Identification of a clinical subset of systemic lupus erythematosus by antibodies to the sm antigen

The clinical and renal histologic attributes of 135 systemic lupus erythematosus (SLE) patients with DNA and/or Sm antibodies were compared to determine if the presence of the Sm antibodies served as a marker for a specific subset of SLE. Although Raynaud's phenomenon was more frequent in patients with Sm antibodies (P < 0.005), serious central nervous system disease was over three times as common in patients with DNA antibodies (P < 0.005). Only one of 23 patients with Sm antibodies had diffuse proliferative glomerulonephritis on renal biopsy, whereas 6 of 14 patients with only DNA antibodies had this histologic finding (P = 0.01). The Sm antibody system may therefore identify a subset of SLE patients with milder central nervous system and renal disease.     

The clinical significance of Raynaud's phenomenon in systemic lupus erythematosus.

In a prospective study of 226 patients with systemic lupus erythematosus (SLE), 91 patients (40%) had Raynaud's phenomenon. These patients were compared to 135 patients without Raynaud's phenomenon. Patients with Raynaud's phenomenon had a greater incidence of arthritis (P less than 0.02), malar rash (P less than 0.003), and photosensitivity (P less than 0.03), and a lesser incidence of severe renal disease as manifested by serum creatinine over 3.0 mg/dl (P less than 0.007) or creatinine clearance below 60 ml/minute. Patients with Raynaud's phenomenon were less likely to have severe, life threatening disease and received a lower average monthly (P less than 0.01) and a lower peak daily corticosteroid dose (P less than 0.01). Fourteen patients (16%) with Raynaud's phenomenon died, compared to 41 without (30%) (P less than 0.03). Raynaud's phenomenon in patients with SLE is associated with milder disease and may be regarded as a favorable prognostic sign.     

Hla type as a predictor of mixed connective tissue disease differentiation ten-year clinical and immunogenetic followup of 46 patients

Objective. To determine any clinical or genetic markers of differentiation and outcome in a previously described cohort of 46 patients with mixed connective tissue disease (MCTD). Methods. Patients were clinically evaluated, chart notes reviewed, and HLA subtyping and immunology profiles performed where possible. Eleven had died and 7 were lost to followup. Results. MCTD had differentiated into systemic lupus erythematosus in 12 patients and into systemic sclerosis in 13. The latter was associated with HLA-DR5 (P = 0.038), and nondifferentiation was associated with HLA-DR2 or DR4 (P = 0.007). Three HLA-DR4 positive patients had MCTD that evolved into rheumatoid arthritis. Erosive and/or deforming arthritis was associated with HLA-DR1 or DR4 (P = 0.015). HLA-DR3 was associated with interstitial lung fibrosis (P = 0.044) and keratoconjunctivitis sicca (0.001 < P < 0.01). Severe Raynaud's phenomenon predicted higher mortality (0.01 < P < 0.05). Conclusion. We suggest that MCTD is, for most patients, an intermediate stage in a genetically determined progression to a recognized connective tissue disease. Those whose disease remains undifferentiated might be considered a distinct subset.     

Rheumatoid arthritis in greek and british patients. a comparative clinical,radiologic, and serologic study

Objective. To compare the clinical, radiologic, and serologic expression of rheumatoid arthritis (RA) in 2 different populations. Methods. Standard protocols and assessment criteria were used in this study of 108 Greek and 107 British patients with RA. Results. British patients had more severe articular involvement than did Greeks, as judged by the duration of morning stiffness (P < 0.005), grip strength (P < 0.0001), and the numbers of swollen (P < 0.001) and tender (P < 0.0001) joints. The British RA patients also had more severe joint damage on radiologic examination, as evidenced by Steinbrocker stage III (P < 0.005) and IV (P < 0.025) disease and had more extraarticular manifestations (P < 0.0001), including rheumatoid nodules (P < 0.0001) and Raynaud's phenomenon (P < 0.05). Greek RA patients, however, more frequently presented with sicca manifestations (P < 0.001) and serum antibodies to Ro/SS-A (P < 0.025). Furthermore, Ro/SS-A antibodies were associated with a high incidence of side effects to D-penicillamine only in the Greeks. Conclusion. Genetic and environmental factors may be responsible for these striking differences in disease expression between these 2 European populations with RA.     

Autoantibodies against C-reactive protein (CRP) in sera of patients with systemic rheumatic diseases

Abstract

An assessment of the frequency of serum autoantibodies against modified C-reactive protein (mCRP) in systemic rheumatic diseases and the association of these autoantibodies with clinical and laboratory findings in patients with systemic lupus erythematosus (SLE). Serum levels of autoantibodies against mCRP were measured by an enzyme-linked immunosorbent assay in 125 patients with SLE and in 213 patients with other systemic rheumatic diseases. The frequency of patients with high antimodified CRP antibody levels was 32% in SLE, 22% in systemic sclerosis (SSc), 19% in polymyositis/dermatomyositis (PM/DM), 43% in primary Sjögren's syndrome (pSS), 29% in rheumatoid arthritis (RA), 33% in mixed connective tissue disease (MCTD), and 43% in overlap syndrome. Serum levels of anti-mCRP antibody were significantly lower in SLE patients with persistent proteinuria (P < 0.001), cellular casts (P < 0.01), and hypoalbuminemia (P < 0.05). Serum anti-mCRP antibody levels in SLE showed a direct correlation with serum IgG levels (P < 0.001), serum anti-SS-A antibody levels (P < 0.01), serum anti-SS-B antibody levels (P < 0.01), and serum anti-U1-RNP antibody levels (P < 0.05). Inhibition experiments revealed that nonnative epitopes on the CRP molecule, termed mCRP, were the main target of the anti-mCRP antibodies detected. Autoantibodies against mCRP were frequently found in sera from patients with systemic rheumatic diseases, and may have a role in the immunopathogenesis of systemic rheumatic diseases, which are characterized by persistent inflammation.     

Familial aggregation of primary Raynaud's disease

Objective. To determine the occurrence of familial aggregation of primary Raynaud's disease. Methods. Twenty-three patients with primary Raynaud's disease and their first-degree relatives were assessed by questionnaire and, when possible, by physical examination. The same procedures were performed on the patients' spouses and the spouses' first-degree relatives, who served as the control group. Results. The prevalence of Raynaud's disease was significantly higher in the families of the probands than in the control families when assessed by questionnaire (26.1% versus 5.5%; P < 10₋₅), and by physical examination (11.2% versus 2.8%; P = 0.015). Conclusion. These findings demonstrate that there is significant familial aggregation of primary Raynaud's disease.     

Course of the modified Rodnan skin thickness score in systemic sclerosis clinical trials: Analysis of three large multicenter,double‐blind,randomized controlled trials

Objective

To assess the course of the modified Rodnan skin thickness score (MRSS) in 3 large, multicenter, double‐blind, randomized controlled trials (RCTs) of patients with diffuse cutaneous systemic sclerosis (dcSSc) with different baseline disease durations, as defined from the date of onset of the first dcSSc symptom (excluding Raynaud's phenomenon) or from the date of onset of the first dcSSc‐related symptom (including Raynaud's phenomenon).

Methods

Data from 3 RCTs examining high‐dose versus low‐dose D‐penicillamine (D‐Pen Trial), recombinant human relaxin versus placebo (Relaxin Trial), and oral bovine type I collagen versus placebo (Collagen Trial) treatment in patients with dcSSc were pooled and analyzed. Patients were divided into 5 groups according to their disease duration at baseline. The linear mixed model for correlated data was used to model the 2 predictors of MRSS: time in study (expressed in months after baseline) and baseline disease duration (expressed in months, calculated from the date of onset of the first symptom characteristic of dcSSc with and without Raynaud's phenomenon).

Results

At study entry, the mean MRSS value was 21.0 in the D‐Pen Trial cohort, 27.3 in the Relaxin Trial cohort, and 26.1 in the Collagen Trial cohort. Time in study was a significant predictor of improvement in MRSS regardless of the disease duration at baseline (P < 0.0001). Patients with a disease duration of ≥24 months showed a greater rate of decline as compared with patients with a disease duration of <24 months (P < 0.05). Similar results were obtained when disease duration was reclassified by including the time of the first Raynaud's phenomenon symptom in the definition.

Conclusion

Our study confirms recent findings that in patients entered into these 3 RCTs, skin thickening did not follow the same trend in natural history as that seen in the dcSSc populations entered into early, open longitudinal studies previously reported. These findings have important implications for study design, in which “prevention of worsening” is the main objective.

     

Symptoms and esophageal motility based on phenotypic findings of scleroderma

Scleroderma esophagus is characterized by ineffective peristalsis and reduced esophageal sphincter pressure. Esophageal disease in scleroderma can precede cutaneous manifestations and has been associated with Raynaud's phenomenon (RP) and pulmonary fibrosis (PF). The objective of the study is to evaluate the impact of cutaneous findings, RP, and PF on demographics, symptoms, and esophageal motility in patients with scleroderma. Scleroderma patients with esophageal involvement were included after review of esophageal manometries and charts over a 6‐year period. High‐resolution esophageal manometry was performed. Patients completed a symptom questionnaire. The study enrolled 28 patients (22 females; mean age 50.3 ± 12.8 years) with scleroderma esophagus. Patients without skin involvement (n= 12) reported more severe heartburn (P= 0.02), while those with cutaneous findings (n= 16) had more frequent dysphagia with solids (P= 0.02). Patients with RP (n= 22) had lower amplitude of distal esophageal contractions (P= 0.01) than those without RP (n= 6). Patients with PF (n= 11) reported more severe coughing and wheezing (both P= 0.03) than those without lung disease (n= 17). This study highlights subgroups of patients with scleroderma esophagus according to phenotypic findings of dermatologic changes, RP, and PF. Heartburn and dysphagia are important symptoms that may be associated with different stages of disease progression based on skin changes in scleroderma. RP was associated with greater esophageal dysmotility. Coughing and wheezing were more severe in patients with PF.     

Time to diagnosis in systemic sclerosis: Is sex a factor?

Objective

To determine whether sex plays a role in the time to diagnosis of systemic sclerosis (SSc).

Methods

In the Canadian Scleroderma Research Group registry, dates of onset of Raynaud's phenomenon, the first non–Raynaud's disease symptom, and diagnosis were recorded based on patient reports. Association between sex and time to diagnosis was assessed for the group as a whole and stratified based on extent of skin involvement, either limited or diffuse.

Results

Of the 408 patients studied (347 women, 61 men, 44% with diffuse cutaneous SSc), the time to diagnosis after the onset of Raynaud's phenomenon was significantly longer for women than men (log rank P = 0.001), but not significantly different after the onset of the first non–Raynaud's disease manifestation. In an analysis stratified by limited or diffuse status, the time to diagnosis from onset of Raynaud's phenomenon was also significantly longer for women than men with diffuse cutaneous SSc (log rank P = 0.008). A trend toward a longer period between onset of Raynaud's phenomenon and SSc diagnosis was observed in women compared with men with limited cutaneous SSc (median 4.6 years in women versus 2.1 years in men; P = 0.085), and there was no sex difference in time to diagnosis after the onset of the first non–Raynaud's disease manifestation.

Conclusion

In SSc, the time to diagnosis is longer for women than men after the onset of Raynaud's phenomenon, suggesting that there may be possible biologic differences in the progression of disease or in the health care trajectories of men and women with early SSc.     

Long-term treatment of systemic lupus erythematosus with cyclosporin A

Objective. To evaluate the efficacy of long-term treatment with cyclosporin A (CSA) in systemic lupus erythematosus (SLE). Methods. Thirty patients with SLE whose condition was either poorly responsive or unresponsive to treatment with steroids and/or cytotoxic drugs were enrolled in a prospective, nonrandomized study of CSA. Patients with hypertension or hypercreatinemia were excluded. Disease activity was evaluated according to the systemic lupus activity measure. Assessments were made prior to study entry and after 6, 12, 18, and 24 months. Results. Twenty-seven patients completed at least 24 months of treatment with CSA. The mean disease activity score significantly decreased after 6 months of therapy (P < 0.01); this result was maintained throughout the study. A conspicuous steroid-sparing effect was observed following administration of CSA (P < 0.01). Side effects included hypertrichosis (63% of patients), paresthesias (23%), gastrointestinal symptoms (20%), gingival hyperplasia (17%), hypertension (10%), tremors (7%), and nephrotoxicity (13%). No significant changes in serum creatinine levels were observed. Conclusion. CSA represents a helpful second-choice treatment for patients with active SLE. Administration of CSA necessitates expert and careful followup of patients.     

Prevalence and clinical correlates of pruritus in patients with systemic sclerosis

Objective

There are no studies of pruritus prevalence or clinical correlates in systemic sclerosis (SSc). The objectives of this study were to document the proportion of SSc patients with pruritus on most days, to determine when in the course of the disease pruritus is most prevalent, and to identify clinical correlates.

Methods

We performed a cross‐sectional, multicenter study of 400 SSc patients from the Canadian Scleroderma Research Group Registry ≥1 year after Registry enrollment. Patients indicated whether they experienced pruritus during the past month on most days and underwent clinical histories and medical examinations. Multiple logistic regression was used to assess the association between sociodemographic and clinical variables and pruritus.

Results

A total of 179 patients (45%) reported pruritus on most days, including 69% (11 of 16) among patients 1.0–1.9 years from onset of non‐Raynaud's symptoms, 41% (38 of 93) for 2.0–4.9 years, 47% (44 of 94) for 5.0–9.9 years, 43% (60 of 140) for 10.0–19.9 years, and 46% (26 of 57) for ≥20 years. In post hoc analysis, patients 1.0–1.9 years from disease onset were significantly more likely to report pruritus (P = 0.049). Patients with pruritus had significantly more skin involvement (P = 0.029), more gastrointestinal (GI) symptoms (P < 0.001), worse breathing problems (P = 0.001), worse Raynaud's symptoms (P = 0.002), and more severe finger ulcers (P = 0.009). Only the number of GI symptoms predicted pruritus in multiple logistic regression analysis (odds ratio 1.25, 95% confidence interval 1.13–1.37; P < 0.001).

Conclusion

Pruritus is common in SSc and is independently associated with GI symptoms. Focused research on sources of pruritus and its management in SSc is needed.     

Levels of vascular endothelial growth factor and hepatocyte growth factor in sera of patients with rheumatic diseases

Abstract

Angiogenesis plays an important role in the progression of rheumatic disease. We measured the levels of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in sera from patients with rheumatic diseases and investigated whether these angiogenic factors would be useful in the evaluation of rheumatic diseases. Serum VEGF and HGF levels were determined using ELISA in 128 patients with rheumatic diseases and in 11 healthy controls. Serum VEGF and HGF levels were significantly higher in patients with rheumatic diseases compared to healthy controls [VEGF, 312 ± 20?pg/ml versus 61 ± 8?pg/ml (mean ± SE), P < 0.001; HGF, 935 ± 36?pg/ml versus 413 ± 49?pg/ml, P < 0.01]. Serum VEGF and HGF levels were significantly elevated in patients with adult Still's disease (VEGF, 1021 ± 258?pg/ml; HGF, 1500 ± 295?pg/ml) and were relatively increased in patients with active rheumatoid arthritis (RA) (VEGF, 359 ± 94?pg/ml) and systemic sclerosis (SSc) (VEGF, 356 ± 43?pg/ml; HGF, 1294 ± 224?pg/ml). HGF levels correlated with the clinical course and disease severity in rheumatic disease patients. VEGF levels correlated with the presence of Raynaud's phenomenon (P < 0.05), interstitial lung disease (ILD) (P < 0.05), and serum KL-6 levels (P < 0.01), whereas HGF levels correlated with cryoglobulinemia (P < 0.05), ILD (P < 0.05), serum C-reactive protein (CRP) (P < 0.05), thrombomodulin (P < 0.05), and KL-6 levels (P < 0.05) in rheumatic disease patients. VEGF levels correlated with the skin scores and KL-6 levels in SSc patients and also correlated with the disease activity of RA patients. These data suggest that serum VEGF and HGF levels are related to rheumatic disease activity and the presence of complications. Analysis of VEGF and HGF may be useful in the clinical evaluation of rheumatic disease patients.     

Systemic lupus erythematosus in a tertiary,east Malaysian hospital: admission,readmission and death

Objective: There are limited data on hospitalization of systemic lupus erythematosus (SLE) patients in Asian countries. Our aim of this study is to describe the characteristics and poor prognostic factors in our patients. Method: We performed a retrospective study of SLE hospitalization during a 1‐year period (2006) in our centre. Results: There were 125 episodes of hospitalization of 79 patients with SLE. This is the first report of SLE patients from the native population of east Malaysia. The cause of admission was flare of SLE (80.8%), infection (23.2%), renal biopsy (22.4%) and others (4%). There was only one admission for thromboembolism. Patients with both flare of SLE and infection have the longest median length of stay of 11 days (IQR 5,24) requiring more intensive care therapy (P < 0.01). Readmission occurred in 31.4% and was associated with admission for other reasons during the first admission. Flare of SLE was protective against readmission (P < 0.05, OR = 0.36). There were six deaths (4.8% of admissions). The deaths were due to infection in three patients, active SLE in two and acute myocardial infarction in one. The deaths have a higher cumulative prednisolone dose than the survivals (P < 0.01). In multivariate modelling, the only predictor of death was high Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index score (P < 0.05, OR = 9.61 per increase of 1 score). Conclusion: Active disease and infection remains the main cause of admission, readmission and death in SLE patients.     

Early expression of E-selectin,tumor necrosis factor α, and mast cell infiltration in the salivary glands of patients with systemic sclerosis

Objective. To assess the predictive value of early endothelial E-selectin and tumor necrosis factor α (TNFα) expression, as well as mast cell infiltration, in the subsequent progression to systemic sclerosis (SSc) in patients with Raynaud's phenomenon (RP) and abnormal nailfold capillaroscopic findings. Methods. Clinical criteria were evaluated, and immunostaining was performed on lip biopsy samples from 22 patients with RP and abnormal capillaroscopic results. None of these patients initially fulfilled the American College of Rheumatology criteria for SSc. Results. E-selectin, TNFα, and mast cell infiltration were found in 9, 10, and 8 of 11 patients, respectively, whose disease progressed to SSc, and in 0, 2, and 1 of 11 patients, respectively, whose disease did not progress to SSc (P < 0.001, P < 0.01, and P < 0.01, respectively). Conclusion. E-selectin, TNFα, and mast cell infiltration are detectable in the very early stages of SSc, prior to the onset of skin changes.     

Anti-C1q antibodies and antiendothelial cell antibodies in systemic lupus erythematosus – relationship with disease activity and renal involvement

The aim of this study was to investigate the relationship between the presence and titre of antibodies against C1q (anti-C1q Ab) and disease activity and renal involvement in patients with systemic lupus erythematosus (SLE). Anti-C1q Ab were measured in 79 patients with SLE (70 women and 9 men; mean age 41.7 years; mean disease duration 8.4 years): 19 patients had active disease with lupus nephritis, 8 active disease without nephritis, 26 inactive disease with nephritis and 26 inactive disease without nephritis. Anti-dsDNA antibodies (EIA and immunofluorescence), antiendothelial cell antibodies (AECA) and complement levels (C3, C4, total haemolytic complement activity) were determined in parallel. Anti-C1q Ab were positive in 49%, anti-dsDNA Ab in 61% and AECA in 19% of the patients, respectively. Significantly higher titres of anti-C1q Ab were found in patients with active disease compared with those with inactive SLE (P < 0.01). Serum levels of anti-C1q Ab showed a positive correlation with anti-dsDNA Ab and SLEDAI score (P < 0.01) and a negative correlation with C3 (P < 0.05), C4 (P < 0.01) and CH50U (P < 0.01). The presence of anti-C1q Ab was not different between patients with or without nephritis. In patients with (P < 0.05) and without nephritis (P < 0.01) the frequency of anti-C1q Ab was significantly higher in active patients compared with inactive patients. Both anti-C1q and anti-ds-DNA Ab were detectable in 74% of patients with active nephritis but only in 30% of all other patients (P=0.001). None of the patients with active nephritis was negative for anti-C1q and anti-dsDNA Ab, whereas 37% of the patients without active nephritis were negative for both antibodies (P < 0.01). Sensitivity, specificity, positive and negative predictive values for active lupus nephritis among SLE patients were 100%, 50%, 51.9% and 100% for anti-dsDNA Ab (EIA) and 74%, 70%, 57% and 89.4% for positive findings of both anti-dsDNA and anti-C1q Ab. The presence and titre of anti-C1q-Ab in SLE are related to disease activity. Absence of anti-dsDNA Ab excludes active nephritis; positive findings of both anti-dsDNA Ab and anti-C1q Ab are of relatively high specificity for active nephritis.     

PTX3 in small‐vessel vasculitides: An independent indicator of disease activity produced at sites of inflammation

Objective

To verify whether the prototypical long pentraxin PTX3 represents an indicator of the activity of small‐vessel vasculitis.

Methods

Concentrations of PTX3, a pentraxin induced in endothelium by cytokines, were measured by enzyme‐linked immunosorbent assay in the sera of 43 patients with Churg‐Strauss syndrome, Wegener's granulomatosis, and microscopic polyangiitis. PTX3 was also measured in the sera of 28 patients with systemic lupus erythematosus (SLE), 22 with rheumatoid arthritis, and 16 with CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias). Serum concentrations of C‐reactive protein (CRP) were measured by immunoturbidimetry. The cells involved in PTX3 production in vivo were identified in skin biopsy samples.

Results

Patients with active vasculitis had significantly higher concentrations of PTX3 than did those with quiescent disease (P < 0.001). PTX3 levels in the latter group were similar to those in healthy controls. PTX3 levels were higher in patients with untreated vasculitis and lower in patients who underwent immunosuppressive treatments (P < 0.005). In contrast, patients with active SLE had negligible levels of the pentraxin. PTX3 levels did not correlate with CRP levels in vasculitis patients. Endothelial cells produced PTX3 in active skin lesions.

Conclusion

PTX3 represents a novel acute‐phase reactant produced at sites of active vasculitis.

     

Cold exposure increases cyclic guanosine monophosphate in healthy women but not in women with Raynaud's phenomenon

Abstract. Objective. To investigate influence of whole-body cooling on cyclic GMP (cGMP) in women with Raynaud's phenomenon and in healthy women. Design. The study was performed as an open, parallel-group comparison between women with Raynaud's phenomenon and healthy women during the winter month of February. Setting. The municipality of Västerås (Sweden). Participants. The Raynaud group comprised 24 female patients. The control group consisted of 21 healthy females. Main outcome measure. The venous levels of cGMP were measured on three different occasions: just before and after 40 min of whole-body cooling and after 20 min rest at room temperature (21°C). Results. Venous cGMP increased significantly in the control group after cold exposure (mean difference 0.43 pmol ml^?1; 95% CI, 0.018–0.848; t = 2.18; df = 20; P = 0.02) and remained at a high level after 20 min rest (mean difference 0.58 pmol mL^?1; 95% CI, 0.063–1.108; t = 2.34; df = 20; P = 0.015). In contrast, the levels of venous cGMP in the Raynaud group did not change significantly. The difference in increase between the two groups was significant (P < 0.02). The diastolic blood pressure in the Raynaud group increased after 40 min of whole-body cooling and was still significantly increased (P < 0.001) after 20 min rest at room temperature (21 °C). Conclusion. These results indicate that women suffering from Raynaud's phenomenon lack the physiological response of cGMP to cold exposure, which may explain their increased vasospastic response.     

Nicardipine in the treatment of raynaud's phenomenon

A new calcium channel blocker, nicardipine, was studied for treatment of Raynaud's phenomenon in a double-blind, placebo-controlled, crossover trial during the winter months. Clinical response was assessed by a patient-kept diary of symptoms and finger systolic pressure that was measured at room temperature and during cold challenge. In vivo platelet activation was determined by measuring plasma levels of the platelet-specific proteins, beta-thromboglobulin and platelet factor 4. When treatment with placebo was compared with treatment with nicardipine, no significant differences were found in the number of Raynaud's attacks per day, the severity of attacks, change in character in Raynaud's phenomenon, use of hands in winter months, patient assessment of medication or objective measurements of finger systolic pressure, and critical closing temperature. There was a reduction of plasma levels of beta-thromboglobulin and platelet factor 4 in the overall study group while taking nicardipine compared with that during the placebo period (mean change 5.0 ± 2.4 ng/ml, P = 0.054, and 1.4 ± 0.6 ng/ml, P < 0.01, respectively). These results demonstrate that while nicardipine was not effective in reducing the episodes of Raynaud's phenomenon, it did inhibit in vivo platelet activation. These findings suggest that platelet activation is not the primary event in the pathogenesis of acute vasospasm in Raynaud's phenomenon, since reduction of platelet activation by the drug did not change the severity of vasospasm.     

Anti-dsDNA antibodies in Brazilian patients of mainly African descent with systemic lupus erythematosus: lack of association with lupus nephritis

Renal disease is associated with morbidity and mortality in systemic lupus erythematosus (SLE) and anti-dsDNA antibodies with SLE immunopathogenesis. We investigated the dsDNA antibody profile of 84 Brazilian SLE patients, 27 with lupus nephritis. Thirty-six (39.1%) patients had dsDNA IgG antibodies shown in enzyme-linked immunosorbent assay (454.7 ± 281.1 WHO units/mL), nine presenting renal disease. The following profile of dsDNA antibodies was demonstrated in Crithidia luciliae test: IgA (seven out of 36; 19.4%), IgG (22 out of 36, 66.1%); IgM (nine out of 36, 25.0%), and IgE (four out of 36, 11.1%). Two or three isotypes of dsDNA antibodies were observed in nine (25.0%) patients, while 11 (30.5%) were seronegative in the C. luciliae test. Patients with dsDNA antibodies had lower serum C3 and C4 when compared with SLE individuals without these immunoglobulins (P < 0.01 and P < 0.001, respectively). There was no association between any dsDNA antibody isotype and lupus kidney disease nor was anti-dsDNA IgM antibody associated with absence of nephritis.     

Prevalence of conventional and lupus‐specific risk factors for cardiovascular disease in patients with systemic lupus erythematosus: A case–control study

Objective

Patients with systemic lupus erythematosus (SLE) are significantly more likely to experience a myocardial infarction or a stroke than age‐matched controls. We compared the prevalence of conventional and lupus‐specific risk factors in patients with SLE just before a cardiovascular event and in matched controls with SLE but no cardiovascular disease (CVD).

Methods

Twenty‐nine patients with SLE and CVD were enrolled. For each patient, 2 ethnically‐ and sex‐matched controls were obtained, 1 matched for age and 1 for SLE duration. Data regarding risk factors were collected for the time immediately preceding the relevant cardiovascular event, or at an equivalent time for controls.

Results

Patients' median age at event was 49 years (interquartile range 43–54 years) and mean disease duration was 12.0 ± 7.1 years. Patients with SLE and CVD were more likely than both age and duration controls to be treated for hypertension (P = 0.01 and P = 0.001, respectively) and to have elevated triglyceride levels (P = 0.05 and P = 0.01, respectively). Compared with duration controls, CVD patients were more likely to have lupus anticoagulant (P = 0.03), but less likely to be receiving treatment with hydroxychloroquine (P = 0.003). Compared with age controls, patients were more likely to be current smokers (P = 0.03), to have taken a mean dosage >7.5 mg/day of prednisolone (P = 0.04), and to have been treated with pulsed methylprednisolone (P = 0.03). In multivariable analysis, only hypertension treatment was an independent risk factor for CVD.

Conclusion

We identified significantly increased prevalence of some conventional and lupus‐specific risk factors in patients with SLE immediately before a CVD event compared with controls matched for age or disease duration.