Preclinical atherosclerosis and rheumatoid arthritis

Cardiovascular disease is an increasingly recognized contributor to excess morbidity and mortality in rheumatoid arthritis [RA]. Traditional cardiovascular risk factors do not adequately account for the extent of cardiovascular disease in RA. To study the relative impact of traditional versus non-traditional cardiovascular risk factors on endothelial dysfunction, as an early essential step for atherosclerosis, in patients with RA. Twenty five consecutive outpatients with RA were collected and compared to 15 healthy, age and sex matched controls.Both groups undergone assessment of traditional cardiovascular risk factors [high blood pressure, diabetes and smoking] as well as other non- traditional cardiovascular risk factors [hs CRP, ESR, serum ICAM] along with bilateral measurement of intima media thickness IMT of common carotid artery [IMT-CCA]. There was highly significant difference in T-chol /HDL [cardiac risk ratio] between the two groups [RA patients and controls]. Also there was a highly significant difference between the two groups as regards inflammatory markers [non-traditional risk factors], IMT and s-ICAM. RA patients with increased IMT-CCA had higher T-chol/ HDL [cardiac risk ratio] [P < 0.05], as well as high DAS and ESR [P < 0.01] compared to RA patients with normal IMT-CCA. Patients with positive RF had increased IMT-CCA [P < 0.05] and higher serum levels ICAM-1[P < 0.01] than those with negative RF. We also found that IMT-CCA was significantly positively correlated to markers of disease activity, while serum levels ICAM-1 was significantly positively correlated to disease duration. Patients with rheumatoid arthritis have a high prevalence of preclinical atherosclerosis independent of traditional risk factors, suggesting that chronic inflammation and disease severity are atherogenic to this population. That is why proper and strict control of disease activity may play a preventive role in this setting

SEN virus detection in Egyptian patients with chronic hepatitis C and hepatitis C related hepatocellular carcinoma

Abstract: SEN virus [SENV] is a single stranded DNA virus that belongs to the Circoviridae family. Nine genotypes [A-I] have been identified. Among them, it has been shown that two SENV genotypes [SENV-D and SENV-H] are significantly associated with transfusion-associated non-A-E hepatitis. The exact role of this virus in the pathogenesis of chronic liver disease, including chronic hepatitis and the development of hepatocellular carcinoma [HCC] remains to be established. Aim of work: to invesigate the presence of SENV-D and SENV-H viremia among Egyptian patients with chronic hepatitis C and hepatitis C virus [HCV] related hepatocellular carcinoma [HCC] and to assess its possible implications

Subjects and Methods: Using polymerase chain reaction [PCR] amplification to detect SENV-D and SENV-H strains in serum, we investigated SENV viremia in 43 patients with chronic liver disease [chronic hepatits C], 25 hepatits C virus related HCC and 25 community based individuals as a control group

Results: SENV-H strain was detected in 18/43[42%] of chronic hepatitis C patients, 11/25 [44%] of HCV related HCC patients compared to 4/25 [16%] of the controls. The difference was statistically significant between patients with Chronic viral hepatitis C and the controls [P=0.0338] and between patients with HCC and the controls [P=0.031]. SENV-D strain was detected only in 7/43 [16%] of the chronic viral hepatitis C cases, 6/25 [24%] of HCC compared to 2/25 [8%] of the controls and the difference was ststistically insignificant between the three studied groups. A statistical insignificant difference was found between SENV positive and SENV negative community based subjects regarding age, sex and ALT level No difference between SENV-infected and non-infected liver patients was demonstrated with respect to ALT level, serum bilirubin, albumin level and prothrombin time

Conclusion: SENV infection is frequent among patients with chronic liver disease and HCC. SENV, at least genotypes D and H are not associated with increased evidence of liver diseases and do not increase the risk for hepatocellular carcinoma in chronic hepatitis C patients

Plasma osteopontin concentration in lupus nephritis

To measure plasma concentration of osteopontin and to correlate these levels with clinical, laboratory, disease activity and histopathological parameters in SLE patients. This study was performed on 20 SLE patients and 10 normal control subjects. Plasma osteopontin concentrations were measured by ELISA technique for both patients and control groups. All patients underwent renal biopsies within 3 months of onset of proteinuria or hematuria. There was a highly significant difference between patients and control groups as regards plasma osteopontin concentration [p<0.001]. There was a significant positive correlation between osteopontin and SLEDAI [p<0.001] and activity index of renal biopsies [p<0.05]. Also there was a highly significant differences as regard osteopontin plasma concentration between patients with and without renal affection [p<0.001]. Osteopontin has been shown at least partly to account for SLE nephritis probably through predominance of Th[1]-type response in both peripheral and renal tissue. Further investigation of this mechanism in lupus nephritis may allow the design of new therapeutic strategies of lupus nephritis such as manipulation of Th[1]/Th[2] and down-regulation of Th[1]-response

Serum vascular endothelial growth factor in collagen diseases: correlation with disease activity

A role for angiogenic factors such as vascular endothelial growth factor [VEGF] in the pathogenesis of collagen diseases through endothelial cell modulation has been suggested. Assessment of serum VEGF level in rheumatoid arthritis [RA], systemic sclerosis [SSc] and systemic lupus erythematosus [SLE] patients to elucidate the potential involvement of VEGF in the pathogenesis of these diseases. Also, to find out a relation between its serum level and the disease activity or the functional impairment in those patients The serum level of VEGF was assessed in 10 RA patients; 10 SSc patients; 10 SLE patients as well as 10 healthy volunteers. Its level was correlated to the different clinical and laboratory parameters of disease activity and functional impairment in the patients. When compared with the control group, each group of patients showed a significantly higher concentration [p<0.001] of serum VEGF. A statistically significant correlation was found between this higher concentration and disease activity in RA and SLE patients as well as the development of lung fibrosis in SSc patients. The results of this study suggest that angiogenesis produced by VEGF may play an important role in the pathogenesis of collagen diseases. Measurement of serum VEGF reflects the disease activity in RA and SLE patients as well as increased frequency of lung fibrosis in SSc patients. In addition, inhibition of VEGF either by drugs or receptor antagonism may improve the clinical manifestations or decrease the progress of these diseases. However, further studies are needed to elucidate the exact role of VEGF in relation to other cytokines involved in the pathogenesis of collagen diseases

Soluble urokinase plasminogen activator receptor in plasma and synovial fluid of rheumatoid arthritis and knee osteoarthritis

To determine the level of soluble urokinase plasminogen activator receptor [suPAR] in the plasma and synovial fluid of rheumatoid arthritis [RA] patients and osteoarthritis [OA] patients in comparison to normal healthy subjects, in order to find out its possible role in the pathogenesis of these diseases and to detect whether it can be used as a marker of disease activity and severity. Our study was conducted on 53 subjects. 23 rheumatoid arthritis [RA] patients, 20 patients having knee osteoarthritis [OA] and 10 healthy subjects served as the control group. suPAR level in plasma and synovial fluid of all subjects was measured by ELISA technique. The mean value of soluble urokinase plasminogen activator receptor [suPAR] in plasma and synovial fluid of RA patients was highly significantly increased in comparison to OA patients and healthy subject [p<0.001]. The mean value of plasma suPAR level was also higher in OA patients than healthy subjects but no significant difference was found between them [p>0.05]. While its value in the synovial fluid was significantly increased in OA patients than healthy subjects. Also, no significant difference was found between plasma and synovial fluid suPAR level in RA, and the control group [p>0.05]. While a highly significant difference in its level was found between them in OA patients. There was a significant positive correlation between plasma and synovial fluid level of suPAR and age, duration of disease and disease severity in RA patients. While no significant correlation was found in RA patients between both plasma and synovial fluid level of suPAR and sex, rheumatoid factor sero reactivity, tenderness, swelling [or any of the clinical data], ESR, disease activity index and type of drug received. Also no significant correlation was found between synovial fluid level of suPAR in OA patients and age, and disease severity. A significant positive correlation was found between plasma and synovial fluid level of suPAR in RA patients. The highly significant in crease in the level of suPAR in both plasma and synovial fluid of RA patients compared to other studied groups and the significant correlation between both plasma and synovial fluid suPAR level and disease severity may clarify its possible role in the pathogenesis of RA and may reflect the destructive and erosive nature of this disease. So suPAR appears to be a useful marker that reflects disease severity in RA patients. Also the significant increase in the synovial fluid suPAR level in OA patients in comparison to the control group suggest that alterations in the PA/PAR system also occur in OA and thus might contribute to the pathogenesis of this disease. Since there was no significant difference in the level of suPAR between plasma and synovial fluid, therefore we suggest measuring plasma suPAR only. Also no correlation was found between plasma and synovial fluid suPAR level and disease activity. This needs further extended studies to confirm this result, as it will determine the value of suPAR as a marker of disease activity