controls

Variables	Cases	Controls	Univariate matched analysis
Variables	(n = 90)	(n = 90)	OR (95% CI)	Pvalue
MBL2 exon variants, n (%)
A/A	56 (62)	59 (66)	Reference
A/O	30 (33)	25 (28)	1.2 (0.7-2.3)	0.5
O/O	4 (4)	6 (7)	0.6 (0.1-3.1)	0.5
MBL2 promoter variant, n (%)
Y/Y	46 (51)	47 (52)	Reference
Y/X	36 (40)	38 (42)	1.0 (0.6-1.7)	1
X/X	8 (9)	5 (6)	1.7 (0.5-6.2	0.4
MBL2 genotypes, n (%)
High producing	48 (53)	54 (60)	Reference
Intermediate producing	24 (27)	18 (20)	1.5 (0.7-3.0)	0.3
Low producing	18 (20)	18 (20)	1.1 (0.5-2.5)	0.8
MBL levels (μg/ml), median (IQR)	1.1	1.0	1.3 (1.0-1.7)^a	0.06
MBL <0.5 μg/ml, n (%)	62 (69)	65 (72)	1.2 (0.6-2.5)	0.6

MBL2 genotypes were classified as low- (XA/YO, YO/YO), intermediate- (XA/XA, YA/YO) or high- (YA/YA, XA/YA) producing genotypes with exon variant alleles collectively designated as O and the wild-type gene as A, and the promoter variant allele and the wild-type gene designated as X and Y, respectively. ^aPer 1 μg/ml increase in MBL serum levels. CI, confidence interval; IQR, interquartile range; MBL, mannose-binding lectin; OR, odds ratio; SSc, systemic sclerosis.

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