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  • Title: Tumour necrosis factor-alpha and microalbuminuria in patients with inflammatory bowel disease.
    Author: Mahmud N, O'Connell MA, Stinson J, Goggins MG, Weir DG, Kelleher D.
    Journal: Eur J Gastroenterol Hepatol; 1995 Mar; 7(3):215-9. PubMed ID: 7743302.
    Abstract:
    OBJECTIVE: To determine whether tumour necrosis factor-alpha (TNF-alpha) is important in the pathogenesis of microalbuminuria in patients with inflammatory bowel disease (IBD). PATIENTS AND METHODS: We measured serum TNF-alpha, interleukin (IL)-6, the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) levels and microalbuminuria in 48 patients with IBD. Serum TNF-alpha was measured by enzyme-linked immunosorbent assay and microalbuminuria was measured using an immunoturbiditimetric method. Clinical disease activity was quantified using the simple index of Harvey and Bradshaw. RESULTS: Microalbuminuria was more severe in patients with IBD than in controls, and in patients with active versus inactive disease. TNF-alpha levels were higher in patients with IBD than in controls (mean +/- SE 16.4 +/- 1.4 versus 6.6 +/- 1.3 pg/ml, respectively; P < 0.01) and in patients with active versus inactive IBD (means +/- SE 20.1 +/- 2 versus 12.8 +/- 2.7 pg/ml; respectively P = 0.056). Microalbuminuria correlated strongly with TNF-alpha (r = 0.60; P < 0.009), ESR (r = 0.67, P < 0.02) and CRP levels (r = 0.935, P < 0.001). TNF-alpha correlated significantly with CRP (r = 0.54, P < 0.01). IL-6 levels were raised significantly in patients with IBD (7 +/- 4 pg/ml, controls undetectable; P < 0.05). Patients with active IBD had higher IL-6 levels than those with inactive IBD (mean +/- SE 13 +/- 8 versus 0.90 +/- 0.35 pg/ml, respectively; P < 0.05). However, IL-6 levels did not correlate with microalbuminuria in patients with IBD (r = 0.105, P = 0.256). CONCLUSIONS: Our findings suggest that TNF-alpha may be important in the pathogenesis of microalbuminuria in patients with IBD, possibly through TNF-induced damage to the glomerular basement membrane. The mechanism for this has not been defined but may relate to TNF-induced disruption of sulphated glycosaminoglycans.
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