Plasma Homocysteine: s marker for coronary atherosclerosis and endothelial dysfunction in rheumatiod arthritis?

The aim of the present work is to assess total homocysteine level [tHcy] in rheumatoid arthritis [RA] patients and its relation to the presence of coronary atherosclerosis and endothelial dysfunction. Subjects and 20 female patients with rheumatoid arthritis and 10 healthy control subjects matched for age and sex were subjected to estimation of total plasma homocysteine concentration by high performance liquid chromatography and fluroscent detection, and von Willebrand factor [vWF], a reliable marker of endothelial cell dysfunction using ELISA technique. Intimal-medial thickness, peak systolic and diastolic velocities in the common carotid artery were measured using Duplex ultrasound, and resistance index was calculated. The results revealed significant increase in total homocysteine level in rheumatoid patients as compared to normal controls [31.33 +/- 14.4 versus 12.5 +/- 2.08, P<0.05] with no significant difference between patients with ischaemic heart disease and without. Also, von Willebr and factor was significantly higher in patients as compared to controls [2.01 +/- 0.5 versus 1.5 +/- 0.3, P<0.05] with positive correlation between homocysteine level and vWF [r=0.881]. Duplex ultrasound evaluation demonstrated mean intima-media thickness wich was significantly greater in RA patients as compared to the control group [0.63 +/- 0.1 versus 0.3+0.6, P<0.05] and positively associated with [tHcy] level [r=0.836310] with high resistance index [62.6 +/- 19.48]. Conclusions: RA patients have fasting hyperhomocysteinemia, which may be a marker for premature atherosclerosis and endothelial dysfunction. Further studies are needed to determine the clinical impact of homocysteine lowering therapy

Osteoporotic changes in Egyptian cirrhotic patients

Aim: Hepatic osteodystrophy occurs in most patients with chronic liver disease. Subjects and In this study, bone density, measured by dual energy X-ray absorptiometry [DEXA], and some biochemical markers of bone turnover were studied in 30 Egyptian schistosomal patients classified equally into 3 groups according to the Child-Pugh score of severity of liver disease. Patients showed significant reduction of BMD in both lumbar spine and femoral neck [LS: -2.87 +/- 1.39; FN: -0.54 +/- 1.13, p< 0.001]. Osteoporosis was found in 56.7% of patients. Urinary D-Pyr/cr, as a marker of bone resorption, showed marked significant increase in Child B and C patients [p<0.001], while serum B-AP and serum PICP, as markers of bone formation, showed less changes. Serum B-AP was significantly increased in the patient group [p<0.05], while serum PICP was insignificantly decreased in patients as compared to controls. The rate of bone loss, determined by the ratio of urinary D-Pyr/cr to PICP, was increased in Child A, B, and C patients. Serum testosterone was significantly decreased in both Child B and C patients and was markedly decreased in the whole patient group [p<0.001]. Conclusions: These results suggest that increased bone resorption is the predominant cause of hepatic osteodystrophy and its risk increases with the severity of liver disease. It also provides bone biomarkers as useful alternatives to bone biopsy in evaluating hepatic bone changes