炎症性肠病患者的肿瘤坏死因子-α与微量白蛋白尿

Tumour necrosis factor-alpha and microalbuminuria in patients with inflammatory bowel disease.

作者信息

Mahmud N, O'Connell M A, Stinson J, Goggins M G, Weir D G, Kelleher D

机构信息

Department of Clinical Medicine, Trinity College, Trinity Centre for Health Sciences, St James's Hospital, Dublin, Ireland.

出版信息

Eur J Gastroenterol Hepatol. 1995 Mar;7(3):215-9.

PMID: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.

摘要

目的

确定肿瘤坏死因子-α（TNF-α）在炎症性肠病（IBD）患者微量白蛋白尿发病机制中是否起重要作用。

患者与方法

我们检测了48例IBD患者的血清TNF-α、白细胞介素（IL）-6、红细胞沉降率（ESR）、C反应蛋白（CRP）水平及微量白蛋白尿。采用酶联免疫吸附测定法检测血清TNF-α，采用免疫比浊法检测微量白蛋白尿。使用Harvey和Bradshaw简单指数对临床疾病活动度进行量化。

结果

IBD患者的微量白蛋白尿比对照组更严重，且活动期患者比非活动期患者更严重。IBD患者的TNF-α水平高于对照组（分别为平均±标准误16.4±1.4与6.6±1.3 pg/ml；P<0.01），活动期IBD患者高于非活动期患者（分别为平均±标准误20.1±2与12.8±2.7 pg/ml；P=0.056）。微量白蛋白尿与TNF-α（r=0.60；P<0.009）、ESR（r=0.67，P<0.02）和CRP水平（r=0.935，P<0.001）密切相关。TNF-α与CRP显著相关（r=0.54，P<0.01）。IBD患者的IL-6水平显著升高（7±4 pg/ml，对照组未检测到；P<0.05）。活动期IBD患者的IL-6水平高于非活动期患者（分别为平均±标准误13±8与0.90±0.35 pg/ml；P<0.05）。然而，IBD患者的IL-6水平与微量白蛋白尿无相关性（r=0.105，P=0.256）。