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مرض كرون Crhon's Disease

Page history last edited by Dr.Ahmed Abdulaziz Nouman 10 years, 4 months ago

Mural inflammation in Crohn disease: location-matched histologic validation of MR imaging features.

Punwani S, Rodriguez-Justo M, Bainbridge A, Greenhalgh R, De Vita E, Bloom S, Cohen R, Windsor A, Obichere A, Hansmann A, Novelli M, Halligan S, Taylor SA.

Department of Specialist X Ray, University College London Hospitals National Health Service Foundation Trust, 235 Euston Rd, Podium Level 2, London NW1 2BU, England.

PURPOSE: To validate proposed magnetic resonance (MR) imaging features of Crohn disease activity against a histopathologic reference. MATERIALS AND METHODS: Ethical permission was given by the University College London hospital ethics committee, and informed written consent was obtained from all participants. Preoperative MR imaging was performed in 18 consecutive patients with Crohn disease undergoing elective small-bowel resection. The Harvey-Bradshaw index, the C-reactive protein level, and disease chronicity were recorded. The resected bowel was retrospectively identified at preoperative MR imaging, and wall thickness, mural and lymph node/cerebrospinal fluid (CSF) signal intensity ratios on T2-weighted fat-saturated images, gadolinium-based contrast material uptake, enhancement pattern, and mesenteric signal intensity on T2-weighted fat-saturated images were recorded. Precise histologic matching was achieved by imaging the ex vivo surgical specimens. Histopathologic grading of acute inflammation with the acute inflammatory score (AIS) (on the basis of mucosal ulceration, edema, and quantity and depth of neutrophilic infiltration) and the degree of fibrostenosis was performed at each site, and results were compared with MR imaging features. Data were analyzed by using linear regression with robust standard errors of the estimate. RESULTS: AIS was positively correlated with mural thickness and mural/CSF signal intensity ratio on T2-weighted fat-saturated images (P < .001 and P = .003, respectively) but not with mural enhancement at 30 and 70 seconds (P = .50 and P = .73, respectively). AIS was higher with layered mural enhancement (P < .001), a pattern also commonly associated with coexisting fibrostenosis (75%). Mural/CSF signal intensity ratio on T2-weighted fat-saturated images was higher in histologically edematous bowel than in nonedematous bowel (P = .04). There was no correlation between any lymph node characteristic and AIS. CONCLUSION: Increasing mural thickness, high mural signal intensity on T2-weighted fat-saturated images, and a layered pattern of enhancement reflect histologic features of acute small-bowel inflammation in Crohn disease.

PMID: 19635832 [PubMed - indexed for MEDLINE]

Smoking and inflammatory bowel diseases: what in smoking alters the course?

El-Tawil AM.

Department of Surgery, University Hospital of Birmingham, Birmingham, UK, atawil20052003@yahoo.co.uk.

Epidemiological studies provide strong evidence to confirm the correlation between cigarette smoking and inflammatory bowel diseases. This relationship is proved to be positive in Crohn's disease and negative in ulcerative colitis. What in smoking alters the course of inflammatory bowel diseases is still a mystery. Different smoking parts have different and may be opponent actions. Smoking has dual effects. Some of its activities are, sometimes, constructive as they are working in an antagonistic manner to the mechanism of the disease, such as reducing rectal blood flow and accordingly less recruitments of inflammatory mediators to the area of inflammation, enhancement of mucosal production, and consequently, strengthening the membranes, and inhibition of pro-inflammatory mediators' liberation and activity in subjects with ulcerative colitis. Yet the outcome of smoking actions may be affected by the existence of other cofactors. Odd factors, such as shortage of zinc in subjects with Crohn's disease, may facilitate liberation of pro-inflammatory mediators and their activities and accordingly exacerbates symptoms.

PMID: 20333390 [PubMed - as supplied by publisher]

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