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Articles by M.A. Mohsen
Total Records ( 2 ) for M.A. Mohsen
  M.A. Mohsen , A.A. Afifi and I. Al-Bagoury
  Generalized bone loss in rheumatoid arthritis (RA) is attributable to several possible factors including inflammatory disease itself. This study was performed to investigate the effect of inflammation on bone mineral density (BMD) and bone turnover in premenopausal women with RA. Thirty two consecutive premenopausal non-steroid user RA female patients without functional impairment and 15 healthy controls were studied. Disease activity was scored using the Activity Score of 28 joints (DAS-28). BMD of lumbar spine and femoral neck was assessed by dual energy x-ray absorptiometry. Urinary excretion rates of bone resorption markers, free pyridinoline (f-PYD) and free deoxypyridinoline (f-DPYD) were assayed. Pro-inflammatory cytokines, IL-1, IL-6, TNF-α and C-reactive protein (CRP) were dosed in blood. Significant lower BMD values in lumbar spine and left femoral neck (p<0.01, <0.001, respectively) and significant higher levels of IL1, IL6, TNF-α and CRP were observed in RA patients versus healthy controls. BMD at lumbar spine and left femoral neck was inversely correlated with DAS-28, CRP and TNF-α levels. BMD at femoral neck was inversely correlated with disease duration (r = -0.463). Urinary f-PYD was positively correlated with DAS-28, CRP and IL-6 (r = 0.624, 0.543, 0.657, respectively) while inversely correlated with BMD at femoral neck (r = -0.6826). In conclusion, elevated pro-inflammatory cytokines, high disease activity and less extent disease duration, appear to be critical determinant for much of systemic bone loss in RA. Urinary f-PYD reflects bone resorption more selectively than f-DPYD. Control of biological activity of IL-6 may be a therapeutic approach to control osteoporosis in RA.
  M.A. Mohsen , S.A. Abdel Karim , W.A. Sultan and T.M. Abbas
  Kidney involvement in systemic lupus erythematosus (SLE) is life threatening complication. Urinary N-acetyl-beta-D glucosaminidase (uNAG) activity has emerged as potentially useful early marker of renal tubular injury. The uNAG excretion was investigated in 72 SLE patients to assess tubular dysfunction and determine its relationship with disease activity and pathological classes of lupus nephritis (LN). SLE patients were divided into two groups: 41 patients with LN and 31 patients without evidence of nephritis. Disease activity was assessed by SLEDAI. Renal disease activity was measured by the Systemic Lupus International Collaborating Clinics Renal Activity Score. uNAG levels were measured using colorimetric assay kit and compared to 25 healthy controls. Renal biopsies were performed for LN patients and glomerular lesions were classified according to WHO criteria. Severity of tubulointerstitial involvement was also assessed. The uNAG activity was significantly higher in LN patients than in lupus non nephritis patients and healthy controls (both p<0.001). Tubular dysfunction with elevated uNAG was present in 6 lupus non-nephritis patients with no evidence of glomerular disease. There was positive significant relation between uNAG and proteinuria (p<0.005) and renal activity score (p<0.001) in LN patients. Conversely, uNAG excretion was not significantly correlated with SLEDAI, WHO classes of nephritis and tubulointerstitial index. In conclusion, increased uNAG activity in lupus non-nephritis patients may predict the development of LN prior to the onset of proteinuria. Increased uNAG activity parallels the degree of renal disease activity in LN patients and is probably more sensitive indicator of tubulointerstitial disease.
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