Resistin in systemic lupus erythematosus: Relation to lupus nephritis and premature atherosclerosis

Lupus nephritis [LN] is one of the most severe complications of SLE. SLE patients have a greater risk of developing premature atherosclerosis. Resistin is an adipocyte-secreted peptide. It has pro-inflammatory and atherogenic effects. To assess the serum levels of resistin in SLE patients and to evaluate it as a marker of nephritis and premature atherosclerosis. This study included 50 SLE nonpregnant female adult [mean age 23.1 +/- 6.9 years] patients as well as 40 healthy volunteers matched in age and sex as a control group. Serum levels of resistin were assayed using enzyme-linked immunosorbent assay [ELISA]. All patients and controls underwent laboratory investigations and carotid duplex. Disease activity was assessed using SLE Disease Activity Index [SLEDAI]. Renal biopsy was performed for SLE patients with LN. There was a highly statistically significant increase in mean serum resistin levels [14.1 +/- 3.88 ng/ml] in patients versus the control group [6.44 +/- 1.34 ng/ml] being more obvious in those with LN. Resistin had a significant positive correlation with markers of inflammation, SLEDAI and carotid intima media thickness [CIMT]. Serum level of resistin may serve as a marker of LN and atherosclerosis in SLE patients. A more aggressive control of the underlying inflammatory process along with the control of traditional risk factors [hypertension and cholesterol] may be beneficial in reducing the risk factors of renal and atherosclerotic involvement in SLE. Therapeutic approaches with drugs that target resistin might be useful in the treatment of SLE

Association of asymptomatic hyperuricemia and endothelial dysfunction in psoriatic arthritis

Cardiovascular disease is an increasingly recognized contributor to excess morbidity and mortality in psoriatic arthritis [PsA]. Traditional cardiovascular risk factors do not adequately account for the extent of cardiovascular disease in PsA. To examine the prevalence of subclinical atherosclerosis in patients with PsA to emphasize the potential role of serum uric acid on endothelial dysfunction, as an early predictor for atherosclerosis in PsA patients. This study included 60 PsA patients as well as 60 age and sex matched healthy controls. Assay of serum uric acid, interleukin-6 [IL-6] and soluble intercellular adhesion molecule-1 [sICAM-1] was done for all patients and controls. Patients were subjected to psoriasis area severity index [PASI] and assessment of disease activity. Patients and controls underwent brachial flow-mediated dilatation [FMD] assessment by color duplex sonography to determine endothelial dysfunction as well as extracranial carotid arteries assessment by high-resolution B-mode ultrasound to measure the common carotid intima-media thickness [CIMT] and the detection of atheromatous plaques. PsA patients have a high significant difference in CIMT, FMD of the brachial artery and mean levels of serum uric acid compared to healthy controls [p < 0.001]. PsA patients with hyperuricemia have a high significant difference in CIMT and FMD of the brachial artery than those with normal serum uric acid. Serum uric acid levels showed a high significant positive correlation with each of CIMT, disease duration, markers of inflammation [ESR, CRP, IL-6, sICAM-1], disease activity score in 28 joints [DAS 28] and PASI [r = 0.71, 0.893, 0.956, 0.858, 0.853, 0.877, 0.907, 0.847, respectively, as p < 0.001]. A high significant negative correlation was found between serum uric acid levels and FMD of the brachial artery as r = -0.634, p < 0.001. Patients with PsA have a high prevalence of subclinical atherosclerosis dependent on serum uric acid, suggesting that chronic systemic inflammation and endothelial dysfunction appear to be the link between asymptomatic hyperuricemia and atherosclerosis. Therefore, proper control of serum uric acid may play a preventive role in the development of atherosclerosis in PsA patients

Serum leptin concentration, bone mineral density and bone biochemical markers in a sample of Egyptian women: a possible relationship

Adipocytokines secreted by adipose tissue participate in bone metabolism; leptin is one of the circulating peptides secreted by adipose tissue. To determine the serum levels of leptin in obese postmenopausal women in order to correlate these levels with bone mineral density and bone biochemical markers to find out the role of leptin in bone metabolism. This was a cross-sectional study which included 37 obese postmenopausal women with body mass index [BMI] >30 kg/m[2]. Thirty-seven lean postmenopausal women with BMI <25 kg/m[2] were included as control group. Serum leptin, bone specific alkaline phosphatase [BAP], osteocalcin and urine C-telopeptide of type collagen [CTx] were assayed. Bone mineral density [BMD] and soft tissue body composition were determined using dual energy X-ray absorptiometry. There was a statistically highly significant increase in serum leptin levels in obese than lean postmenopausal women [p < 0.0001]. There was a highly significant decrease in BMD of spine and hip [p < 0.0001] in obese than lean postmenopausal women. After adjustment of fat mass, a highly significant positive correlation was found between leptin and BAP [r = 0.562, p < 0.0001], a significant positive correlation was found between leptin and each of osteocalcin and urine CTx [r = 0.423, 0.456 respectively, p < 0.05] but there was no statistically significant correlation between leptin and BMD. Our results support the hypothesis that leptin can act directly or indirectly on bone remodeling by modulating osteoblast activities. Leptin was found to be associated with decreased BMD at different sites of the body and was positively correlated with bone biochemical markers. However, leptin did not come out to be an independent predictor of BMD whereas; fat mass was found to have a role in bone metabolism in postmenopausal women. However these comparisons of a single measurement of leptin with BMD, does not exclude possible long-term strong relationships between leptin and BMD