Correction to: Psoriasis in systemic lupus erythematosus: a single-center experience

Clinical Rheumatology - Prof. Ari Polachek on of the author of the published version of this article missed to add his second affiliation which is the Department of Rheumatology, Tel Aviv Sourasky...     

Accumulation of coronary artery disease risk factors over three years: data from an international inception cohort

OBJECTIVE: To examine the accumulation of risk factors over 3 years in a multicenter, international inception cohort of patients with systemic lupus erythematosus (SLE). METHODS: The Systemic Lupus International Collaborating Clinics registry for atherosclerosis comprises 27 centers from 11 countries. An inception cohort of 935 patients with SLE was assembled, according to a standardized protocol, from 2000 to 2006 to study risk factors for atherosclerosis. Both classic and other coronary artery disease (CAD) risk factors were collected at entry and through 3 years of followup. Therapy was documented over the 3 years. The Framingham 10-year risk factor profile was calculated for each patient at year 1 and year 3. RESULTS: A total of 278 patients from the inception cohort were followed for 3 years and constituted the population for this study. At enrollment a substantial number of patients already demonstrated several risk factors for CAD, both classic and other. All risk factors increased from enrollment over the 3 years of followup. Treatment of hypertension and hypercholesterolemia also increased over 3 years, but less so for hypercholesterolemia. The Framingham 10-year CAD risk profile was higher in men than in women both at entry and at 3 years, and remained unchanged over the 3 years. Corticosteroid use increased only slightly over 3 years, but use of antimalarials and immunosuppressive agents increased to a greater extent. CONCLUSION: Patients with SLE should be monitored for CAD risk factors from the time of diagnosis and appropriate treatment should be instituted early.     

Pericardial fluid analysis in scleroderma (systemic sclerosis)

A patient with scleroderma who presented with pericarditis and effusion is described. Aspirates from this pericardial effusion had the characteristics of an exudate with no evidence of autoantibodies, immune complexes or complement depletion. These findings suggest that the mechanisms operating in the production of pericardial effusion in scleroderma may be different from those found in rheumatoid arthritis and systemic lupus erythematosus.     

Sacroiliac joint abnormalities in calcium pyrophosphate crystal deposition disease

Summary Three cases of generalized calcium pyrophosphate dihydrate deposition disease and roentgenographic sacroiliac abnormalities (chondrocalcinosis, inflammatory change and degenerative change) are described.     

Single photon emission computed tomography dual isotope myocardial perfusion imaging in women with systemic lupus erythematosus. II. Predictive factors for perfusion abnormalities

OBJECTIVE: We have reported that 40% of patients with systemic lupus erythematosus (SLE) had abnormal myocardial perfusion studies. Here we investigated risk factors for abnormal myocardial perfusion in a cohort of women with SLE without history of coronary artery disease. METHODS: Consecutive women with SLE followed at a large lupus clinic underwent single photon emission computed tomography dual isotope myocardial perfusion imaging (DIMPI) following pharmacological stress using dipyridamole. At the time of study each patient had a clinical and laboratory assessment performed by a standard protocol. We compared traditional risk factors as well as disease and therapy related factors in those with and without perfusion abnormalities. RESULTS: A total of 129 patients were studied. The mean +/- SD age was 44.8 +/- 10.9 yrs, and mean SLE Disease Activity Index was 4.2 +/- 5.1. Forty-nine (38%) patients had an abnormality of myocardial perfusion. Factors associated with an abnormal DIMPI included current hypertension (OR 2.11, p = 0.05), elevated cholesterol ever (OR 2.51, p < 0.05), and total cholesterol:high density lipoprotein-cholesterol ratio (OR 1.96 for each increase of 1.0, p < 0.008). CONCLUSION: Myocardial perfusion abnormalities are common in women with SLE without known coronary artery disease (CAD), suggesting a high burden of subclinical CAD. Several metabolic and therapy related factors appear to be associated with the process of atherogenesis in SLE. These results suggest that SLE should be considered a predisposing factor for atherosclerosis.     

Do current arterial hypertension treatment guidelines apply to systemic lupus erythematosus patients? A critical appraisal

Objective

Arterial hypertension (HTN) is reported to burden up to 74% of systemic lupus erythematosus (SLE) patients and contributes significantly to accelerated atherosclerosis and increased cardiovascular (CV) risk. Current HTN treatment guidelines have not incorporated lupus patients in their recommendations; whether these guidelines can be fully implemented in SLE is doubtful.

Methods

A critical appraisal of the existing HTN guidelines in regard to SLE is presented in this review, based upon clinical and experimental data. Particular issues addressed are the time of antihypertensive therapy initiation, the optimal blood pressure level, the antihypertensive agent of first-choice and the need for reduction of the total cardiovascular risk in SLE.

Results

Antihypertensive therapy should be recommended at levels of 140/90 mmHg (systolic and diastolic BP, respectively) in newly diagnosed lupus patients without overt target organ involvement. In the case of lupus nephritis (LN) or diabetes mellitus (DM), therapy should be implemented at lower levels, such as 130/80 mmHg. Hypertensive lupus patients should be considered at high or very high CV risk and, consequently, the optimal BP level should be less than 130/80 mmHg. Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) seem to be a safe and efficacious first-choice antihypertensive treatment in lupus patients. Total CV risk should be considered and co-morbidities (dyslipidemia, antiphospholipid syndrome, etc.) should be managed promptly.

Conclusions

Current HTN therapeutic guidelines, lacking data from large-scale clinical trials, may not adequately apply to SLE patients. The assessment of the aforementioned recommendations in randomized clinical trials is expected to confirm their value in reducing CV risk in SLE.     

Prevalence of antibodies to beta2-glycoprotein I in systemic lupus erythematosus and their association with antiphospholipid antibody syndrome criteria: a single center study and literature review

OBJECTIVE: To determine the prevalence of anti-beta2-glycoprotein I antibodies (anti-beta2-GPI) in patients with systemic lupus erythematosus (SLE), and to assess their association with and predictive value for the clinical classification criteria of the antiphospholipid antibody syndrome (APS). METHODS: One hundred thirty-three consecutive patients with SLE were recruited from 2 lupus clinics in the University of Toronto. Serum and plasma samples were tested for IgG anticardiolipin antibodies (aCL), prolonged partial thromboplastin time (PTT), a panel of lupus anticoagulant (LAC) assays, and anti-beta2-GPI (IgG, IgM, IgA). Normal ranges for the assays were established using 129 healthy controls. A literature review from 1992 to 2000 was performed using beta2-GPI, SLE, APS, thrombosis, and recurrent pregnancy loss as key search words. RESULTS: The distribution of anti-beta2-GPI antibodies (of any isotype) in each group were as follows: all patients with SLE, 36.8%; SLE with clinical features of APS, 40.4%; SLE without clinical features of APS, 34.9%; and healthy controls, 3%. The positive predictive values of prolonged PTT, IgG aCL, and anti-beta2-GPI for at least one clinical feature of APS in SLE were 59.3, 50.0, and 38.8%, respectively. There were 27 patients with SLE who had antibodies to beta2-GPI but a normal PTT and negative aCL and LAC. Six (20.7%) of these had a history of thrombosis and/or recurrent pregnancy loss. Twelve studies (including ours) were identified in which patient groups were similar and the same antibody isotype was measured. No agreement was apparent after reviewing the literature regarding an association of anti-beta2-GPI IgG and clinical features of APS in patients with SLE. CONCLUSION: Antibodies to beta2-GPI were frequently seen (35%) in our SLE population. The prevalence of anti-beta2-GPI was similar in those with (19/47) and without (39/86) APS. Anti-beta2-GPI did, however, identify 6 patients with clinical features of APS who were negative for aCL and prolonged PTT. Our results indicate that anti-beta2-GPI may provide additional information for the diagnosis of APS in SLE, but do not supercede other established assays. However, when we attempted to place our results in the context of other reports, the literature review revealed that secondary diagnoses of patient groups and assay techniques are too variable among different investigators to allow useful comparison. Thus, no conclusions could be drawn regarding anti-beta3-GPI and clinical features of secondary APS in SLE.