CD95 and BCL-2 expression as apoptotic markers in rheumatoid arthritis patients

Dysregulation of apoptosis of the different immune cells including the peripheral blood mononuclea, cells [PBMNC], lymphocytes have been incriminated as a pathogenetic factor in rheumatoid arthrjts [RA]. CD95 [Fas] as a death receptor and Bcl-2 as an antiapoptotic protein are among the important factors responsible for controlling lymphocytes apoptosis. To assess the expression of CD95 and Bcl-2 as apoptotic markers in PBMNs in RA patients and correlate them with RA activity and functional capacity of RA patients. Twenty RA patients and 10 healthy controls were included in this study. All patients were maintained on 7.5 mg methotrexate /week and concomitant NSAIDs. All patients were examined clinically and disease activity measures including Ritchie articular index [RAI] and the number of swollen joints [SW44] were assessed and disease activity score [DAS] was calculated for each patient. Health assessment questionnaire [HAQ] was also determined. CD95 and Bcl-2 expression on the PBMNC were assessed in serum samples by flow cytometry in patients and controls, in addition to complete blood count, Rose Waaler test and ESR. Plain X-ray for both hands was also performed for all patients to detect joint erosions. The mean CD95 expression on PBMNC was significantly higher in RA patients compared to healthy controls [t=3.222, P= 0.004]. CD95 was also significantly and positively correlated with RAI, [DAS] and [ESR] [r=0.463, r=0.736, r=0.542 respectively and P<0.05 for all]. There was no statistically significant difference regarding the mean expression of Bcl-2 in RA patients and controls [t=0.122, P>0.05]. It did not also correlate with any of the studied variables. Increased CD95 expression on PBMNC in RA patients seems to be related to the inflammatory process [disease activity] in rheumatoid disease rather than to the apoptotic process as it is correlated with disease activity measures of the studied patients. Moreover, the normal expression of Bcl-2 in PBMNC indicated that the possibility of dysregulation of apoptosis in this study is unlikely

Transforming growth factor beta 1 gene [T869C] polymorphism in rheumatoid arthritis: association with disease severity

The aim of the work is to investigate the possible association of polymorphism in the transforming growth factor beta-1 [TGF beta 1] gene with the disease severity in rheumatoid arthritis. The study was conducted on 50 patients with rheumatoid arthritis [group I] diagnosed according to the American College of Rheumatology [ACR]. They were divided according to the activity of the disease [Ritchieis articular index-RAI- and ESR] into: Active group [group A]: 29 RA patients with signs of activity [having RAI >/= 16 and ESR >/= 30 mm/h]. In-active group [group B]: 21 RA patients without signs of activity [having RAI

IL-6 and thyroid hormones in critically ill patients with sepsis

The aim of this study was to investigate whether the activation of the cytokine system, in particular, activation of interleukin-6 production, has a role in pathogenesis of thyroid hormones changes in critically ill patients with sepsis. Thirty one patients with sepsis were studied at the Critical Care Medicine department at Alexandria Main University Hospital. Clinical evaluation of the severity of illness was done using sepsis related organ failure score [SOFA score]. Blood samples were obtained within 6 hours after admission and were collected with EDTA. Plasma was separated by centrifugation at 3000rPM for 10 minutes and stored at -80°C until assayed. 10 blood samples were obtained from healthy volunteers [5 males and 5 females] as control group. These plasma samples were used for measurement of inerleukin-6 [IL-6], free thyroxine [fT4], free triiodothyronine [f T[3]] and thyroid stimulating hormone [TSH]. Serum interleukin-6 level was significantly higher in patients with sepsis than control group [mean +/- SD was 100.904 +/- 10.941 pg/ml versus 26.652 +/- 5.125 pg/ml respectively, P = 0.0001*]. The patients were divided into 4 groups according to SOFA score. It was found that fT3 and FT4 levels were significantly decreased with increased severity of sepsis [F= 20.306, P=.000* and F= 7.025, P= .001* respectively], while serum levels of IL-6 were increased significantly with the increased severity of sepsis [F =18.55, p =.000*]. A significantly positive correlation was found between IL-6 and SOFA score, [r = .823, P .000*] while significantly negative correlation was found between levels of fT3 and serum IL-6 levels and SOFA score, [r= -.887, P = .000* and r = -.866, P= .000* respectively]. Also, a significant negative correlation was found between levels of fT4 and serum IL-6 levels and SOFA score [r= -.597. P =.000* and r= -.579, P = .000* respectively]. Also, there was a negative correlation between TSH, IL-6 and SOFA score levels but significant only with IL-6 levels [r= -0.407, P= .023* and r= -.0085, P= 0.649 respectively.] This study demonstrated that there is a positive correlation between serum level of IL-6 and severity of sepsis as it was significantly increased with increased SOFA score. While fT3, fT4 and TSH levels are significantly decreased with increased levels of IL-6. So, these suggest that the activation of the cytokine system, in particular, activation of interleukin-6 production, has a role in pathogenesis of thyroid hormones changes in critically ill patients with sepsis

Soluble tumor necrosis factor receptor -2 in acute coronary heart diseases

The aim of this study was to evaluate the impact of soluble tumor necrosis factor receptor -2 in acute coronary heart diseases. This prospective study had been carried on 30 patients with acute coronary heart diseases [group I] admitted consecutively in the critical care medicine department at Alexandria main university hospital. Demographic data and medical history had been taken. Thorough clinical examination, Troponin, CKMB, ECG, x ray chest and echocardiography had been done for each patient on admission. In addition, samples of plasma had been taken from each patient and also, from 10 healthy volunteers of matched age and sex [control group] [group II] to determine plasma level of soluble tumor necrosis factor receptor -2 [sTNFR-2] by ELISA test. Plasma level of sTNFR-2 in group [I] was significantly higher than the group [II], [mean +/- SD was 15.315 +/- 8.909 versus 5.03 +/- 2.01ng/ml respectively, t=5.22. p = 0.0001*]. It was found non significant positive correlation between both ejection fraction [EF] and fraction shorting [FS] [left ventricular systolic function] and sTNFR-2, [r=0.121, p=0.526, r=0.293 and p=0.116 respectively]. Non significant, negative correlation was found between both early filling left ventricle/late filling left ventricle [E/A ratio] [left ventricular diastolic function] and mitral valve regurgitation [MR] and sTNFR-2 [r=- 0.108, p=0.569, r=-0.320 and p=0.085 respectively]. A negative significant correlation was found between wall motion score index [WMSI] and sTNFR-2 [r=-0.419, p=0.021*]. Measurement of sTNFR-2 may be of value in evaluation of the TNF system in acute coronary heart diseases. sTNFR-2 is increased in acute coronary heart diseases and may modulate the in vitro cytotoxicity of TNF. In this work, it is not clear whether the elevation of sTNFR-2 in acute coronary heart diseases is due to an actual increase or to a reduced breakdown or elimination of these receptors. Further explorations are needed to more precisely define the meaning, molecular basis, and interaction ofsTNFR-2 and TNF