ABSTRACT
Despite their recognition in systemic lupus erythematosus [SLE] patients more than 30 years ago, the prevalence and disease associations of anti-ribosomal P[anti-P] antibodies are controversial. We attempted in this study to evaluate the prevalence, the clinical significance and the pathogenesity of anti-ribosomal antibodies in SLE patients. Our study included 82 patients with SLE [71 females and 11 males] with age ranging from 17 to 50 years [27.6 +/- 9.2] in addition to twenty age and sex matched healthy individuals as a control group. Routine investigations, together with urine microscopy, 24-hour urinary protein quantitation, creatinine clearance, liver function tests and serum C3 level were performed. Renal biopsy was performed for most patients with lupus nephritis. Brain Computed tomography [C.T], Electroencephalogram [EEG] and Magnetic Resonance Immaging [MRI] were done for patients with neuropsychiatric lupus. The clinical activity of the disease was assessed by the SLE disease activity index [SLEDAI] after full clinical examination including rheumatological examination. Immunologic investigations included: 1] determination of anti-P antibodies by an enzyme linked immunosorbent assay [ELISA] method using a highly purified COOH terminal 22 amino acid peptide as an antigen. 2] indirect immunofluoresent technique for the detection of antideoxy ribonucleic acid [dsDNA], anti-smooth muscle antibodies [ASA] and anti-mitochondrial antibodies [AMA]. 3] ELISA methods for the detection of anticardiolipin antibodies [ACA] IgG and IgM, hepatitis C virus antibodies [HCV] IgG and hepatitis B surface antigen [HBsAg]. Anti-P antibodies were positive in 22/82 [26.8%] of patients with SLE and in none of the normal control subjects. Accordingly we classified our patients into two groups: Group I with positive anti-P antibodies [22 patients] and group II with negative anti-P antibodies [60 patients]. Hepatitis [which could be attributed to SLE and not to other causes since they were negative for ASA, AMA, HCV and HBV] was reported in 21/82 [25.6%] of our SLE patients. Fifteen of them were from the anti-P positive group [15/22, 68.1%] and 6 were from the anti-P negative group [6/60,10%]. This difference was statistically highly significant [p<0.001]. Regarding the incidence of lupus nephritis, it was [18/22, 81.8%] in the anti-P positive group, while in the anti-P negative group it was [24/60, 40%], the difference was statistically significant [p<0.001]. There was no statistically significant difference between anti-P positive and anti-P negative patients with regard to the presence of anti-ds DNA antibodies. Lupus psychosis was reported in 12/22 [54.5%] of anti-P positive patients [group I] and in 6/60 [10%] of anti-P negative patients [group 11], the difference was statistically highly significant [p<0.001]. The level of ACA in the sera of our patients was correlated significantly with the level of anti-P antibodies [r = 0.573 and p<0.001 for IgG ACA and r = 0.773 and p<0.001 for IgM ACA]. Clinical observations revealed that the presence of anti-P antibodies was significantly correlated with disease severity determined by systemic lupus erythematosus disease activity index [SLEDAI]. The SLEDAI score was significantly elevated with a mean of 26.9 +/- 2.6 in anti-P positive patients [group I] and a mean of 17.2 +/- 1.6 in the anti-P negative patients [group II] [p<0.001]. The level of C3 was significantly reduced in anti-P positive patients when compared with anti-P negative patients [p<0.001]. We concluded that, although anti-P antibodies were present in a small percentage of SLE patients, yet they were significantly associated with more aggressive disease, with increased incidence of hepatic, renal and central nervous system [CNS] involvements. Thus, the determination of anti-P antibodies may be one of the useful prognostic tools in identifying a subset of SLE patients with more severe disease associations and early major organe affections, that necessitate close clinical observations and frequent follow up visits. Large scale prospective study can better illuminate the relationship of anti-P antibodies to clinical disease expression, especially hepatitis and CNS involvement