Scleroderma specific autoantibodies in rheumatoid arthritis and Sjögren's syndrome patients with interstitial lung disease: Prevalence and associations.

Systemic sclerosis (SSc) has been classically linked to interstitial lung disease (ILD) development, often in association with specific SSc autoantibodies. In the present report, we aimed to estimate the prevalence of SSc autoantibodies in 60 seropositive RA and 41 primary SS patients complicated or not by ILD. SSc autoantibodies were determined in patients' sera by a commercial immunoblot assay. RA ILD patients displayed higher frequency of SSc-specific antibodies at strong titers compared to RA-with no lung involvement (25% vs 3.1%, p = 0.01)[OR 95% CI:10.9 (1.2-94.5)], with no differences detected between primary SS groups. These data indicate that many seropositive RA ILD patients probably represent an overlap RA/SSc entity, requiring tailored diagnostic and therapeutic approach.

Atherosclerosis in SLE: a potential role for serum parathormone levels.

OBJECTIVE: A link between bone metabolism and cardiovascular (CV) disease has been suggested mainly in the general population. In the current study we explored whether altered bone metabolism influence CV risk in patients with SLE. METHODS: In 138 consecutive patients with SLE, atherosclerosis was assessed by the presence of plaque and/or arterial wall thickening in carotid/femoral arteries by ultrasound. Bone mineral density (BMD) levels and hip/spinal cord fractures together with classical CV disease and osteoporosis risk factors including serum 25(OH) vitamin D3 and parathormone (PTH) levels were recorded in all patients. Serum osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-Β ligand were quantitated by commercial ELISA. Statistical analysis included both univariate and multivariate models. RESULTS: Abnormal PTH serum concentrations (>65 pg/mL)-but not 25(OH) vitamin D3 serum levels-were identified as a risk factor for both plaque formation and arterial wall thickening in patients with SLE (ORs (95% CIs): 8.2 (1.8 to 37.4) and 3.9 (1.3 to 11.8), respectively). This association remained significant following adjustment for vitamin D3 levels and classical CV risk factors. Moreover, an independent association between osteoporosis with plaque formation and arterial wall thickening was detected following adjustment for total steroid dose, premature menopause and disease duration (ORs (95% CIs): 5.3 (1.1 to 26.2) and 3.5 (1.1 to 11.4), respectively). An inverse correlation between femoral neck BMD values and intima-medial thickness scores was also observed (r: -0.42, p=0.008). CONCLUSIONS: These findings further strengthen the concept of shared pathophysiological mechanisms between atherogenesis and altered bone metabolism in autoimmune populations, revealing heightened PTH levels as a potential marker for atherosclerosis among patients with SLE.

Cardiovascular disease in systemic lupus erythematosus: A comprehensive update.

Heightened rates of both cardiovascular (CV) events and subclinical atherosclerosis, documented by imaging and vascular function techniques are well established in systemic lupus erythematosus (SLE). While traditional CV factors such as smoking, dyslipidemia, diabetes mellitus (DM), hypertension, central obesity and hyperhomocysteinemia have been reported to be prevalent in lupus patients, they do not fully explain the high rates of ischemic events so far reported, implying that other factors inherent to disease itself could account for the enhanced risk, including disease duration, activity and chronicity, psychosocial factors, medications, genetic variants and altered immunological mechanisms. Though the exact pathogenesis of atherosclerosis in the setting of lupus remains ill defined, an imbalance between endothelial damage and atheroprotection seems to be a central event. Insults leading to endothelial damage in the setting of lupus include oxidized low density lipoprotein (oxLDL), autoantibodies against endothelial cells and phospholipids, type I interferons (IFN) and neutrophil extracellular traps (NETs) directly or through activation of type I IFN pathway. Increased oxidative stress, reduced levels of the normally antioxidant high density lipoprotein (HDL), increased levels of proinflammatory HDL (piHDL) and reduced paraoxonase activity have been related to increased oxLDL levels. On the other hand, impaired atheroprotective mechanisms in lupus include decreased capacity of endothelial repair-partly mediated by type I IFN- and dampened production of atheroprotective autoantibodies. In the present review, traditional and disease related risk factors for CV disease (CVD) in the setting of chronic autoimmune disorders with special focus on SLE will be discussed.