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PubMed1991

[Serum concentration of hyaluronic acid in healthy populations and patients with rheumatoid arthritis--relationship to clinical disease activity of RA].

With the sandwich binding protein assay utilizing hyaluronic acid binding protein, we measured serum concentration of hyaluronic acid in 458 healthy persons, 71 patients with rheumatoid arthritis (RA) and 51 patients with various rheumatic diseases such as osteoarthritis (OA), progressive systemic sclerosis (PSS), systemic lupus erythematosus (SLE) and gout. The mean concentration +/- standard deviation (SD) of healthy persons whose age ranged 2 to 92 years old was 38.5 +/- 35.7ng/ml, and those with over 50 years old had apparently higher concentrations (51.9 +/- 40.5ng/ml) than those with below 50 of age (20.6 +/- 14.8ng/ml). When the upper limit of normal range was set up at 130 ng/ml, abnormal percentages were 62.0% (44/71) in RA, 0% (0/18) in OA, 6.3% (1/16) in PSS, 18.2% (2/11) in SLE and 0% (0/6) in gout. Patients who apparently had arthritis but not RA revealed normal or near to the upper limit in serum hyaluronic acid compared to RA patients having the mean +/- SD of 351.4 +/- 463.7ng/ml. When patients with RA were classified into stage I to IV with X ray of bone destruction, patients with more advanced X ray stage showed significantly higher serum concentrations of hyaluronic acid. Similarly, patients with lower activity of daily living revealed significantly higher serum concentrations of hyaluronic acid. In addition, serum hyaluronic acid level did correlate to concentration of serum CRP and sialic acid. Lansbury's index, strength of grip, joint score and erythrocyte sedimentation rate, but did not to duration of morning stiffness and titer of rheumatoid factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMed2004

Autoantibody against matrix metalloproteinase-3 in patients with systemic sclerosis.

Systemic sclerosis (SSc) is characterized by multi-organ fibrosis with an autoimmune background. Although autoantibodies are detected frequently in SSc patients, the role of autoantibody in the development of fibrosis remains unknown. Connective tissue homeostasis is a balance between the synthesis and degradation of the extracellular matrix (ECM); ECM degradation is regulated mainly by matrix metalloproteinases (MMPs). Anti-MMP-1 antibody is suggested to inhibit MMP-1 and be involved in the development of the fibrosis in SSc. However, the accumulation of various ECM components in the tissue of SSc cannot be explained by the anti-MMP-1 antibody alone. In this study, we examined the presence or levels of antibody to MMP-3, a protein which degrades various ECM components relevant to SSc fibrosis. Enzyme-linked immunosorbent assay (ELISA) using human recombinant MMP-3 revealed that IgG anti-MMP-3 autoantibody levels were elevated significantly in the sera from SSc patients, but not in patients with active systemic lupus erythematosus or dermatomyositis. IgG and IgM anti-MMP-3 antibody levels were significantly higher in diffuse cutaneous SSc, a severe form, than those in limited cutaneous SSc. Consistently, IgG anti-MMP-3 antibody levels correlated significantly with fibrosis of the skin, lung and renal blood vessels. The presence of IgG anti-MMP-3 autoantibody in sera from SSc patients was confirmed by immunoblotting analysis. Remarkably, MMP-3 activity was inhibited by IgG anti-MMP-3 antibody. These results suggest that anti-MMP-3 antibody is a serological marker that reflects the severity of SSc and also suggest that it may contribute to the development of fibrosis by inhibiting MMP-3 activity and reducing the ECM turnover.

Autoantibodies↗
PubMed1999

Association of human leukocyte antigen class II genes with autoantibody profiles, but not with disease susceptibility in Japanese patients with systemic sclerosis.

OBJECT: To examine the role of human leukocyte antigen (HLA) class II genes in the development of systemic sclerosis (SSc) as well as in the clinical and serologic expression of SSc in patients. METHODS: HLA-DRB1, DRB3, DRB4, DQB1, and DPB1 alleles were determined by genotyping; and serum antinuclear antibodies were identified using indirect immunofluorescence, double immunodiffusion and immunoprecipitation. PATIENTS: One hundred and five Japanese patients with SSc and 104 race-matched healthy controls. RESULTS: Frequencies of DRB1 and DQB1 alleles were not different between SSc patients and healthy controls, while DPB1*0901 was marginally increased in SSc patients. In contrast, SSc-related autoantibodies were closely associated with the clinical features. HLA class II genes were detected as follows: anti-DNA topoisomerase I antibody with diffuse cutaneous involvement, pulmonary fibrosis, and DRB1*1502-DQB1*0601-DPB1*0901; anti-U1RNP antibody with overlapping features of lupus and/or myositis and DRB1*0401/*0802-DQB1*0302; and anticentromere antibody with limited cutaneous involvement and DRB1*0101-DQB1*0501-DPB1*0402. In the analysis of the association of HLA class II and the clinical features in SSc patients significant differences were obtained only for the increased frequencies of arthritis and rheumatoid factor in patients with DRB1*0405 compared to those without. CONCLUSION: HLA class II genes strongly influence the production of SSc-related autoantibodies rather than the development of SSc. In addition, SSc is a composite disease of distinctive subsets defined by serum autoantibodies, which have specific clinical and HLA class II associations.

Adolescent↗
PubMed2003

Bactericidal/permeability-increasing protein and cathepsin G are the major antigenic targets of antineutrophil cytoplasmic autoantibodies in systemic sclerosis.

OBJECTIVE: To study the prevalence and antigenic specificity of antineutrophil cytoplasmic autoantibodies (ANCA) in patients with systemic sclerosis (SSc). METHODS: Sera from 68 patients with SSc were screened for ANCA by indirect immunofluorescence (IIF) assay and for antibodies to myeloperoxidase (MPO) by ELISA. All sera positive for ANCA on IIF were analyzed for reactivity against antigenic targets other than MPO [bactericidal/permeability-increasing protein (BPI), cathepsin G, lysozyme, elastase, PR3, and lactoferrin]. Twenty-three sera negative for ANCA were also tested for antibodies to BPI and cathepsin G using ELISA. RESULTS: The study included 33 patients with diffuse and 35 with limited SSc. ANCA was detected in 24 of the 68 sera (35.3%). In these 24 sera the antigenic targets were BPI in 14, cathepsin G in 13, and MPO in 8. Sera of 11 patients had reactivity against both BPI and cathepsin G. In sera, that were negative for ANCA, antibodies to BPI (4/23), cathepsin G (3/23), and MPO (1/44) were found in a small proportion of patients. Patients with antibodies to BPI had lower skin score, whereas no patient with antibodies to MPO had renal disease. CONCLUSION: BPI and cathepsin G are the major antigenic targets of ANCA seen in patients with SSc. Patients with antibodies to BPI had lower skin scores.

Adolescent↗
PubMed1998

Mortality and causes of death in a Swedish series of systemic sclerosis patients.

OBJECTIVES: To analyse survival rates and the causes of death in a systemic sclerosis (SSc) population, and to evaluate the occurrence of fatal malignant neoplasms and their possible association with oral cyclophosphamide (CYC) treatment. METHODS: Survival was calculated for 249 SSc patients followed up for up to 13 years. Mean (SD) follow up was 5.8 (4.2) years. The 49 decreased patients were subdivided according to causes of death and its relation to SSc. Fatal malignancies in CYC treated patients were compared with those occurring in non-CYC treated patients. RESULTS: The overall 5 and 10 year survival rates were 86% and 69% respectively. There was a 4.6-fold increased risk of death, as compared with the general population. Prognosis was worse in the diffuse cutaneous involvement (dSSc) and male subgroups than in the limited cutaneous involvement (1SSc) and female subgroups. Of the 49 deaths, 24 were attributable to pulmonary complications such as pulmonary fibrosis, pulmonary hypertension, pneumonia or pulmonary malignancy. Treatment with oral CYC did not increase the risk of dying of cancer. CONCLUSIONS: Mortality is increased both in the SSc population as a whole and in its different subsets (dSSc and 1SSc). Prognosis is worst among male patients with dSSc. However, the 5 year survival rate was better than those reported from earlier studies. Most patients die of cardiopulmonary disease. Five of seven fatal lung cancers were adenocarcinomas, possibly caused by chronic inflammatory disease of the lung. In this study, CYC treatment was not associated with an increased incidence of fatal malignant neoplasms.

Adenocarcinoma↗
PubMed2000

Serum levels of KL-6 as a useful marker for evaluating pulmonary fibrosis in patients with systemic sclerosis.

OBJECTIVE: KL-6 is a mucin-like glycoprotein that is strongly expressed on type II pneumocytes in the lung. Circulating KL-6 has been shown to be a sensitive marker of the disease activity of interstitial lung diseases. We determined the serum levels of KL-6 in patients with systemic sclerosis (SSc) and investigated whether these levels would serve as a useful marker of pulmonary fibrosis (PF) in patients with SSc. METHODS: The serum KL-6 levels were determined using a specific ELISA in 91 patients with SSc, and in 38 healthy controls. RESULTS: The serum levels of KL-6 were significantly higher in patients with SSc than in healthy controls (923+/-860 vs. 382+/-55 U/ml; p<0.0001). The serum KL-6 levels of the patients with diffuse cutaneous SSc (dSSc) tended to be higher than those with limited cutaneous SSc (ISSc) (1054+/-1000 vs. 800+/-694 U/ml), but there was no significant difference between these 2 groups. The serum KL-6 levels in the patients with PF were significantly elevated compared to those without PF (1283+/-1056 vs. 520+/-148 U/ml; p<0.0001). Moreover, DLCO and VC were also significantly decreased in the patients with elevated KL-6 levels compared to those with normal levels (62+/-22% vs. 72+/-17%, p<0.05; 87 +/-20% vs. 100+/-18%, p<0.01, respectively). CONCLUSION: Serum KL-6 level may be a useful serum marker for evaluating pulmonary fibrosis in patients with SSc.

Adult↗
PubMed1994

Circulating endothelin-1 levels in systemic sclerosis subsets--a marker of fibrosis or vascular dysfunction?

OBJECTIVE: To investigate the circulating levels of endothelin-1 (ET-1) in serum (sET-1) in patients with pulmonary disease [pulmonary fibrosis (PF) and pulmonary hypertension (PHT)], and renal involvement [hypertensive renal crisis (HRC)] in the 2 major subsets of systemic sclerosis (SSc) in order to determine the significance of sET-1 levels in relation to specific organ involvement or to the underlying pathogenic mechanisms of vascular damage and fibrosis. METHODS: In addition to the measurement of ET-1 in serum using a competitive radioimmunoassay, the circulating levels of angiotensin converting enzyme (ACE) and plasma von Willebrand factor (vWF) were measured as markers of endothelial damage in the various disease groups. RESULTS: Levels of sET-1 were significantly increased in 64 patients with diffuse systemic sclerosis (dSSc) and 17 patients with primary Raynaud's phenomenon (RP) compared with 22 healthy individuals. sET-1 levels were equally elevated in diffuse cutaneous disease (dcSSc) with only fibrotic dermal or lung pathology compared with patients with additional PHT or HRC crisis. These observations were in marked contrast to the sET-1 levels seen in patients with the limited cutaneous form of SSc (lcSSc) where only patients with lcSSc with hypertensive lung or renal disease had significantly higher levels of sET-1 than comparable lcSSc patients with only fibrotic dermal and lung disease. sET-1 levels were additionally found to correlate with plasma vWF, skin fibrosis (skin score) and duration of disease in patients with SSc. CONCLUSION: The presence of significantly raised sET-1 levels in patients with dcSSc with widespread fibrosis and patients with lcSSc with hypertensive disease and the relationship seen between sET-1 levels and markers of fibrosis and vascular damage suggest that ET-1 may be important in the pathogenesis of both the fibrotic and vascular manifestations in SSc.

Biomarkers↗
PubMed1995

Autoantibodies to pyruvate dehydrogenase complex in patients with systemic sclerosis. Possible role of anti-E1 alpha antibody as a serologic indicator for development of primary biliary cirrhosis.

OBJECTIVE: To determine the prevalence and clinical significance of anti-pyruvate dehydrogenase complex (anti-PDC) antibodies in systemic sclerosis (SSc). METHODS: Serum samples from patients with limited cutaneous SSc (n = 81) or diffuse cutaneous SSc (n = 63) were examined for anti-PDC antibodies by enzyme-linked immunosorbent assay (ELISA) and immunoblotting. RESULTS: IgG- and/or IgM-isotype anti-PDC antibodies were demonstrated by ELISA in 26 of 144 patients with SSc (18%). By immunoblotting, 19 patients had IgG anti-PDC antibodies. Among these patients with IgG anti-PDC antibodies, antibody to the E1 alpha subunit was significantly associated with the presence of laboratory abnormalities typical of primary biliary cirrhosis (PBC). CONCLUSION: Antibody to the E1 alpha subunit of PDC may be a serologic indicator for the development of PBC in patients with SSc.

Adult↗
PubMed2000

Elevated serum KL-6 levels in patients with systemic sclerosis: association with the severity of pulmonary fibrosis.

BACKGROUND: Serum KL-6 has been suggested to be a useful marker for the evaluation of interstitial lung disease activity. OBJECTIVE: To determine the correlation between serum KL-6 levels and pulmonary fibrosis in patients with systemic sclerosis (SSc). METHODS: Serum samples from patients with limited cutaneous SSc (lSSc; n = 19), diffuse cutaneous SSc (dSSc; n = 26) and normal individuals (n = 15) were examined by ELISA. RESULTS: Serum KL-6 levels in SSc patients were significantly higher than those in normal controls. KL-6 levels in dSSc patients were significantly elevated compared with those in lSSc patients. Elevated KL-6 levels were associated with the presence of pulmonary fibrosis in SSc patients or dSSc patients. Furthermore, KL-6 levels inversely correlated with percentages of diffusion capacity of carbon monoxide and vital capacity in SSc patients or dSSc patients. CONCLUSION: KL-6 may be a simple, serologic indicator for the severity of pulmonary fibrosis in SSc.

Adult↗
PubMed1995

Adenosine deaminase in progressive systemic sclerosis.

The aim of the present study was to confirm the increase of adenosine deaminase (ADA) activity in progressive systemic sclerosis (PSS), described by Sasaki & Nakajima, and to compare plasma ADA activity of patients in different stages of the disease. Enzyme activity was measured with a colorimetric assay. The 48 patients were subdivided into 3 groups: subgroup 1 (n = 10), disease still limited to the skin; subgroup 2 (n = 21), involvement of the skin and oesophagus; and subgroup 3 (n= 17), involvement of the skin and multiple internal organs. ADA levels were highest in subgroup 3. However, the difference with respect to subgroup 2 did not reach statistical significance. Subgroup 1 was different from controls and subgroups 2 and 3 (p<0.001). Our results confirm that ADA activity is increased in PSS, and that this finding is observed even in the early stages of the disease process. We speculate that the increase in ADA, a well-known marker of T-cell activation, might be an indicator of disease activity in PSS, in the beginning as well as during phases of exacerbation in later stages of the disease.

Adenosine Deaminase↗
PubMed1996

Digital calcification in systemic sclerosis: effective treatment with good tissue preservation using the carbon dioxide laser.

Tissue calcification of the fingers associated with limited systemic sclerosis is a common problem and is the source of considerable morbidity as it may be extremely tender and cause considerable functional disability. The current treatment of digital calcification is unsatisfactory. We evaluated the use of the carbon dioxide (CO2) laser in the management of this condition in six patients with the limited form of systemic sclerosis. A total of 21 areas of symptomatic digital calcification of the fingers were treated. Complete resolution of symptoms occurred in 12, moderate response with partial improvement was seen in five, little improvement was observed in two, and recurrence of calcinosis was found in two. The patient's average healing time was 6 weeks (range 4-10). The median duration of follow-up was 20 months (range 12-40). Postoperative infection was seen in two patients, and resolved completely in both with the use of topical and oral antibiotics. We found the CO2 laser a simple and effective treatment for most of the symptomatic lesions of digital calcification, and it may obviate the need for deforming surgery in many cases.

Adult↗
PubMed1999

Distribution and antigen specificity of anti-U1RNP antibodies in patients with systemic sclerosis.

Systemic sclerosis (SSc) is a generalized connective tissue disease which is characterized by the presence of several autoantibodies. To determine the prevalence and antigen specificity of anti-U1RNP antibodies (anti-U1RNP) in patients with SSc, serum samples from 223 patients with SSc, 117 patients with systemic lupus erythematosus (SLE), 18 patients with mixed connective tissue disease (MCTD) and 40 healthy control subjects were examined by indirect immunofluorescent analysis (IIF), double immunodiffusion, and immunoblotting using nuclear extract of HeLa cells. Eighteen of the 223 (8%) serum samples from patients with SSc were shown to be positive for anti-U1RNP. The frequency of anti-U1RNP positivity in limited cutaneous SSc (14%) was significantly higher than that in those with diffuse cutaneous SSc (3%). Anti-Sm antibodies were detected in patients with SLE positive for anti-U1RNP, but not in those with SSc positive for anti-U1RNP or those with MCTD. Immunoblotting demonstrated that anti-70-kD antibodies were detected more often in patients with SSc positive for anti-U1RNP and in those with MCTD than in those with SLE. Furthermore, anti-U1RNP was closely correlated with pulmonary fibrosis and joint involvement in patients with SSc. These results suggest that anti-70-kD antibodies are useful in the classification of patients with anti-U1RNP.

Antibodies, Antinuclear↗
PubMed2000

Association of markers for TGFbeta3, TGFbeta2 and TIMP1 with systemic sclerosis.

OBJECTIVES: To investigate whether six microsatellite markers known to map closely to genes involved in fibrosis are associated with systemic sclerosis (SSc). METHODS: Markers mapping to TGFbeta1, TGFbeta2, TGFbeta3, PDGFB, TIMP1 and COL5A2 were genotyped and allele frequency distributions compared in 191 patients and 196 controls. As TIMP1 maps to the X chromosome, male and females were analysed separately. Markers associated with SSc were further investigated according to whether patients had limited (lcSSc) or diffuse (dcSSc) cutaneous fibrosis. RESULTS: Associations were found between SSc and markers for TGFbeta3 (chi(2)=17.3, df=8, P=0.02), TGFbeta2 (chi(2)=25.2, df=13, P=0.02) and TIMP1 (with male SSc, chi(2)=11.9, df=5, P=0.03), between lcSSc and the TGFss2 marker (chi(2)=25.6, df=13, P=0.02), and between dcSSc and TGFbeta3 marker (chi(2)=27.1, df=8, P=0.001). Between lcSSc and dcSSc patients, the allele frequency distribution differed only for the TGFbeta3 marker (chi(2)=16.5, df=6, P=0.01). CONCLUSION: These associations indicate a possible role for TGFbeta3, TGFbeta2 and TIMP1 in genetic susceptibility to SSc and for TGFbeta3 in determining the degree of cutaneous fibrosis.

Adult↗
PubMed1995

The repertoire of T-cell receptors in systemic sclerosis.

Certain T cell subsets are increased in systemic sclerosis patients, particularly V delta 1+ gamma delta T cells in the blood and lungs and CD8+ alpha beta T cells in the lungs. The repertoires of T cell antigen receptor (TCR) V delta 1, V alpha, and V beta gene families were examined by two methods of analysis. First, the relative abundance of V alpha and V beta gene transcripts was determined in the blood and bronchoalveolar fluid of the patients. Second, the diversity of the junctional regions in TCR V delta 1 transcripts and in different V alpha and V beta gene families was analyzed. Limited V delta 1-C delta junctional region lengths were observed in the patients compared with controls. This was confirmed by sequence analysis of V delta 1-C delta junctional regions after subcloning amplified products in a bacterial vector. Evidence for selection of the V delta 1+ T cells in the tissues of patients came from the findings that the same V delta 1-C delta junctional sequences persisted in an individual patient over time and that identical junctional sequences were isolated from multiple sites. A restricted diversity of the junctional region lengths was also detected in a number of V alpha and V beta gene families, particularly within bronchoalveolar CD8+ T cell subset. These data suggest that the oligoclonal expansion of the corresponding alpha beta and gamma delta T cells is antigen-driven and may be important in the pathogenesis of systemic sclerosis.

Humans↗
PubMed2003

Function blocking autoantibodies against matrix metalloproteinase-1 in patients with systemic sclerosis.

Systemic sclerosis is characterized by fibrosis and systemic autoimmunity; however, roles of autoantibodies in the development of fibrosis remain unknown in systemic sclerosis. The net accumulation of extracellular matrix is dependent on the balance between the synthesis and degradation of extracellular matrix components, the latter process regulated by matrix metalloproteinases. Matrix metalloproteinase-1 (interstitial collagenase-1) can initiate degradation of collagen types I-III that are major extracellular matrix constituents in affected skin of systemic sclerosis. In this study, we tested the hypothesis that systemic autoimmunity in systemic sclerosis induced anti-matrix metalloproteinase-1 autoantibodies that inhibited matrix metallo-proteinase-1 activity, resulting in collagen accumulation. Enzyme-linked immunosorbent assay using human recombinant matrix metalloproteinase-1 revealed that IgG anti-matrix metalloproteinase-1 autoantibody levels were significantly elevated in sera from patients with systemic sclerosis, but not patients with active systemic lupus erythematosus or dermatomyositis, relative to normal controls. IgG anti-matrix metalloproteinase-1 autoantibody levels were significantly higher in patients with diffuse cutaneous systemic sclerosis than those found in patients with limited cutaneous systemic sclerosis. Furthermore, IgG anti-matrix metalloproteinase-1 antibody levels significantly correlated with the extent of fibrosis in the skin, lung, and renal blood vessels. The presence of IgG anti-matrix metalloproteinase-1 autoantibody in sera from systemic sclerosis patients was confirmed by immunoblotting analysis. Remarkably, IgG anti-matrix metalloproteinase-1 autoantibody in sera from systemic sclerosis patients inhibited matrix metalloproteinase-1 collagenase activity. Collectively, the results of this study suggest that anti-matrix metalloproteinase-1 autoantibody contributes to the development of fibrosis by inhibiting matrix metalloproteinase-1 collagenase activity and reducing the extracellular matrix turnover and suggest that the presence of anti-matrix metalloproteinase-1 autoantibody in systemic sclerosis is the link between systemic autoimmunity and fibrosis.

Adult↗
PubMed2000

Circulating collagen metabolites in systemic sclerosis. Differences between limited and diffuse form and relationship with pulmonary involvement.

OBJECTIVE: To study collagen metabolites in systemic sclerosis (SSc) and their relationship with clinical manifestations of the disease. METHODS: Forty-eight SSc patients, 13 with a diffuse form (dcSSc), 23 with a limited form (lcSSc) and 12 with suspected SSc not fulfilling the ACR criteria, and 31 healthy controls were examined. Serum concentrations of aminoterminal type III procollagen peptide (PIIINP), aminoterminal and carboxyterminal type I procollagen peptides (PINP and PICP) and cross-linked carboxyterminal telopeptide of collagen I (ICTP) were determined by radioimmunoassay. RESULTS: Increased serum concentrations of ICTP were found in SSc patients compared with controls. Distinctly higher levels of ICTP were observed in dcSSc than in lcSSc. High serum ICTP was correlated with skin score and acute phase reactants, and with reduced pulmonary function. Serum PIIINP concentration was elevated in both lcSSc and dcSSc. CONCLUSION: Augmented collagen catabolism accompanies the increased collagen synthesis in SSc. Serum ICTP concentration is a marker of this feature and also reflects clinical severity.

Adult↗
PubMed2003

Parallel detection of autoantibodies with microarrays in rheumatoid diseases.

BACKGROUND: Clinical needs often dictate testing for several autoantibodies in a single patient with evidence of autoimmune disease. We developed a microarray containing 15 autoantigens for the detection of autoantibodies in rheumatoid autoimmune diseases. METHODS: We synthesized recombinant centromere protein B, cytokeratin 19, SSA 52-kDa antigen, SSA 60-kDa antigen, SSB antigen, and Jo-1 antigen and prepared anti-nuclear antibody antigens. Cyclic citrullinated peptide, histone, goat IgG for detection of rheumatoid factor, double-stranded DNA, and single-stranded DNA were purchased, as were recombinant small nuclear ribonucleoprotein U1, topoisomerase I, and Smith antigen (Sm). All 15 antigens were of human origin except calf thymus Sm. Proteins were printed on polystyrene. The arrays were incubated with serum samples and then with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent substrates, and light signals were captured by a charge-coupled device camera-based chip reader. Antibodies were quantified by use of calibration curves. Positive samples were confirmed by commercially available methods. RESULTS: The detection limit of the microarray system was 20 pg of IgG printed on the polystyrene support. More than 85% of the confirmed positive sera were detected as positive with the microarray system based on cutoff values established with the microarray system. The imprecision (CV) of the microarrays was <15% for all 15 autoantibody assays, with the exception of single-stranded DNA (18% and 23%) within and between batches. Characteristic autoantibody patterns were seen in patients with clinical diagnoses of rheumatoid arthritis (n = 83), systemic lupus erythematosus (n = 71), systemic sclerosis (n = 36), polymyositis (n = 38), and Sjogren syndrome (n = 20). CONCLUSIONS: This microarray system provides results similar to those by conventional methods. Assessment of the diagnostic accuracy of the system remains to be done.

Adolescent↗
PubMed1997

Elevated serum levels of interleukin 4 (IL-4), IL-10, and IL-13 in patients with systemic sclerosis.

OBJECTIVE: To determine whether serum interleukin 4 (IL-4), IL-10, and IL-13 levels in patients with systemic sclerosis (SSc) are elevated and whether they correlate with the clinical or serologic features of this disease. METHODS: Serum samples from patients with limited cutaneous SSc (ISSc) (n = 45), diffuse cutaneous SSc (dSSc) (n = 28), and control subjects (n = 30) were examined by ELISA. RESULTS: Serum IL-4 and IL-13 levels were significantly higher in patients with ISSc and dSSc than in the controls. Serum IL-10 levels were significantly higher in the patients with dSSc compared with controls. Elevated IL-10 levels were detected frequently in patients with arthralgia. Serum IL-13 levels correlated with erythrocyte sedimentation rates and C-reactive protein levels in patients. CONCLUSION: We suggest that IL-4, IL-10, and IL-13 may be some of the cytokines that contribute to the disease process, and that IL-13 may be a serologic indicator of systemic inflammation in patients with SSc.

Adolescent↗