Value of tumor necrosis factor-like weak inducer of apoptosis and chemokine CXC ligand 13 as biomarkers for disease activity in systemic lupus Erythematosus

Tumor necrosis factor -like weak inducer of apoptosis [TWEAK] triggers multiple cellular activities in a wide variety of cells, ranging from proliferation to cell death. It also causes upregulation of chemokine [C-X-C motif] receptor 5, and its ligand, chemokine [C-XC motif] ligand 13 [CXCL13]. However, the precise roles of TWEAK and CXCL13 in the pathogenesis of SLE and their association with disease activity still obscure. The study included forty SLE patients and twenty control subjects. SLE disease activity was evaluated by Systemic Lupus Erythematosus Disease Activity Index [SLEDAI] 2000 score. Anti-dsDNA antibodies, serum complement C3, high sensitivity CRP [hsCRP] concentrations, TWEAK and CXCL 13 serum concentrations were detected by ELISA. TWEAK mRNA expression in peripheral blood mononuclear cells was estimated by relative quantitative Real Time-PCR. Serum concentrations of TWEAK and CXCL13 were significantly elevated in SLE patients compared to controls [p < 0.05] with significant increase in patients with active SLE compared to those with inactive disease [p< 0.05], they also significantly correlated with SLEDAI score and anti-dsDNA antibodies. TWEAK mRNA levels increased significantly in active lupus compared to inactive disease. It can be concluded that TWEAK serum and expression levels together with its inducible chemokine CXCL13 serum levels may benefit as biomarkers for prediction of SLE disease activity, as well as possible targets for personalized therapies due to their involvement in the pathogenesis of SLE

Prevalence of peripheral neuropathy in Egyptian hepatitis C virus patients: correlation to some clinical and laboratory parameters

The present study was undertaken to assess prevalence and characteristics of peripheral neuropathy [PN] in Egyptian hepatitis C virus [HCV] patients. Eighty newly diagnosed HCV patients were enrolled, with 20 healthy volunteers. All were subjected to: full clinical examination, neurological examination, laboratory assessment including; routine blood tests, ESR, CRP, RF, ANA, C4, cryoglobulins [CGs], anti-GM1 antibodies, HCV antibodies, Quantitative PCR, abdominal ultrasonography, liver biopsy, and electrophysiological assessment. Thirty-six patients [45%] had clinical neuropathy, 18 patients [22.5%] had subclinical neuropathy. Thirty-eight out of the 54 PN patients [70.3%] showed axonal neuropathy which is mainly sensory affecting lower limbs. Twelve patients showed +ve cryoglobulinemia, all of them had neuropathy [10 clinical, 2 subclinical]. Abnormal titers of anti-neuronal antibodies were associated with electrophysiological abnormalities in 50 out of the 54 PN patients. PN correlated with age, disease duration, ESR, CRP, RF, HCV viraemia, CGs, anti-GM1 and hypocomplementinemia. PN exists in high prevalence among Egyptian HCV patients, and is associated with CG. It is mainly of axonal sensory type more affecting lower limbs. HCV patients should be investigated for the presence of CGs even in the absence of clinical manifestations

Assessment of lipid peroxidation and antioxidant status in rheumatoid arthritis and osteoarthritis patients

The aim of the present study was to assess the lipid peroxidation [LPO] and antioxidant status of patients with rheumatoid arthritis compared with osteoarthritis. This study included 30 RA, 30 OA patients and 15 healthy subjects. Parameters of activity of RA patients and clinical parameters of OA patients were assessed. Erythrocyte sedimentation rate [ESR], C reactive protein [CRP], serum malondialdehyde [MDA], the activities of erythrocyte superoxide dismutase [SOD] and catalase [CAT], glutathione [GSH] level, plasma glutathione-S-transferase [GST] activity and ceruloplasmin [Cp] level were measured. Increased MDA, plasma GST activity and Cp levels with reduction of the activities of SOD, CAT and GSH levels were demonstrated in RA and OA patients. A positive correlation was detected between the clinical and laboratory parameters in both RA and OA patients with GST and Cp. A direct correlation was found between previous parameters and serum MDA in RA. Meanwhile, a negative correlation was observed between these parameters with erythrocyte SOD, CAT activities and GSH level. Direct correlation also existed between MDA and GST with Cp, between erythrocyte SOD with CAT activities and negative correlations of GST activity with GSH level. Increased oxidative stress in RA and OA patients have led to compensatory changes in the levels of antioxidants. These changes provide additional protection against LPO. These findings confirm the role of oxidative stress in the pathogenesis of RA and OA, and that LPO markers and antioxidants can serve as surrogate markers for disease activity