• HLA polymorphism
• systemic lupus erythematosus

Recently, a comprehensive study was published on HLA class II DNA typing in a large cohort of European patients with SLE.¹ Independently of this collaborative study, we have examined similar DRB1, DQA1, and DQB1 allele polymorphisms and clinical features in Hungarian patients with SLE.

Fifty patients with SLE (48 female; mean age at the time of the examinations 41 years (range 21–76)) and 50 healthy blood donors matched for age and sex with the controls were examined. Genotyping of HLA-DRB1 alleles was carried out with the Dynal RELI SSO HLA-DRB kit, and the DRB1*15/16 subtyping by the method of Ota et al.² DQA1 determination was performed by the method of Ota et al.³ The DQB1 typing was carried out with the INNO-LiPA DQB kit. A χ² test with Yates’s correction was used for statistical analysis. The significance levels (p<0.05) were adjusted by using Bonferroni’s correction to eliminate chance associations (pc value). Odds ratio (OR) values were also calculated.

The main clinical manifestations were articular involvement (92%), anaemia (72%), leucopenia (54%), pericarditis and/or pleuritis (54%), and nephritis (32%).

The DRB1*1501, DRB1*03, and DRB1*07 alleles occurred more frequently in the patients with SLE than in the controls (12/50 (24%) v 3/50 (6%); 20/50 (40%) v 10/50 (20%) and 17/50 (34%) v 6/50 (2%), respectively; ORs 4.4, 2.25, and 3.2, respectively). The DQA1*0102 and *05011 alleles were also more common in the SLE group than in the controls (25/50 (50%) v 13/50 (26%), and 20/50 (40%) v 9/50 (18%), respectively; ORs 2.23 and 2.3, respectively). Of the DQB1 alleles, *0201 and *0602 were detected more frequently in the patients with SLE than in the controls (20/50 (40%) v 8/50 (16%), and 11/50 (22%) v 2/50 (4%), respectively; ORs 2.87 and 6.05, respectively). After the Bonferroni’s correction the above mentioned differences did not reach significance.

In contrast, the DRB1*04 and DRB1*11/12 alleles were less common in the patients with SLE than in the controls (3/50 (6%) v 16/50 (32%) and 15/50 (30%) v 25/50 (50%)). The *04 allele was linked with resistance to leucopenia (pc=0.01), the *11/12 alleles with resistance to discoid skin lupus (pc=0.001). The 1106 subtype of the DRB1*11 alleles occurred only in the patients with SLE (4/16 (25%) v 0/25 (0%)).

Connections between the genetic and clinical characteristics were as follows: the DRB1*1501 positivity was less frequent in the patients with than in those without lupus nephritis (LN) (3/16 (19%) v 15/34 (44%)). In contrast, the DRB1*03 and DRB1*07 alleles were more frequent in the patients with than in those without LN (8/16 (50%) v 11/34 (32%) and 7/16 (44%) v 8/34 (24%)). In the patients with pleuritis and/or pericarditis, only the DRB1*07 positivity was more frequent than in the patients without serositis (12/27 (44%) v 3/23 (13%)). The *07 allele was detected more frequently in the patients with one or more severe renal, cardiorespiratory manifestations than in the patients without these potentially fatal features of the disease (16/36 (44%) v 0/14 (0%)). In the patients with anti-SSA and anti-SSB positivity the renal and cerebral involvement was more common, but the differences were not significant (4/8 (50%) v 9/33 (27%) and 2/8 (25%) v 3/33 (9%)).

A comparison with the results of the comprehensive European study showed that agreement was complete for the increased prevalence of the DRB1*1501, DRB1*03, DQA1*0102, DQB1*0201, and DQB1*0602 alleles in the patients with SLE. We could not detect increased frequencies of the DQB1*0303 and DQB1*0502 alleles in our patients with SLE, and our patients with DRB1*1501 positivity exhibited a milder clinical course and a negative correlation with LN.