Autoantibodies against platelet-derived growth factor receptor alpha in patients with systemic lupus erythematosus

Abstract

Autoantibody against platelet-derived growth factor receptors (PDGFRs) has been reported in scleroderma (SSc). However, it remains unknown whether anti-PDGFRs antibody exists in collagen vascular diseases other than SSc. To answer the question, we developed an ELISA system and examined sera from patients with SLE (n = 75), SSc (n = 31), RA (n = 25) and control individuals. We also reviewed medical records to clarify clinical features of patients with anti-PDGFRα antibody. To examine the functions of anti-PDGFRα antibody in patients, fibroblasts were cultured and stimulated in the presence of purified IgG from patients, and their cell numbers were counted. Anti-PDGFRα antibody was detected in 29% of patients with SLE and in 21% of patients with SSc. Anti-PDGFRα antibody was found in 36% with active SLE, but in 10% in an inactive phase. Immunosuppressive therapy decreased the titer of the antibody. Patients with anti-PDGFRα antibody frequently developed a rash and hematological abnormalities, particular hemolytic anemia. Moreover, anti-PDGFRα antibody in SLE failed to demonstrate agonistic or antagonistic activities on PDGFR signaling. These findings indicate that nonfunctional anti-PDGFRα autoantibody exists in patients with SLE as well as those with scleroderma, and that the antibody could be a marker of disease activity and may be a marker of a subgroup of SLE.     

Altered adhesion molecules expression on peripheral blood mononuclear cells from patients with systemic sclerosis and clinical correlations

The aim of the study was to evaluate the expressions of adhesion molecules (AM) on peripheral blood mononuclear cells (PBMNC) from systemic sclerosis (SSc) patients. Thirty-one SSc patients (ACR) and 20 normal subjects were selected for the study. PBMNC were analyzed for LFA-1α, LFA-1β, ICAM-3, ICAM-1, and l-selectin expressions. ICAM-3 expression was decreased while ICAM-1 was increased on SSc PBMNC, compared to controls (p = 0.04 and 0.003, respectively). A positive association was found between LFA-1α (r = 0.37, p = 0.03), LFA-1β (r = 0.38, p = 0.002), ICAM-3 (r = 0.42, p = 0.01), and l-selectin (r = 0.38, p = 0.03) expressions and greater number of immunosuppressive drugs taken by SSc patients. Also, anti-centromeric positive SSc patients had lower expressions of LFA-1α, LFA-1β, ICAM-3, and l-selectin. Lower expression of ICAM-3 and higher expression of ICAM-1 suggest that AMs may be involved in the pathogenesis of scleroderma.     

Malignancy in scleroderma patients from south west England: a population-based cohort study

The pathophysiological relationship between scleroderma and malignancy remains poorly understood. Although some previous studies have demonstrated an increased malignancy risk in patients with scleroderma, others have been inconclusive. We aimed to determine if patients with scleroderma had an increased risk of malignancy compared to an age- and sex-matched local South West England population, and if there were any important differences between scleroderma patients with and without malignancy. Methods of this study are as follows. Notes were obtained on all local scleroderma patients (n = 68) locally, and those diagnosed with malignancy verified by contacting each patient’s general practitioner. Expected malignancy figures were obtained from age- and sex-stratified regional prevalence data provided by the South West Cancer Intelligence Service registry. Among the patients, 22.1% with scleroderma were identified with concurrent malignancy. Affected sites were of the breast (n = 5), haematological system (n = 5), skin (n = 4), and unknown primary (n = 1). Overall, malignancy risk was found to be increased in scleroderma (RR = 3.15, 95% CI 1.77–5.20, p = 0.01). In particular, this risk was the highest for haematological malignancies (RR = 18.5, 95% CI 6–43, p = 0.03), especially for non-Hodgkin’s lymphoma (RR = 25.8, 95% CI 5–75, p = 0.10). The majority of patients (86.7%) developed malignancy after the onset of scleroderma (mean = 6.9 years). Age of >70 and patients with limited scleroderma were significant risk factors for a patient with scleroderma to have a concurrent malignancy; however, no increased risk was found in patients with any particular pattern of organ involvement, cytotoxic usage or serology. To conclude, in this small patient cohort, we have found that scleroderma is associated with an increased risk of malignancy. This risk is statistically significant in patients with limited scleroderma. Patients who are elderly and those with limited disease should be closely scrutinized at follow-up appointments.     

Anti-cyclic citrullinated peptide antibodies in scleroderma patients

Anti-CCP (cyclic citrullinated peptide) is considered the most useful laboratory tool in the diagnosis of rheumatoid arthritis (RA). Some authors have also found this autoantibody in patients with scleroderma (SSc). The study aimed to investigate the prevalence of anti-CCP antibodies in SSc patients from Southern Brazil and their association with clinical and serological profile of the disease. We studied 76 patients with SSc and 100 healthy volunteers for presence of anti-CCP. SSc patients charts were reviewed for clinical and laboratory data. In the SSc group, the diffuse form was present in 20.5%; 62.8% had the limited form; 14.1% had overlap with systemic lupus or polymyositis and 2.5% had SSc sine scleroderma. Anti-CCP was found in nine of 78 (11.5%) SSc patients and in one of 100 healthy volunteers (p = 0.0054). No relationship was found with arthritis, skin Rodnan m score, esophageal dysmotility, myocarditis, pulmonary hypertension and lung fibrosis. Positive association was observed with arthralgias (p = 0.02). Also, no relationship was noted with the presence of anti-centromere antibodies, anti-Scl-70, anti-RNP or rheumatoid factor. Anti-CCP are more common in SSc patients than in controls. Arthralgias but not arthritis or rheumatoid factor are more frequent in anti-CCP positive patients.     

Anti-agalactosyl IgG antibodies in Thai patients with rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis

This study was performed to determine the prevalence of anti-agalactosyl IgG antibodies in Thai patients with RA, systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), and determine the sensitivity and specificity of anti-agalactosyl IgG antibodies in the diagnosis of RA in comparison with IgM-rheumatoid factor (IgM-RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies. Serum samples were obtained from 100 patients with RA, 50 cases of SLE, 50 cases of SSc, and 100 healthy controls and analyzed for the presence of anti-agalactosyl IgG antibodies, IgM-RF and anti-CCP antibodies. A serum value greater than mean + 2 standard deviation of normal value of anti-agalactosyl IgG antibodies and anti-CCP antibodies was considered positive. The prevalence of anti-agalactosyl IgG antibodies in RA, SLE, and SSc patients was 88.0%, 14.0%, and 12.0%, respectively. The serum level of anti-agalactosyl IgG antibodies in patients with RA (227.10 ± 353.64 AU/mL) was significantly higher than those in SLE (11.84 ± 52.04 AU/mL), SSc (18.85 ± 99.60 AU/mL), and healthy controls (2.14 ± 1.97 AU/mL), (p < 0.001). There was a good correlation between the log serum level of anti-agalactosyl IgG antibodies and IgM-RF (r = 0.92, p < 0.001), anti-CCP antibodies and IgM-RF (r = 0.49, p < 0.001), and anti-agalactosyl IgG antibodies and anti-CCP antibodies (r = 0.55, p < 0.001). The sensitivity and specificity in the diagnosis of RA was 88.00% and 96.00% for anti-agalactosyl IgG antibodies, 90.00% and 99.00% for anti-CCP antibodies, and 91.00% and 95.00% for IgM-RF, respectively. The serum level of anti-agalactosyl IgG antibodies was significantly higher in RA than in SLE, SSc, and healthy controls. There was a good correlation between serum levels of anti-agalactosyl IgG antibodies, anti-CCP antibodies, and IgM-RF. These three tests had comparable sensitivity and specificity.     

Vitamin D may not be a good marker of disease activity in Korean patients with systemic lupus erythematosus

Vitamin D is a pleiotrophic hormone with immunoregulatory properties. Low levels of vitamin D have been discovered in various autoimmune diseases. Here, we investigated serum vitamin D levels in Koreans with systemic lupus erythematosus (SLE) and examined whether levels correlate with disease activity of SLE. Blood samples were prospectively collected from patients with SLE (n = 104) and normal controls (NC, n = 49) during the spring from March to May 2008. The level of serum 25-hydroxyvitamin D (25(OH)D3) was measured by radioimmunoassay. The serum 25(OH)D3 levels of patients with SLE (42.49 ± 15.08 ng/ml) were significantly lower than NC (52.72 ± 15.19 ng/ml, P < 0.001). Additionally, 17 patients with SLE (16.3%) had vitamin D insufficiency, while two NC had vitamin D insufficiency (4.1%). The risk of vitamin D insufficiency was 4.6-fold increased in SLE (P = 0.032). The serum 25(OH)D3 levels, adjusted with BMI, were positively correlated only with hemoglobin (β = 0.256, P = 0.018) and serum complement 3 (β = 0.365, P = 0.002). Serum vitamin D levels were lower, and vitamin D insufficiency was more common in Korean patients with SLE, however, our study demonstrated that vitamin D levels might not be a good marker of disease activity.     

Significance of serum uric acid in pulmonary hypertension due to systemic sclerosis: a pilot study

Systemic sclerosis is a connective tissue disease, which may lead to elevated pulmonary arterial pressure due to pulmonary arterial hypertension and/or left ventricular diastolic dysfunction. Uric acid (UA) has been shown to be elevated in patients with pulmonary hypertension (PH) and heart failure. We aimed to investigate the potent relationship between serum UA and pulmonary pressure as well as functional capacity in patients with SSc. We studied 66 patients (mean age 57.7 ± 12.1 years, 63 women), presenting with SSc. Systolic pulmonary artery pressure assessed by echocardiography, lung function tests, six-minute walk test (6MWT) and serum UA levels were recorded in all patients. In 24 (36%) patients, the diagnosis of PH was established by echocardiography (systolic pulmonary artery pressure ≥40 mmHg). Patients with PH had higher UA serum levels compared to patients without PH (5.1 ± 2.1 mg/dl vs. 4.2 ± 0.9 mg/dl, p = 0.04). Among patients with PH, UA values were inversely correlated with the SMWT distance (r = −0.51, p = 0.01). Serum UA values increased in proportion to the functional capacity in PH patients with scleroderma. Further investigations in prospective studies will unfold in detail the pathophysiological significance of UA in SSc patients with PH and determine its role as a prognostic marker in the assessment and monitoring of the disease.     

Foot health needs in people with systemic sclerosis: an audit of foot health care provision

The vascular and cutaneous alterations evident in systemic sclerosis/scleroderma (SSc) place the foot at risk of ulceration. The UK Podiatry Rheumatic Care Association (PRCA)/Arthritis and Musculoskeletal Alliance standards of care recommend that all people with SSc should receive at least basic information about their foot health, and that those with foot problems should have access to self-management advice and care where needed. The aim of this study was to evaluate foot health services offered in Leeds (UK) for people with SSc, against nationally agreed standards of care. Ninety-one consecutive patients with SSc were selected from either the connective tissue disease outpatient clinic (n = 70) or the specialist rheumatology foot health clinic (n = 21) at Chapel Allerton Hospital, Leeds Teaching Hospitals NHS Trust. All the patients completed a disease-specific audit tool developed by the UK PRCA that evaluates provision of foot health care for patients with SSc. Sixty-one patients (67%) reported having had foot problems at some point in time and 54 (59%) had current foot problems. Of these 54 patients, 17 (32%) had not received any foot care. Only 36 (39%) of the 91 patients had received any foot health information. This audit demonstrates that patients with SSc have a relatively high prevalence of self-reported foot problems. Foot health care and information are inadequate for people with SSc and foot problems, and preventative information is almost non-existent. Improved foot health information will better empower patients to self-manage low risk problems, and help identify high risk problems which require specialist care.     

Third generation anti-cyclic citrullinated peptide antibodies do not predict anti-TNF-α treatment response in rheumatoid arthritis

Objective of this study is to retrospectively compare the third generation anti-cyclic citrullinated peptide (anti-CCP3) test with the second generation (anti-CCP2) assay as markers of disease activity and predictors of clinical response in rheumatoid arthritis (RA) patients treated with TNF-α blocking agents. This study was performed in 42 RA patients treated either with infliximab (n = 11), etanercept (n = 7) or adalimumab (n = 24). Serum anti-CCP3 and anti-CCP2 levels were tested before and 6 months after starting a TNF-α blocking treatment using commercially available ELISA kits. Anti-CCP3 and anti-CCP2 antibody levels did not significantly change after 6 months of TNF-α blocking treatment. Furthermore, neither anti-CCP3 nor anti-CCP2 was useful to predict anti-TNF-α treatment response using receiving operating characteristic curve and logistic regression analyses. Both anti-CCP3 and anti-CCP2 are not differentially influenced by TNF-α blocking agents in RA patients and failed to predict anti-TNF-α treatment response.     

Systemic sclerosis overlap and non-overlap syndromes share clinical characteristics but differ in prognosis and treatments

ObjectivesTo screen for concomitant autoimmune disease in patients with systemic sclerosis (overlap SSc) and to describe their clinical characteristics and prognosis.MethodsThis was a two-center retrospective observational study. Patients diagnosed with SSc according to the 2013 ACR-EULAR scleroderma classification criteria were screened for concomitant rheumatoid arthritis (RA), Sjögren syndrome (SgS) and systemic lupus erythematosus (SLE). Patient characteristics were retrieved from the medical records and were compared to those of a non-overlap SSc cohort.ResultsAmong the 534 SSc patients studied, thirty-four (6.4%) were identified as having overlap SSc. There were 21 (3.9%) patients with RA, 14 (2.6%) with SgS and 4 (0.7%) with SLE (5 patients had 2 AISD) . The disease phenotype of overlap SSc was similar to that of non-overlap SSc in terms of cutaneous phenotype, prevalence of pulmonary arterial hypertension, interstitial lung disease, digital ulcers and mortality. Using a multivariate Cox model, age (HR = 1.04, 95% CI [1.02–1.07]), the modified Rodnan skin score (HR = 1.08 per point, 95% CI [1.05–1.11]), and the presence of concomitant SgS (HR = 3.79, 95% CI [1.38–10.40]) were significantly associated with mortality. Overlap SSc were more likely to receive corticosteroids (85.3% vs. 45%, p < 0.001), immunosuppressive drugs (82.4% vs. 49.2%, p < 0.001) and biologics (52.9% vs. 3.8%, p < ZZ0.001).ConclusionsWhile overlap and non-overlap SSc shared common characteristics, patients with SgS/SSc had a higher risk of mortality, and those with RA/SSc received more corticosteroids, methotrexate and biologics. Screening for an associated AISD should be promoted since their co-occurrence with SSc may affect prognosis and treatments.     

What is the relationship between disease activity, severity and damage in a large Canadian systemic sclerosis cohort? Results from the Canadian Scleroderma Research Group (CSRG)

We studied the relationships between physician-assessed damage, severity and activity in a large, multicentre systemic sclerosis (SSc, scleroderma) cohort. We hypothesized that there is a relationship between disease activity and severity and damage, but that severity would be more strongly related to damage. A total of 520 SSc patients (87% women, mean age 56 years, mean 8.6 years disease duration, 39% diffuse SSc) were studied. The correlations between physician's global assessments of damage, activity and severity were determined overall and in a subset of early, diffuse SSc (n = 74). The mean (SD) patient global health score was 3.6 (2.4) on a 0–10 scale. Physician-rated severity, activity and damage were 2.8 (2.2), 2.3 (2.0), and 3.4 (2.4) respectively. Damage was more strongly related to severity (r = 0.744, P < 0.001) than activity (r = 0.596, P < 0.001). Damage was not related to disease duration (r = 0.046, P = 0.3). In early diffuse SSc, the correlations were: damage and severity 0.771 (P < 0.001), damage and activity 0.596 (P < 0.001), severity and activity 0.809 (P < 0.001). The relationships vary in the overall cohort versus the early diffuse SSc subset where activity, severity and damage appear more strongly related. Thus, the exact nature of the relationship between damage, activity and severity will depend upon the characteristics of the population studied.     

Genetic variation in the interleukin-10 gene promoter in Polish patients with systemic lupus erythematosus

Identification of susceptibility genes in systemic lupus erythematosus (SLE) has recently become a topic of interest. The IL-10 promoter contains three single base-pair substitutions at −627C > A, −854C > T and −1117G > A. These single base-pair substitutions produce three different haplotypes, GCC, ACC and ATA, which affect IL-10 expression. We examined the distribution of −627C > A, −854C > T and −1117G > A IL-10 promoter polymorphisms in patients with SLE (n = 103, women only) and matched controls (n = 300). Despite the higher prevalence of the GCC/GCC, GCC/ATA and ATA/ATA genotypes in SLE patients than in controls, we observed that only GCC/GCC genotype frequency distribution was significant between these groups. We observed that women with the GCC/GCC genotype displayed an approximately twofold increased risk of SLE OR = 2.245 (95% CI = 1.354–3.721, P = 0.0022). We did not find any associations between various genotypes of IL-10 promoter haplotypes and clinical manifestations or autoantibody production in patients with SLE. Our observations indicate that the GCC/GCC promoter genotype may contribute to SLE incidence in Polish patients.     

Abnormal surface markers expression on bone marrow CD34<Superscript>+</Superscript> cells and correlation with disease activity in patients with systemic lupus erythematosus

Defects of hematopoietic stem cells (HSCs) have been suggested to contribute to the development of systemic lupus erythematosus (SLE). The aim of this study was to investigate the phenotypic characteristics of bone marrow (BM) CD34⁺ cells in patients with SLE and its relationship with SLE disease activity. Ten SLE patients and 10 healthy subjects were recruited and their BM CD34⁺ cells were analyzed by flow cytometric analysis with CD45/SSC gating for the expression of CD90, CD95, CD117, CD123, CD164, CD166, FAS-L, and HLA-DR. The percentage of BM CD34⁺ cells was significantly decreased in active SLE patients (1.48 ± 0.41%, n = 7) compared to the healthy controls (2.31 ± 0.75%, n = 10, p < 0.01), but no significant difference was found between the inactive patients (2.04 ± 0.44%, n = 3) and the controls. The expression of CD95, CD123, and CD166 on BM CD34⁺ cells were significantly increased in SLE patients (48.31 ± 10.59%, 44.9 ± 21.5%, 30.9 ± 19.54%, respectively, n = 10) when compared with the control subjects (24.33 ± 11.1%, 19.5 ± 4.4%, 10.7 ± 5.5%, respectively, n = 10, p < 0.05). The increased CD123 expression was negatively correlated with the number of peripheral white blood cells (r = −0.700, p < 0.05, n = 10). The percentage of CD166 expression was found significantly correlated with the index of SLE disease activity (r = 0.472, p < 0.05, n = 10) and 24 h proteinuria (r = 0.558, p < 0.05, n = 10), but negatively correlated with serum C3 level (r = −0.712, p < 0.01, n = 10). Our study found that the surface marker expression of CD95, CD123, and CD166 on BM CD34⁺ cells were significantly increased in patients. This supports the hypothesis that there are abnormalities of the HSC in SLE. Since CD166 and CD123 correlated with the overall lupus activity, their role as a biomarker of inflammatory disease activity also requires further study.     

The diagnostic utility of the anti-CCP antibody test is no better than rheumatoid factor in South Africans with early rheumatoid arthritis

To establish the diagnostic utility of the anti-cyclic-citrullinated peptide antibody (aCCP) test in Black South Africans with early rheumatoid arthritis (RA). A cross-sectional study comparing the rheumatoid factor (RF) and aCCP status in RA patients and a control group consisting of healthy subjects, and patients with systemic lupus erythematosus (SLE) and scleroderma. The sensitivity, specificity, positive (PPV) and negative predictive values of the aCCP test alone were 82.5%, 84.9%, 87.6% and 79% versus 81.7%, 90.7%, 92.5% and 78% for RF alone. The best specificity (95.3) and PPV (95.8%) was observed when both aCCP and RF tests were positive. Patients with erosive disease had a significantly higher mean RF titre compared with those with non-erosive disease (p = 0.007). There was a trend towards an association of smoking (OR = 4.1, 95% CI = 0.9–18.6) and functional disability (p = 0.07) with RF-positive status. No similar clinical associations were observed with aCCP. Almost a third of SLE patients were aCCP positive. Despite the best specificity and PPV observed when both the aCCP and RF tests were positive, our findings suggest that testing for aCCP is only cost-effective in the RF-negative patient in whom there is a strong clinical suspicion of RA.     

IL-18 105 A>C polymorphism contributes to renal manifestations in patients with SLE

Systemic lupus erythematosus (SLE) is a multisystem autoimmune connective tissue disorder characterized by various aberrations including increased production of IL-18. As IL-18 105 A>C polymorphic variants have been linked to increased production of this cytokine, we investigated the prevalence of IL-18 105 A>C (rs549908) polymorphic variants in SLE patients (n = 111) and controls (n = 152). There were no significant differences in the distribution of IL-18 105 A>C polymorphic variants in SLE patients and controls. However, there was a significant association between the IL-18 105 AA genotype (recessive model) and renal manifestations OR = 3.360 (1.523–7.415, P = 0.0039) and the P value remained statistically significant after Bonferroni correction (P _corr = 0.0351).Our findings indicate that the IL-18 105 AA genotype variant can contribute to renal manifestations in patients with SLE.     

Antitopoisomerase I antibody in patients with systemic lupus erythematosus/sicca syndrome without a concomitant scleroderma: two case reports

 We describe two female patients with classic systemic lupus erythematosus (SLE) and secondary sicca syndrome associated with topoisomerase I (topo-I, Scl-70) antibody, a specific marker for scleroderma (SSc), which is rarely found in other collagen diseases. During the course of the disease, the sera of these two patients were repeatedly found to be positive for topo-I antibody following a positive screening by ANA-EIA. Neither patient had clinical evidence of scleroderma. One patient remains well nearly 4 years from the first positive serological test. The progression to sicca syndrome in that patient occurred 2 years after having tested positive for antitopo-I antibody. Her frozen serum also tested positive for anti-Scl-70 by the Western blot technique. The other patient, however, died after developing renal and cardiopulmonary complications of lupus, including Libman Sachs endocarditis and pulmonary hypertension. Contrary to the previous patient, the onset of sicca syndrome in this case had preceded the expression of positive antitopo-I antibody. The present cases and other similar previously reported ones are therefore unique in the sense of being a serological challenge to the high specificity of antitopo-I to scleroderma. In addition, they may also represent a new subset of SLE with or without sicca syndrome, which is characterised by the absence of features of scleroderma despite the presence of antitopo-I antibody. Received: 27 May 2002 / Accepted: 12 August 2002     

Serum nitric oxide metabolites and disease activity in patients with systemic sclerosis

There is no surrogate marker in serum for defining disease activity in scleroderma (SSc). Nitric oxide (NO), which regulates vasodilation and possesses pro-inflammatory actions, has been implicated in the pathogenesis of SSc. We compared serum NO _x (total nitrate and nitrite) level in SSc patients to healthy controls and evaluated its correlation with detailed symptomatology and scoring systems for various organ involvement. Symptoms and physical findings that suggested disease activity in regard to various organs were documented. Lung function test, high-resolution computed tomographic (HRCT) scan of thorax and echocardiography were performed. Serum NO _x was measured by chemiluminescence. Serum NO _x levels in SSc (n = 43) were significantly higher (72.4 ± 47.8 μM) than age- and sex-matched controls (n = 41; 37.1 ± 13.5 μM; p < 0.001). Serum NO _x were not found to be associated with lung fibrosis defined by lung function parameters or inflammation and fibrosis scores on HRCT. Twenty-two patients were found to have elevated serum NO _x level defined as mean ± 2 SD of normal controls. Logistic regression analysis revealed that age (OR 1.12, p = 0.02) and elevated pulmonary arterial pressure (PAP) (n = 9; OR 145.3, p = 0.01) were predictive factors for elevated serum NO _x . Prednisolone use was associated with lower serum NO _x level (OR 0.06, p = 0.04). Elevated PAP of increasing severity was found to be associated with higher level of serum NO _x (p = 0.004 by trend). Serum NO _x in SSc patients were elevated compared to healthy controls. Serum NO _x level was determined by multiple factors including age, prednisolone use, and elevated PAP.     

A positive correlation between homocysteine and brachial–ankle pulse wave velocity in patients with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is associated with premature atherothrombotic complications. Hyperhomocysteinemia is considered a cardiovascular risk factor. Increased vascular stiffness may increase cardiovascular mortality. Pulse wave velocity (PWV) is a noninvasive method of analyzing vascular stiffness in the assessment of atherosclerosis. The objective of this study was to identify the relationship between plasma homocysteine levels and brachial–ankle pulse wave velocity (baPWV) measurement in SLE. Plasma homocysteine, baPWV, ankle–brachial index, blood pressure, C3, C4, anticardiolipin antibody (aCL), and anti-double-stranded DNA antibodies were determined in a total of 58 female patients with SLE. The control group comprised 32 age-matched healthy females. In addition, all patients were further classified into subgroups according to the presence of aCL (SLE/aCL+, n=27 vs SLE/aCL−, n=31) to determine the effect of aCL on the tested variables. The mean values for plasma homocysteine and baPWV were 13.19 μmol/l and 1,482 cm/s, respectively. Plasma homocysteine levels were significantly elevated in SLE patients when compared with the healthy controls. SLE patients with aCL had a significantly higher plasma homocysteine level than those without aCL. A significant positive correlation between plasma homocysteine and baPWV was found in patients with SLE (r=0.335, P=0.028, n=58). Plasma homocysteine also significantly correlated with right baPWV in all SLE patients (r=0.371, P=0.014, n=58) and in the SLE/aCL+ group (r=0.523, P=0.031, n=27). These findings indicate a possible link between plasma homocysteine and baPWV in SLE. In conclusion, SLE patients had an increased level of plasma homocysteine, and this phenomenon appeared to be related to vascular stiffness.     

Low prevalence of hepatitis B virus infection in patients with systemic lupus erythematosus in southern China

To investigate the prevalence of hepatitis B virus (HBV) infection in systemic lupus erythematosus (SLE) patients in southern China, SLE inpatients were retrospectively investigated for their HBV infection rate. Fifteen SLE patients positive for hepatitis B surface antigen (HBsAg) were followed up. Furthermore, serum interferon (IFN)-α levels among SLE patients were detected by ELISA. Results showed estimated HBsAg-positive rate was 10.74% in general population. The HBsAg-positive rate was lower in SLE patients compared with controls (2.33 vs. 9.57%, P < 0.01). Interestingly, 13 out of 15 SLE patients converted from HBsAg positive to HBV surface antibody (HBsAb) positive even under glucocorticoid therapy. In addition, we found significantly increased IFN-α levels in SLE patients.The prevalence of HBV infection in SLE patients was lower than that in sex- and age-matched non-SLE controls in southern China. The characteristic IFN signatures in SLE may favor the subsequent clearance of HBV.     

Increased serum soluble CD147 levels in patients with systemic sclerosis: association with scleroderma renal crisis

CD147 is a glycosylated membrane protein that belongs to the immunoglobulin superfamily. This study aimed to determine serum soluble CD147 (sCD147) levels and their clinical associations in patients with systemic sclerosis (SSc). Serum sCD147 levels were examined by enzyme-linked immunosorbent assay in 61 SSc patients and 24 healthy individuals. Serum sCD147 levels were significantly elevated in SSc patients compared with healthy individuals (P < 0.001). Among patients with SSc, there were no differences in serum sCD147 levels between limited cutaneous (n = 30) and diffuse cutaneous SSc (n = 31). Patients with SSc who had elevated sCD147 levels had renal crisis more often than those with normal sCD147 levels (13% vs 0%; P < 0.05). Serum sCD147 levels were increased in patients with SSc and associated with the presence of renal crisis. These results suggest that sCD147 may have a role in the development of renal crisis in SSc. Measurement of serum sCD147 may be useful for risk stratification for renal crisis in SSc.