Epidemiology of spondyloarthritis: a review.

The classification of Spondyloarthritis (SpA) has been revised with the introduction of the ASAS classification criteria. Although this has best been described in ankylosing spondylitis and psoriatic arthritis, there are population studies evaluating the epidemiology of the different subgroups of SpA. In this paper, we present data on the incidence and prevalence of the subgroups of SpA in different populations, and point to data indicating how the introduction of new classification criteria, with the altered perception of the SpA entity, might impact on the epidemiology.

Quantitative salivary gland scintigraphy can distinguish patients with primary Sjøgren's syndrome during the evaluation of sicca symptoms.

Abnormal findings on salivary gland scintigraphy (SGS) are part of the classification criteria for Sjøgren's syndrome (SS), but SGS is operator dependent and poorly standardised. We studied the use of quantitative data on the uptake, concentration and excretion of the four major salivary glands in the evaluation of sicca patients. During an initial clinical evaluation for sicca symptoms (mean duration, 51 months), 24 subjects were classified as either SS (n = 8) or isolated sicca (IS; n = 16). SGS was then performed after i.v. injection of 200 MBq pertecnetat. Digitalised quantitative data on time-to-peak uptake (Tmax), peak tracer distribution (C%) and stimulated excretion (E%) were calculated from time-activity curves and compared between groups and controls (n = 8) and correlated to clinical data. Statistical analysis was performed with non-parametric tests. SS patients had longer Tmax in both parotic glands (18.1 min; p < 0.01)) and both submandibular glands (mean 13.7 min, p < 0.05); whereas Tmax in IS patients was similar as in controls in both parotic (10.4 min; p > 0.2) and submandibular glands (9.4 min; p > 0.4). C% was significantly lower in the parotic glands of both the SS and the IS group compared to the controls (p < 0.01). E% was significantly reduced in SS patients (16.3% for parotic and 17.4% for submandibular glands; p < 0.01); whereas in the IS patients, excretion (32, 2% for parotic and 26, 9% for submandibular glands) was similar from all glands as in the control groups (35, 2% for parotic and 27, 8% for submandibular glands). No correlation was found between these SGS results and age, focus score, erythrocyte sedimentation rate, serum creatinin or immunoglobulin levels. No IS patient progressed to full-blown pSS during the 4 years of follow-up. Quantitative SGS data are useful and objective tools to distinguish patients with SS.

[Systemic lupus erythematosus and pregnancy]. / Systemisk lupus erythematosus og svangerskap.

BACKGROUND: Systemic lupus erythematosus (SLE) often starts in women of fertile age. Due to the unpredictable nature of the disease and the increased risk of the disease flaring up during pregnancy, women with SLE have previously often been advised to avoid pregnancy. This summary reviews current insights in pregnancy management of women with SLE. METHOD: Search in the Medline database (period 1980-2005) using keywords: SLE, lupus nephritis, antiphospholipid antibody, neonatal lupus and pregnancy. RESULTS: Previous studies of pregnant women with SLE have had different designs, sample sizes, selections of patients, definitions and measures of outcome. Women with previous pregnancy losses, an ongoing active disease with nephritis or hypertension and positive antiphospholipid antibodies, have an increased risk of pregnancy loss. The most favourable pregnancy outcomes are achieved when conception takes place during a remission of the disease. INTERPRETATION: There are few absolute contraindications for pregnancies in women with SLE. Women with SLE may experience uncomplicated pregnancies, but they need to plan their pregnancies as the risk for complications is increased. Best results are achieved through the cooperation of rheumatologists, gynaecologists and nephrologists. Glucocorticosteroids, hydroxychlorocine, azathioprine and anticoagulation may be used during pregnancy.

[Treatment with etanercept in chronic polyarthritis]. / Behandling med etanercept ved kronisk polyartritt.

BACKGROUND: In randomised trials, treatment with anti-tumour necrosis factor alpha drugs has been shown to be efficacious for patients with rheumatoid arthritis. We analysed the effectiveness and toxicity of etanercept treatment in our day-to-day rheumatology practice at the University Hospital of Northern Norway. MATERIAL AND METHODS: Patients with active polyarthritis who had failed at least three different disease-modifying anti-rheumatic drugs including methotrexate and/or combination therapy were consecutively included in an open study when they started etanercept therapy (25 mg twice per week subcutaneously). During follow up we noted the number of swollen and tender joints, took visual analogue scores (0-100 millimetre) for pain and global well-being, administered the Modified Health Assessment Questionnaire, performed laboratory tests, and took note of side effects. RESULTS: Between April 1999 and July 2001, etanercept treatment was initiated in 71 patients. An ACR-20 response (20% improvement according to American College of Radiology criteria) occurred in 57% of patients after one month of treatment and in 70 % after three months, ACR-50 response in 24% and 42%, and ACR-70 response in 6% and 20%. While half of all patients reported side effects, only five patients (7%) discontinued treatment because of them. INTERPRETATION: Etanercept is effective therapy for many patients with severe chronic polyarthritis in clinical practice. Short-term side effects occur more frequently than reported and seem less frequent with concomitant methotrexate therapy. Long-term side effects are still unknown and require close monitoring.

Inflammatory cell infiltrates in vessels with different susceptibility to atherosclerosis in rheumatic and non-rheumatic patients: a controlled study of biopsy specimens obtained at coronary artery surgery.

BACKGROUND: The main aim of the present study was to compare the occurrence of inflammatory cell infiltrates in the aorta, a vessel with a high occurrence of atherosclerosis, with that in the saphenous vein (SV) and internal mammary artery (IMA), which are protected from atherosclerosis. METHODS AND RESULTS: Samples from the aorta, SV, and IMA of 65 patients with inflammatory rheumatic diseases (IRD) and from 51 control patients undergoing coronary artery bypass graft surgery were examined for the presence and location of inflammatory cell infiltrates and atherosclerotic lesions. Mononuclear cell infiltrates (MCIs) in the media or adventitia were observed in 2% IMAs, 17% SVs, and 35% aortic specimens (SV vs IMA: p=0.006; SV vs aorta: p=0.001). Atherosclerotic lesions were present in none IMA, 3% SVs and 18% aortic specimens. IRD and smoking increased the odds of MCI in the aorta (odds ratio (OR)=3.6, 95% confidence interval (CI): 1.6-8.5 and OR=4.0, 95% CI: 1.5-10.9), but not in the SV or IMA. CONCLUSIONS: The occurrence of medial and adventitial MCI in the aorta, SV, and IMA paralleled each vessel's susceptibility to atherosclerosis: it was highest in the aorta and lowest in IMA. Local vascular inflammation may be involved in atherogenesis, and influence the patency of vascular grafts.

Inflammatory rheumatic disease and smoking are predictors of aortic inflammation: a controlled study of biopsy specimens obtained at coronary artery surgery.

OBJECTIVE: Several inflammatory rheumatic diseases are associated with accelerated atherosclerosis. Atherosclerosis may result from systemic and/or local vascular inflammation. The aim of this study was to evaluate the occurrence of chronic inflammatory infiltrates in the aortas of patients with and those without inflammatory rheumatic disease who had undergone coronary artery bypass graft (CABG) surgery, and to assess the relationship between the infiltrates and other factors thought to play a role in atherosclerosis, such as smoking. METHODS: Aortic specimens routinely removed during CABG surgery in 66 consecutive patients with inflammatory rheumatic disease and 51 control patients without inflammatory rheumatic disease were examined by light microscopy for the occurrence, location, and severity of chronic inflammatory infiltrates and atherosclerotic lesions. RESULTS: Mononuclear cell infiltrates in the inner adventitia (apart from those localized along the epicardium) were more frequent in the group of patients with inflammatory rheumatic disease (47% versus 20%; P = 0.002, odds ratio [OR] OR 3.6, 95% confidence interval [95% CI] 1.6-8.5), and the extent of these infiltrates was greater. Multivariate analyses revealed that the occurrence of mononuclear cell infiltrates was associated with inflammatory rheumatic disease (OR 2.99, P = 0.020) and current smoking (OR 3.93, P = 0.012), and they were observed in 6 of 7 patients with a history of aortic aneurysm. Inflammatory infiltrates in the media were seen only in patients with inflammatory rheumatic disease. The frequency of atherosclerotic lesions, inflammation within the plaques, and epicardial inflammatory infiltrates in the 2 groups was equal. CONCLUSION: Among aortic samples collected during CABG surgery, those obtained from patients with inflammatory rheumatic disease had more pronounced chronic inflammatory infiltration in the media and inner adventitia than those obtained from control patients. Current smoking was an independent predictor of chronic inner adventitial infiltrates. The infiltrates may represent an inflammatory process that promotes atherosclerosis and formation of aneurysms.

Damage accumulation in systemic lupus erythematosus and its relation to disease activity and mortality.

OBJECTIVE: To describe damage accrual and the interconnections between disease activity measures, damage accrual, and death in a Nordic lupus cohort. METHODS: Longitudinal study in the population-based Tromso lupus cohort. Disease activity [SLE Disease Activity Index (SLEDAI)] and disease damage [by Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology (ACR) Damage Index (SDI)] were recorded for each visit. Weighted average SLEDAI scores (WAS) were calculated to correct for variable observation times. Development of damage (SDI > 0), severe damage (SDI >or= 3), and death were used as separate endpoints. Univariate nonparametric analysis identified and hazard ratios (HR) by Cox regression techniques confirmed the independence of predictors for each outcome. RESULTS: Through 11.9 years of followup, 72 patients (46%) remained free of damage, 51 (32%) developed moderate damage, and 35 (22%) developed severe damage. SDI scores were higher in 37 nonsurvivors (23.4%; SDI 2.1) than in survivors (SDI 0.9; p < 0.05). Damage accrual was linear throughout the first decade of disease. The only independent predictor for SDI >/= 3 was a WAS score > 3 (hazard ratio 2.34; 95% CI 1.1-4.9). Age > 40 years at diagnosis (HR 5.6, 95% CI 2.4-12.7) and WAS > 3 (HR 2.4, 95% CI 1.2-4.9) were significant predictors for death. CONCLUSION: Damage accrual in SLE occurred in 54% of patients in a linear fashion over the first decade of disease. Global disease activity was the main determinant of damage accrual. Accrued damage was not an independent risk factor for death, which was predicted by age > 40 years and WAS > 3.

Is closer linkage between systemic lupus erythematosus and anti-double-stranded DNA antibodies a desirable and attainable goal?

The anti-double-stranded DNA (anti-dsDNA) antibody test incorporated in the 1982 revised American College of Rheumatology criteria for the classification of systemic lupus erythematosus needs updating to reflect current insights and technical achievements, including allowance for the presence of nonpathogenic anti-dsDNA antibodies. As we need to develop at least some measure of pathogenicity of anti-dsDNA antibodies, we propose that initial anti-dsDNA antibody screening is done by sensitive ELISA and supplemented by more stringent assays. Simultaneously the relevance of anti-dsDNA antibody presence needs to be restricted to clinical manifestations, thought to be caused by anti-dsDNA antibody and within an appropriate time frame.

Incidence and prevalence of ankylosing spondylitis in Northern Norway.

OBJECTIVE: To determine the incidence and prevalence of ankylosing spondylitis (AS) over a prolonged period in the 2 northernmost counties of Norway, where HLA-B27 has a high prevalence in the population. METHODS: We conducted a cohort study of all patients registered with a diagnosis of AS between 1960 and 1993 at the University Hospital of Northern Norway, which is the sole rheumatology department serving these counties. We registered demographics, year of disease onset (clinical disease), and year of diagnosis (radiograph confirmation) for all patients. The date of onset of clinical disease in patients with AS was used in the calculation of incidence rates. Annual incidence and point/period prevalence rates were expressed per 100,000 adults. Primary AS was defined as AS in the absence of psoriasis or inflammatory bowel disease (IBD). RESULTS: A total of 534 patients (75.1% male, mean age at clinical diagnosis 24.2 years, 93.0% HLA-B27 positive) had a confirmed diagnosis of AS (by the modified New York criteria). Median time from disease onset to radiologic confirmation was 8.0 years. Annual incidence of primary AS (n = 417) was 7.26, while estimated point prevalence rose from 0.036% in 1970 to 0.10% in 1980 and to 0.21% in 1990 with a period prevalence of 0.26%. AS was secondary to psoriasis or IBD in 117 patients (18.1%), with a diagnostic delay similar to that in primary AS. Annual incidence (14.1) and period prevalence in 1982-1993 (0.41%) were significantly higher in the town of Tromsø than in the surrounding rural region (5.21 and 0.22%, respectively). Mortality in patients with AS was low. CONCLUSION: The incidence of AS was relatively stable in the northern part of Norway over a 34-year period. Incidence and prevalence are higher than reported in similar studies from Finland and Minnesota, possibly due to a higher population prevalence of HLA-B27.