Prevalence of 13 autoantibodies and of the 16/6 and related pathogenic idiotypes in 465 patients with systemic lupus erythematosus and their relationship with disease activity.
With a cross sectional study of 465 consecutive systemic lupus erythematosus (SLE) patients tested for 13 autoantibodies (Aab) and two idiotypes we determined the prevalence of Aab according to disease activity, both general and at particular organ systems. Seventy seven percent of SLE sera had at least one Aab and 56% had it at high titres. Pathogenic idiotypes had a prevalence of less than 10% and 166 sera had Aab to 5 or more antigens and 9 sera had Aab against all 13 antigens tested. Patients with active disease had increased prevalence of Aab to DNP, ssDNA, ENA, mitochondria and histones when considered at 5 s.d. above the mean of normal controls. The higher positivity of Aab in patients with active disease was confirmed in logistic regression analysis adjusted by age, disease duration, and intensity of treatment. A trend was observed of increased prevalence and titres of Aab from inactive disease without treatment, to inactive disease but still being treated, to active disease. Only 22% of patients with active disease had no Aab and the higher the number of Aab the higher the frequency of active disease. Patients with active arthritis, and to a lesser degree those with active mucocutaneous involvement, had higher prevalence and titres of most autoantibodies than patients with disease activity at other organ systems. Active renal disease associated only with anti-dsDNA, whereas active CNS disease associated with anti-mitochondrial Aab. Our findings support the vision of SLE as an immune dysregulation leading to polyclonal B cell activation with resulting production of multiple Aab. Their profiles seem influenced by genetical, hormonal and environmental factors and, in turn, they contribute to the clinical picture in each patient. Disease activity influences the presence of some, but not all, Aab and some of them may remain present in some patients, even in remission.
Villarreal
G M
GM
Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico.
Drenkard
C
C
Villa
A R
AR
Slor
H
H
Shafrir
S
S
Bakimer
R
R
Shoenfeld
Y
Y
Alarcón-Segovia
D
D
D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood / Q000276:immunology; D000974:Antibodies, Antinuclear / Q000097:blood / Q000276:immunology; D000918:Antibody Specificity; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000097:blood / Q000276:immunology*; D003430:Cross-Sectional Studies; D004247:DNA / Q000276:immunology; D004277:DNA, Single-Stranded / Q000276:immunology; D005260:Female; D006657:Histones / Q000276:immunology; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000097:blood*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D008297:Male; D008800:Mexico / Q000453:epidemiology; D008875:Middle Aged; D008928:Mitochondria / Q000276:immunology; D020733:RNA, Small Cytoplasmic; D012343:RNA, Transfer / Q000276:immunology; D012261:Ribonucleoproteins / Q000276:immunology; D017411:Ribonucleoproteins, Small Nuclear / Q000276:immunology; D012720:Severity of Illness Index; D000097585:SS-B Antigen; D000099207:SS-A Antigen
D017153:Antibodies, Anticardiolipin; D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D001324:Autoantigens; D004247:DNA; D004277:DNA, Single-Stranded; D006657:Histones; D007130:Immunoglobulin Idiotypes; D020733:RNA, Small Cytoplasmic; D012343:RNA, Transfer; D012261:Ribonucleoproteins; D017411:Ribonucleoproteins, Small Nuclear; D000097585:SS-B Antigen; D000099207:SS-A Antigen; C116006:RO60 protein, human