SUMMARYWe have investigated the following pulmonary related parameters in 22 patients with Crohn's disease who were free of clinical pulmonary symptoms and had normal chest roentgenograms and in 25 controls: serum angiotensin converting enzyme, pulmonary function tests, bronchoalveolar lavage (lymphocyte count and subpopulations, macrophage viability and superoxide anion release by macrophages) and pulmonary scannings. Serum angiotensin converting enzyme was lower in Crohn's disease (14-1±5 1) than in controls (25-2±4-7) (p18% alveolar lymphocytes). Bronchoalveolar lavage lymphocytes subpopulations were quite variable. Twelve of 17 Crohn's disease (71%) had an increase spontaneous and/or stimulated superoxide anion production by alveolar macrophages. Six of 12 Crohn's disease (50%) had an increase physiologic dead space in the upper part of their lung against one of 11 controls (9%). These data suggest that most patients with Crohn's disease have a latent pulmonary involvement.Systemic manifestations are frequent in inflammatory bowel disease, but classically the lung was regarded as rarely involved. 1 2 A few recent reports, however, have described pulmonary manifestations occuring in patients with inflammatory bowel disease: bronchial suppuration, or bronchiectasis,3-5 granulomatous lung disease,6 diffuse or localised interstitial fibrosis71-2 and sulphasalazine pneumonitis. 1321 The rarity of pulmonary clinical manifestations contrasts with striking abnormalities of pulmonary function tests described in patients with inflammatory bowel disease: reduced lung transfer factor, increased residual volume, or decreased forced expiratory volume in one second.22 26We have attempted to determine the actual frequency of pulmonary tests and bronchoalveolar abnormalities in patients with Crohn's disease and without clinical or radiological pulmonary abnormalities.27 28 Furthermore, we tried to clarify
sCD146 is a novel marker of the endothelial intercellular junction that reflects endothelial remodeling more effectively than soluble CD31. Further studies are warranted to determine whether sCD146 will provide a serological assay reflecting alterations in vascular permeability and vessel proliferation in the inflamed IBD intestine.
Background:
Crohn’s disease is associated with vascular injury and dysregulation of the intestinal immune system which together can provide disturbance of mesenteric circulation functional properties.
Aim:
To evaluate the vascular reactivity of mesenteric arteries from patients with Crohn’s disease.
Methods:
Phenylephrine‐induced contractions were assessed from 10 patients with Crohn’s disease and 8 control organ donors. NG‐nitro‐L‐arginine‐methyl‐ester (L‐NAME) was used to test the presence of inducible NO synthase. Endothelium dependent and independent relaxation was assessed using acetylcholine, bradykinin, calcium ionophore A23187 and sodium nitroprusside.
Results:
The contractile response to phenylephrine was significantly decreased in arteries without endothelium from patients with Crohn’s disease. Exposure to the NO synthase inhibitor L‐NAME restored the contractile response to phenylephrine. Relaxation remained unaltered in both groups.
Conclusion:
These data provide direct evidence for fading of contraction caused by phenylephrine in Crohn’s disease. The restored mesenteric artery tone by a specific NO synthase inhibitor suggests that an increased production for NO in vascular smooth muscle might be responsible of this altered vascular reactivity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.