Liver abnormalities and liver membrane autoantibodies in systemic lupus erythematosus.

The hepatic involvement of 57 patients with systemic lupus erythematosus (SLE) was studied with special reference to liver membrane autoantibody (LMA). Liver abnormalities were found predominantly in patients with active SLE (27/48 (56%) in active SLE v 3/20 (15%) in inactive SLE). They were, however, rather mild or moderate and tended to disappear as the disease activity of SLE decreased. In this respect the liver abnormalities observed in this study differed from those in patients with lupoid hepatitis. The incidence of LMA in active SLE (8/11 (73%] was significantly greater than that in inactive SLE (4/12 (33%)). The mean LMA index value in active SLE was 8.3, which was also greater than the 2.9 in inactive SLE. Furthermore, in active SLE the mean LMA titre was significantly higher in patients with liver abnormalities than in those without. These results suggest that LMA may be associated with the activity of SLE and may be one of the factors which cause transient liver abnormalities.     

Oxidative stress and antioxidant parameters in a Turkish group of patients with active and inactive systemic lupus erythematosus

Aim: Although the pathogenesis of systemic lupus erythematosus (SLE) is likely to be multifactorial, the inflammatory nature of SLE implies that a state of oxidative stress may exist in this disease, which may contribute to immune cell dysfunction, auto‐antigen production and auto‐antibody reactivity. This study was conducted to investigate the oxidant/antioxidant status of patients with SLE and to correlate this with disease activity. Methods: Sixteen clinically active, 12 clinically inactive SLE patients and 11 healthy controls were included into the study and antioxidant potential (AOP), catalase (CAT), glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD), adenosine deaminase (ADA), malondialdehyde (MDA), and xanthine oxidase (XO) activity levels in erythrocytes and AOP, GSH‐Px, MDA, and XO activity levels in plasma were measured. Results: In erythrocytes; AOP was higher in SLE patients (both active and inactive), CAT activity was higher in inactive SLE patients, GSH‐Px, SOD and XO activity were lower in SLE patients (active and inactive) than the control group. In plasma; SLE patients (active and inactive) had higher AOP levels, activity of GSH‐Px was lower in SLE groups (active and inactive), activity of MDA was lower in active SLE patients, and activity of XO was higher in the active SLE patients than the control group. Conclusion: Antioxidant status was impaired in SLE patients but there was no significant difference between the active and inactive SLE groups, so oxidative stress may play a role in the pathogenesis of SLE but probably is not correlated with disease activity.     

Antibody testing for ulcerative colitis--more letters?

The presence of perinuclear antineutrophil cytoplasmic antibodies (P-ANCAs) and antibodies against cathepsin G, a target antigen for P-ANCAs, was determined in the sera of patients with ulcerative colitis (UC), relative to endoscopic severity and disease activity. P-ANCAs were detected by indirect immunofluorescent assay on ethanol-fixed human neutrophils. Antibodies to cathepsin G were detected by ELISA and Western blotting. P-ANCAs were detected by immunofluorescent assay in 62.5% of 32 patients with active UC. Anti–cathepsin G antibodies were detected in 40.6% of 32 patients with active UC, and their prevalence was significantly higher in patients with severe colitis, as determined by endoscopy, than in those with mild or moderate colitis. The prevalence and titers of anti–cathepsin G antibodies were significantly higher during the active phase of the disease than during the inactive phase.     

Value of anticardiolipin antibodies for monitoring disease activity in systemic lupus erythematosus and other rheumatic diseases

Summary The prevalence of anticardiolipin antibodies in active systemic lupus erythematosus (SLE) was compared with that in inactive SLE and other rheumatic and non-rheumatic diseases to determine the value of these autoantibodies in monitoring rheumatic diseases. Pairs of IgG- and IgM-aCL were measured by ELISA in 173 consecutive hospitalised patients, including 141 with rheumatic diseases (18 active SLE, 21 inactive SLE, 19 rheumatoid arthritis, 13 reactive arthritis, 7 other spondyloarthropathies, 16 vasculitis, 47 other autoimmune diseases) and 32 non-rheumatic controls. A further 101 aCL pairs were determined during follow-up in 19 patients with SLE. Serum concentrations were analysed with respect to SLE activity and compared between the different patient groups. IgG- and IgM-aCL levels in excess of 10 GPL and 9 MPL respectively were considered positive. 30.6% of all patients (53/173) were found to be positive for IgG-aCL, as against only 9.8% (17/173) for IgM-aCL. IgG-aCL serum levels in active SLE differed significantly from all other groups, including inactive SLE (all p<0.005). Median IgM-aCL levels were below the cut off point in all groups, although measurable values were obtained almost exclusively in active SLE and RA. In this study IgM-aCL measurement was of less value in monitoring rheumatic diseases. IgG-aCL positivity in SLE was associated with a significantly higher odds ratio (OR) for active disease (OR 16.0, 95% confidence interval: 2.8–90.0). The results show that disease activity in SLE was accompanied by significantly increased IgG-aCL, whereas no elevation was found in other diseases. This parameter may therefore be useful in monitoring SLE activity.     

Cardiac magnetic resonance imaging abnormalities in systemic lupus erythematosus: a preliminary report

The purpose of this prospective, pilot study was to determine whether differences in myocardial T2 relaxivity can be identified among active systemic lupus erythematosus (SLE) patients with clinically suspected SLE myocarditis, other active SLE patients, inactive SLE patients and age and gender matched controls. Eleven consecutive female patients (six with active SLE and five with inactive SLE), and five age, gender and race matched healthy controls underwent imaging with echocardiography and cardiac magnetic resonance imaging (MRI). Echocardiographic measurements included left ventricular end diastolic (LVEDV) and end systolic volumes (LVESV), and mass (LVM) (all indexed to body mass); ejection fraction and cardiac output. The cardiac MRI measurement was the T2 relaxation time (an index of soft tissue signal, with higher levels suggestive of increased tissue water content). Patients with active SLE had significantly higher LVEDV and LVM than inactive SLE patients and healthy controls, and significantly larger LVESV than healthy controls. Myocardial T2 relaxation times were significantly higher in patients with active SLE compared to those with inactive SLE and to healthy controls, and remained higher even after excluding the two active SLE patients who had clinical myocarditis. The four active SLE patients who underwent repeat cardiac imaging studies after clinical improvement showed normalization of these myocardial abnormalities. The conclusion was that active SLE patients demonstrate abnormalities in myocardial structure manifested by high myocardial T2 relaxation times that normalized after clinical improvement in disease activity. These findings suggest that T2 relaxation values are a sensitive indicator of myocardial disease in patients with SLE and that myocardial T2 relaxation abnormality frequently occur in patients with active SLE, even in the absence of myocardial involvement by clinical criteria.     

Toxic effects of SLE serum on normal monocytes in vitro: cell death induced by apoptosis related to complement dysfunction

The aim of this study was to assess toxic effects of systemic lupus erythematosus (SLE) serum on blood peripheral mononuclear cells from healthy donors and to evaluate if complement activation was involved. Monocytes from a healthy donor were incubated with 20 sera from ten SLE patients in both high and low disease activity states. After incubation non-adherent cells were analysed by flow cytometry. Serum from six SLE patients induced an increased cell death, four in active disease only, one in the inactive state and one in the active and the inactive state. Five of these sera, three with high and two with low disease activity, induced an increased apoptosis in the monocytes. Proportion of apoptotic cells correlated inversely with C1q and C3 concentration in the active disease sera, but not with disease activity as evaluated by SLEDAI. Apoptosis could be induced by addition of active C1s or antigen/antibody complexes to normal serum before incubation. Serum with complexes added induced increased tumour necrosis factor-alpha secretion from mononuclear cells, but SLE patient sera did not. The results demonstrate that the toxic effect of serum from SLE patients on healthy monocytes is explained by induction of apoptosis. The induction process is suggested to be connected with complement activation in the serum.     

Myocardial tissue characterization in systemic lupus erythematosus: value of a comprehensive cardiovascular magnetic resonance approach

Systemic lupus erythematosus (SLE) is a multi-organ inflammatory disorder mainly affecting women and is associated with high cardiovascular morbidity and mortality. We tested the utility of a comprehensive cardiovascular magnetic resonance approach to assess myocardial involvement and to determine its relation to disease activity in SLE patients. We studied 20 SLE patients (19 females, 35+/-10 years) and 13 healthy volunteers (nine females, 28+/-11 years). Classification followed the criteria of the American College of Rheumatology and assessment of SLE activity was based on the European Consensus Lupus Activity Measurement index. Cardiovascular magnetic resonance (CMR) was performed on a 1.5T scanner and included the following sequences: steady-state free precession, T2-weighted, early and late T1-weighted after gadolinium-DTPA injection. Ejection fraction was not significantly different between groups (controls: 63+/-6, inactive SLE: 67+/-7, active SLE 64+/-8; P=0.003 for all groups). In contrast, relative T2 ratio (myocardium to skeletal muscle) was significantly higher in active SLE than in the other groups (controls: 1.7+/-0.3, inactive: 1.8+/-0.2, active: 2.1+/-0.2; P=0.003). Similarly, early enhancement ratio was significantly higher in active SLE (controls: 2.4+/-1.4, inactive: 2.8+/-1.1, active: 4.5+/-2.0, P=0.39). Both relative T2 and early enhancement ratios significantly correlated with disease activity. Intramural foci of late enhancement were observed in three of eight patients (all with active SLE). Of the five patients with no late enhancement, only one had active disease. An imaging approach combining T2-weighted, early and late enhancement imaging is a useful tool to assess possible myocardial involvement in SLE. CMR parameters of global myocardial involvement correlate well with disease activity, but not with usual clinical signs as summarized in a cardiac score.     

Abnormal telomerase activity and telomere length in T and B cells from patients with systemic lupus erythematosus

OBJECTIVE: To evaluate the clinical significance of telomerase activity and telomere length in T and B lymphocytes from patients with systemic lupus erythematosus (SLE). METHODS: CD3+ (T cell) and CD19+ (B cell) lymphocytes were isolated from the peripheral blood of SLE patients and healthy controls by means of magnetic bead-coupled antibodies. SLE patients were classified as active or inactive cases according to the SLE Disease Activity Index (SLEDAI). Telomere activity of lymphocytes was measured by telomeric-repeat amplification protocol. Telomere length was measured by flow cytometry-fluorescence in situ hybridization. RESULTS: T cell telomerase activity was significantly higher in patients with both active and inactive SLE than in controls, but was lower than B cell telomerase activity in patients with active SLE, and was not correlated with SLEDAI results. B cell telomerase activity was only significantly higher than in controls in patients with active SLE, and was strongly correlated with SLEDAI. Four laboratory results, anti-dsDNA antibody titer, IgG level, C3 level, and CH50 level, were correlated with B cell telomerase activity. Telomere length in T cells was significantly shorter than in controls. In contrast, the telomere length in B cells did not differ significantly from controls. CONCLUSION: In patients with SLE, many T cells divide continuously. Their telomerase activity was higher than that in control T cells, but not so high as to prevent telomere shortening. In contrast, B cells do not divide abnormally in the inactive phase of SLE, but divide rapidly in the active phase.     

Increased endothelial cell adherence, aggregation, and superoxide generation by neutrophils incubated in systemic lupus erythematosus and Felty's syndrome sera

The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated. PMN from normal healthy donors were incubated in sera from 19 patients with active SLE, 12 with inactive SLE, 20 with Felty's, 24 with rheumatoid arthritis, and 34 normal persons. After incubation, the degree of adherence of the PMN to human endothelial cells in culture, their aggregation, and superoxide (O2-) generation were determined. Sera from patients with both active SLE and Felty's syndrome induced significantly increased PMN adherence to endothelial cells and PMN aggregation in vitro, compared with normal sera. This increased adherence to endothelial cells was maintained after heat treatment (56 degrees C for 30 minutes) of the sera. In O2- generation experiments, sera from patients with active SLE induced significantly increased O2- release from normal PMN using both fresh and heat-treated sera. Sera from Felty's patients demonstrated the same effect with heat-treated sera but not ith fresh sera. When sera from patients with active SLE and Felty's syndrome were used, all three parameters correlated significantly with each other in individual patients. In contrast, sera from the 12 patients with inactive SLE and 24 rheumatoid arthritis patients without Felty's failed to induce significant differences in the three parameters studied when compared with 34 normal controls. Fractionation of 3 SLE sera and 1 Felty's serum on Sephadex G-200 demonstrated that the adherence enhancing factor was present in both IgG and IgG-excluded fractions. The observed increased adhesiveness of PMN induced by SLE and Felty's sera may, at least in part, contribute to the neutropenia which is common in these diseases. Increased O2- release associated with PMN adherence may contribute to endothelial cell damage and vascular injury, which is also a common manifestation of these diseases.     

Immunoglobulin class of rheumatoid factors detected by enzyme-linked immunosorbent assay

Summary The immunoglobulin class of rheumatoid factor (RF) in sera and synovial fluids of patients with rheumatic diseases was measured by a solid-phase enzyme immunoassay. IgG-RF was frequently found in seronegative sera as well as in seropositive sera of rheumatic patients. Titers of IgG-RF were higher in the active phase than in the inactive phase of SLE and showed a correlation to the levels of hypocomplementemia and circulating immune complexes in SLE sera. Titers of IgA-RF were likewise higher in the active-phase of SLE with a correlation to titers of circulating immune complexes. IgA-RF was also found frequently in sera of patients with Sjögren's syndrome.     

Cerebrospinal fluid and serum prolactin in systemic lupus erythematosus with and without central nervous system involvement

Aim: Recent research has shown that prolactin (PRL) may participate in the pathogenesis of systemic lupus erythematosus (SLE), and hyperprolactinemia may be related to disease activity. The current study investigated both serum and cerebrospinal fluid (CSF) PRL in SLE patients and their possible relationship to central nervous system (CNS) involvement. Methods: Prolactin levels were determined by immunoradiometric assay. Serum PRL levels were detected in 80 patients with SLE and 25 matched healthy controls. Disease activity was scored by SLEDAI. CSF PRL levels were detected in 7 cases of CNS‐involved SLE, eight cases of non‐CNS‐involved inactive SLE and eight cases of non‐SLE CNS disorders. Results: Hyperprolactinemia was present in 40% of SLE patients. Serum PRL levels were significantly correlated with SLEDAI scores. There was no significant difference of serum PRL levels between SLE patients with or without CNS involvement, but the mean CSF PRL levels were higher in CNS‐involved SLE patients than in non‐CNS‐involved SLE and non‐SLE patients. There was no significant correlation between serum and CSF PRL levels. Conclusions: Our results suggest that high serum PRL levels correlate with active disease in SLE, but not with CNS involvement. CSF PRL levels in SLE patients correlate with CNS involvement, which indicates that CSF PRL may be involved in the pathogenesis of CNS‐SLE.     

Detection of anti-interferon antibodies in systemic lupus erythematosus

In this study, we show that sera from 2 of 13 patients with clinically active systemic lupus erythematosus (SLE) contained anti-interferon alpha (anti-IFN alpha) antibody. In contrast, anti-IFN alpha activity was not detected in sera from patients with clinically inactive SLE, rheumatoid arthritis (RA), Sj?gren's syndrome, or in normal individuals. None of the sera exhibited anti-IFN gamma activity. These studies show that anti-IFN antibody, like IFN itself, is most frequently observed in patients with clinically active SLE. It is also possible that the presence of IFN-anti-IFN complexes may contribute, in part, to the pathogenesis of this disease.     

Clinical significance of rheumatoid factor--its complement activating property and isotype]

We investigated the relationship between complement-activating properties of rheumatoid factors (RF) and their isotypes. Active and inactive RA patients without extra-articular symptoms (EAS) and those with EAS were studied. Patients with SLE, liver cirrhosis (LC) and normal volunteers were served as controls. Isotype of RF was measured by ELISA and complement activation (CA) of RF was measured by hemolytic assay. The CA values were significantly higher in RA patients with EAS than those in RA patients without EAS and with other diseases. The IgG and IgM-RF values were significantly higher in active RA without EAS than in inactive RA. Positive correlations between IgM-RF values and CA values were observed in RA with or without EAS, SLE and LC. The Sephadex G-200 gel filtration analysis of sera revealed CA in only 19S IgM fraction. Additionally, we purified 19S IgM-RF from sera of RA, SLE and LC patients by affinity chromatography, and found 19S IgM-RF had CA. These data suggest that serum IgM-RF may play a critical role in the pathogenesis of RA, especially in RA with EAS.     

Cerebrospinal fluid and serum prolactin in systemic lupus erythematosus with and without central nervous system involvement

Aim: Recent research has shown that prolactin (PRL) may participate in the pathogenesis of systemic lupus erythematosus (SLE) and hyperprolactinemia may be related to disease activity. The current study investigated both serum and cerebrospinal fluid (CSF) PRL in SLE patients and their possible relationship to central nervous system (CNS) involvement. Methods: Prolactin levels were determined by immunoradiometric assay. Serum PRL levels were detected in 80 patients with SLE and 25 matched healthy controls. Disease activity was scored by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). CSF PRL levels were detected in seven cases of CNS involving SLE, eight cases of non‐CNS involved inactive SLE and eight cases of non‐SLE CNS disorders. Results: Hyperprolactinemia was present in 40% of SLE patients. Serum PRL levels were significantly correlated with SLEDAI scores. There was no significant difference in serum PRL levels between SLE patients with or without CNS involvement, but the mean CSF PRL levels were higher in CNS‐involved SLE patients than in non‐CNS‐involved SLE and non‐SLE patients. There was no significant correlation between serum and CSF PRL levels. Conclusions: Our results suggest that high serum PRL levels correlate with active disease in SLE, but not with CNS involvement. CSF PRL levels in SLE patients correlate with CNS involvement, which indicates that CSF PRL may be involved in the pathogenesis of CNS‐SLE.     

Clinical significance of selected endothelial activation markers in patients with systemic lupus erythematosus

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease in which immunologically mediated vascular endothelial cell activation is regarded as a potential pathophysiological mechanism of systemic organ damage. We investigated selected endothelial cell activation markers in serum of patients with SLE and their relationships with systemic organ manifestations and disease activity. METHODS: Serum levels of endothelin-1 (ET-1), soluble E-selectin, and thrombomodulin (sTM) were determined by ELISA in 76 SLE patients and in 34 healthy controls. RESULTS: Higher serum concentrations of ET-1, sE-selectin (p < 0.05), and sTM (p < 0.001) were observed in SLE patients in comparison with controls. Significant differences of ET-1, (p < 0.01), sTM (p < 0.001), and sE-selectin serum concentrations (p < 0.01) were found between SLE patients with systemic involvement and controls. Patients with organ manifestations (n = 34) showed significantly higher serum levels of ET-1 than patients without systemic involvement (n = 42) (p < 0.05). Comparison between patients with active and inactive SLE according to SLE Disease Activity Index (SLEDAI) score showed significantly higher concentration of ET-1 in the sera of patients with active SLE compared with inactive patients and the controls (p < 0.001). CONCLUSION: Our findings suggest that the elevated serum concentrations of ET-1, sTM, and sE-selectin reflect persisting endothelial cell activation in SLE, and point to an important role of ET-1 in the pathogenesis of internal organ involvement. Moreover, elevated ET-1 concentrations are related to disease activity, suggesting a key role of endothelial cell activation in systemic manifestations in SLE patients.     

Anti-cathepsin G antibodies in the sera of patients with ulcerative colitis

The presence of perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCAs) and that of antibodies against cathepsin G, a target antigen for P-ANCAs, was determined in the sera of patients with ulcerative colitis (UC), relative to the endoscopic severity and disease activity. P-ANCAs were detected by indirect immunofluorescent assay (IIF) on ethanol-fixed human neutrophils. Antibodies to cathepsin G were detected by an enzyme-linked immunosorbent assay (ELISA) and Western blotting. P-ANCAs were detected by IIF in 62.5% of 32 patients with active UC. Anti-cathepsin G antibodies were detected in 40.6% of 32 patients with active UC, and their prevalence was significantly higher in patients with severe colitis, as determined by endoscopy, than in those with mild or moderate colitis (P < 0.05). The prevalence and titers of anti-cathepsin G antibodies were significantly higher during the active than the inactive phase of the disease (P < 0.05). Measurement of titers of anti-cathepsin G antibodies by ELISA in the serum is useful for evaluating the activity of UC. Received: June 21, 1999 / Accepted: March 24, 2000     

Expression of human tumor necrosis factor-like weak inducer of apoptosis in patients with systemic lupus erythematosus

The aim of this study was to compare the mRNA and serum expression of tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) in patients with systemic lupus erythematosus (SLE) and healthy controls. Sixty-two SLE patients and 15 healthy controls were recruited in the study. TWEAK messenger RNA (mRNA) expression in peripheral blood mononuclear cells (PBMCs) from 33 of 62 patients was detected by relative quantification RT-PCR. TWEAK concentrations in the sera of all 62 patients were measured by ELISA. TWEAK mRNA expressions in PBMCs were decreased in SLE patients compared with healthy controls. Lower TWEAK mRNA expression was also found in the active SLE patients when compared to inactive ones. However, there was no significant difference between patients with lupus nephritis (LN) and those without. The level of serum TWEAK (sTWEAK) in SLE patients was increased when compared to healthy controls. In addition, the sTWEAK level was higher in SLE patients with vasculitis than those without vasculitis, and so was in comparison between patients with and without headache. Nevertheless, no significant differences were found between active SLE patients and inactive patients, or between LN patients and non-LN SLE patients. In this study, patients with SLE express low levels of TWEAK mRNA but high levels of sTWEAK. Additionally, sTWEAK level was associated with several clinical manifestations of SLE, indicating that TWEAK may play a complex role in SLE.     

Serum soluble interleukin 2 receptor in systemic lupus erythematosus: effects of disease activity and infection.

Serum soluble interleukin 2 receptor (sIL2R) was measured in patients with active and inactive systemic lupus erythematosus (SLE). The concentration of sIL2R was higher in inactive SLE than in normal controls and was significantly increased in active compared with inactive SLE. When patients with active SLE were followed up serially it was found that the sIL2R concentration fell when the disease became inactive. There was no statistically significant association between sIL2R and the grades of disease activity, however. In patients with either active or inactive SLE and infection the sIL2R concentration was much higher than in those without infection. Chronic infection (tuberculosis or candida) was associated with a much higher concentration of sIL2R than pyogenic or herpes zoster infection. The sIL2R concentration helps to distinguish infection in patients with SLE.     

系统性红斑狼疮患者外周血TB淋巴细胞Fas FasL表达及与凋亡的关系研究

目的探讨系统性红斑狼疮(SLE)患者外周血T、B淋巴细胞Fas、FasL表达及与凋亡的关系.方法采用流式细胞术(FCM)检测了30例SLE活动期患者、30例SLE非活动期患者和30名正常人外周血T、B淋巴细胞的凋亡率及Fas、FasL表达率.结果T、B淋巴细胞的Fas表达率依次为:活动期组＞非活动期组＞正常对照组(P＜0.01);FasL的表达率除B淋巴细胞在SLE活动期显著高于正常对照组外(P＜0.01),其余各组间差异无统计学意义;细胞的凋亡率在活动期显著高于非活动期(P＜0.01),而非活动期与正常对照组差异无统计学意义(P＞0.05):SLE的活动性与T或B细胞的Fas、FasL表达率间无相关关系,而与T或B细胞的凋亡率呈正相关(P＜0.01);无论是T或B细胞,Fas、FasL的表达率与凋亡率间无相关性.结论SLE患者体内外周血淋巴细胞的凋亡受到多种因素影响,但最终仍表现为凋亡率的异常增高,特别是活动期SLE,推测外周血淋巴细胞凋亡率的增高在SLE发病机制中起着重要作用.     

Enzyme-linked immunosorbent assays for antibodies to poly(A), poly dAT and histones: possibly useful tools for the evaluation of prognosis and disease activity in systemic lupus erythematosus

Summary In a prospective study 222 sera from 56 patients with systemic lupus erythematosus (SLE) were tested for antibodies to poly(A), poly dAT and histones using enzyme-linked immunosorbent assay (ELISA). Patients with active disease had significantly more often antibodies to poly(A), poly dAT and histones than patients with inactive disease. There was a positive correlation between the activity score of the disease and the levels of poly(A)-antibodies of IgG and IgM class, poly dAT-antibodies and antibodies to histones.Patients with SLE-nephritis had a higher level of poly dAT and IgG class poly(A) antibodies than patients without nephritis. Interestingly, patients with an SLE-nephritis had lower levels of IgM-poly(A)-antibodies than those without nephritis. Attempts to use the ELISAs in predicting the SLE exacerbations were unsuccessful. However, the assays can be used as parameters in the estimation of the disease activity.