PMID- 19758197
OWN - NLM
STAT- MEDLINE
DCOM- 20091029
LR  - 20220408
IS  - 1749-6632 (Electronic)
IS  - 0077-8923 (Linking)
VI  - 1173
DP  - 2009 Sep
TI  - Human leukocyte antigen-DRB1 and -DQB1 genotyping in lupus patients with and 
      without antiphospholipid syndrome.
PG  - 545-51
LID - 10.1111/j.1749-6632.2009.04642.x [doi]
AB  - We investigated the genetic background regarding major histocompatibility complex 
      (MHC) II alleles in patients with systemic lupus erythematosus (SLE) only, in 
      patients with SLE with secondary antiphospholipid syndrome (SLE+SAPS), and in 
      patients whose clinical course began as primary antiphospholipid syndrome (PAPS) 
      and subsequently progressed to SLE (PAPS+SLE) in order to explain the 
      phenotypical differences found in our previous study. Those with primary or 
      secondary APS present more thrombotic and less inflammatory activity. Fetal 
      wastage was the highest in the PAPS+SLE group. We performed human leukocyte 
      antigen (HLA)-DRB1 and HLA-DQB1 genotyping in 63 patients (26, 22, and 15 in SLE 
      only, SLE+SAPS, and PAPS+SLE groups, respectively) and in 57 healthy controls, 
      using PCR with sequence-specific primers. We found that, as reported in the 
      literature, the occurrence of DRB1*03 and DQB1*0201 alleles was higher in SLE 
      patients than in controls, but these alleles were rare in the PAPS+SLE group (13% 
      in PAPS+SLE vs. 46% in the SLE only group; P = 0.044). HLA-DRB1*04 alleles were 
      expressed frequently in both primary and secondary APS. DRB1*13, DQB1*06, and 
      DQB1*0302 alleles were present more frequently in the PAPS+SLE patients than in 
      the other groups, while the DQB1*0301 allele was rare. In this study we have 
      shown that the SLE-associated DRB1*03/DQB1*02 alleles occurred frequently in our 
      lupus patients as well as in SLE patients with secondary APS. In patients who 
      started as PAPS and later progressed to SLE, the allele frequency was 
      fundamentally different. Taken together, our results confirmed that the HLA-DRB1 
      and HLA-DQB1 profile of PAPS and SAPS is different. Therefore it is unlikely that 
      these alleles are responsible for the partly similar phenotype of the two groups.
FAU - Kapitany, Aniko
AU  - Kapitany A
AD  - Third Department of Internal Medicine, Medical and Health Science Center, 
      University of Debrecen, Debrecen, Hungary.
FAU - Tarr, Tunde
AU  - Tarr T
FAU - Gyetvai, Agnes
AU  - Gyetvai A
FAU - Szodoray, Peter
AU  - Szodoray P
FAU - Tumpek, Judit
AU  - Tumpek J
FAU - Poor, Gyula
AU  - Poor G
FAU - Szegedi, Gyula
AU  - Szegedi G
FAU - Sipka, Sandor
AU  - Sipka S
FAU - Kiss, Emese
AU  - Kiss E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Antibodies, Anticardiolipin)
RN  - 0 (Autoantibodies)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ beta-Chains)
RN  - 0 (HLA-DQB1 antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (beta 2-Glycoprotein I)
SB  - IM
MH  - Alleles
MH  - Antibodies, Anticardiolipin/blood
MH  - Antiphospholipid Syndrome/complications/*genetics/immunology
MH  - Autoantibodies/blood
MH  - Female
MH  - Gene Frequency
MH  - Genotype
MH  - HLA-DQ Antigens/*genetics
MH  - HLA-DQ beta-Chains
MH  - HLA-DR Antigens/*genetics
MH  - HLA-DRB1 Chains
MH  - Humans
MH  - Lupus Erythematosus, Systemic/complications/*genetics/immunology
MH  - Male
MH  - Retrospective Studies
MH  - beta 2-Glycoprotein I/immunology
EDAT- 2009/09/18 06:00
MHDA- 2009/10/30 06:00
CRDT- 2009/09/18 06:00
PHST- 2009/09/18 06:00 [entrez]
PHST- 2009/09/18 06:00 [pubmed]
PHST- 2009/10/30 06:00 [medline]
AID - NYAS4642 [pii]
AID - 10.1111/j.1749-6632.2009.04642.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2009 Sep;1173:545-51. doi: 10.1111/j.1749-6632.2009.04642.x.