Prevalence of portal hypertensive duodenopathy in cirrhosis: clinical and haemodynamic features.

OBJECTIVES: To estimate the prevalence of portal hypertensive duodenopathy (PHD) in patients with cirrhosis and portal hypertension, and to evaluate its relationship with clinical and haemodynamic parameters. PATIENTS AND METHODS: Endoscopy reports and clinical history of 549 consecutive patients with cirrhosis and portal hypertension were evaluated retrospectively. A diagnosis of PHD was obtained in those patients with a congestive vascular pattern of the duodenum. RESULTS: PHD was found in 46 patients (8.4%). Previous endoscopic band ligation and coexistence of severe gastropathy were significantly more frequent in PHD group. Systemic and hepatic haemodynamic evaluations were performed in 20 patients with PHD and 160 without PHD: the mean hepatic venous pressure gradient was higher in those cases with PHD (22.5 (5.4) vs. 19.8 (5.5) mmHg, P=0.045). Hypertensive colopathy was found in seven out of the 10 patients with PHD and a colonoscopic evaluation. In five of six patients PHD disappeared after liver transplant. CONCLUSIONS: PHD is an uncommon finding of portal hypertension in cirrhotic patients. It is associated with previous endoscopic band ligation, to manifestations of portal hypertension in other sites of the gastrointestinal tract and to greater values of hepatic venous pressure gradient. The clinical relevance of this syndrome remains to be determined.

[Study of predictive factors of severe digestive lesions due to caustics ingestion]. / Estudio de los factores predictivos de lesiones digestivas graves tras la ingestión de cáusticos.

OBJECTIVE: Our purpose was to analyze the predictive factors of severe upper gastrointestinal injury by caustic substances in adult patients. PATIENTS AND METHOD: Retrospective study between February 1995 and February 2001 of adult patients who underwent an urgent upper endoscopy due to caustic ingestion. Endoscopic caustic ingestion criteria by Zargar et al were used to determine the degree of injury. We performed a univariate study of factors associated with sever digestive injury and, lately, a logistic regression analysis of predictive factors. Sensitivity, specificity, positive and negative predictive values of these factors were calculated. RESULTS: One hundred and fifty nine patients were included in the study, whose mean age was 48.9 (20.1) years and 49.7% were men. The more frequent caustic ingested was lye (47.8%). A severe caustic injury was found in urgent upper endoscopy in 18.4% of patients, which was located in esophagus in 14.6%, stomach in 8.2% and duodenum in 0.6% of cases. Male sex, voluntary ingestion, oropharingeal lesions, significant clinical symptoms and dishwasher and detergents ingestion were associated with severe upper gastrointestinal tract (GIT) injury. Voluntary ingestion, oropharingeal lesions and significant clinical symptoms at admission were independent predictive factors of severe GIT injury. The existence of one of these factors had an 89.7% of sensitivity while two or more displayed a specificity of 91%. CONCLUSIONS: Clinical and exploratory data may determine, before upper endoscopic procedure, the probability of severe GIT injury by caustic ingestion. Therefore, these data could play a significant role in the diagnostic, prognostic and therapeutic management of caustic ingestion.

The role of PPARgamma on restoration of colonic homeostasis after experimental stress-induced inflammation and dysfunction.

BACKGROUND & AIMS: Psychological stress has been implicated in the clinical course of several gastrointestinal diseases, but the mechanisms implicated and the effects of stress on the normal colon are not yet fully understood. METHODS: Male Wistar rats were exposed to various immobilization periods as a stress paradigm. Colon was processed to assess myeloperoxidase activity, nitric oxide synthase 2, cyclooxygenase 2, and peroxisome proliferator-activated receptor gamma (PPARgamma) expression and production of prostaglandins. Colonic permeability, bacterial translocation, tight junctions ultrastructure, and immunoglobulin (Ig) A levels were also evaluated. RESULTS: Exposure to acute (6 hours) immobilization stress produced an increase in myeloperoxidase activity and nitric oxide synthase 2 and cyclooxygenase 2 expression. All these parameters remained increased after 5 days of repeated stress exposure, showing a trend to normalize after 10 days. Levels of the anti-inflammatory eicosanoid 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) and expression of PPARgamma run parallel with these changes. Colonic epithelial barrier was altered after stress exposure, and a significant decrease in colonic IgA levels after acute stress exposure was observed. Pretreatment with PPARgamma agonists 15d-PGJ(2) and rosiglitazone prevented colonic inflammation and barrier dysfunction as well as the decrease of IgA production induced after acute stress; PPARgamma specific antagonist T0070907 reverted these effects. CONCLUSIONS: Activation of PPARgamma in rat colon in vivo seems to counteract colonic inflammation and dysfunction induced by stress. On the other hand, PPARgamma ligands may be therapeutically useful in conditions in which inflammation and barrier dysfunction takes place in colon after exposure to stress.

Activity of inducible and neuronal nitric oxide synthases in colonic mucosa predicts progression of ulcerative colitis.

OBJECTIVE: The present study analyzes inducible and neuronal nitric oxide synthase activity and expression in colonic mucosa of patients with ulcerative colitis, and correlates them with the progression of disease extent. METHODS: Thirty patients with ulcerative colitis were included. Synthases activity and expression were analyzed both in inflamed and noninflamed mucosa. After 2 yr, disease extent was determined and compared with extent at inclusion. RESULTS: Ca(2+)-independent activity, expressed as median with (interquartile range), in inflamed mucosa was higher than in noninflamed and control mucosa (102 (165-66), 24 (50-3), 1 (2.5-0.1) pmol.min(-1) mg prot(-1), respectively, p < 0.005), whereas Ca(2+)-dependent activity was significantly lower in inflamed than in noninflamed and control mucosa. Western blot analysis identified inducible and neuronal isoforms and confirmed these differences. Patients with more extended disease after 2 yr had higher levels of Ca(2+)-independent activity in noninflamed mucosa at inclusion and lower levels of Ca(2+)-dependent activity than patients with persistence of similar extent of inflammation (50 (78-29) vs 8 (30-0.1), p < 0.005; 51 (100-36) vs 150 (156-106), p < 0.05, respectively). Values of Ca(2+)-independent activity in noninflamed mucosa greater than 30 pmol. min(-1) mg prot(-1) showed 80% sensitivity and 87.5% specificity in the detection of patients with subsequent progression of disease extent, whereas values of Ca(2+)-dependent activity in noninflamed mucosa greater than 125 pmol. min(-1) mg prot(-1) showed 75% sensitivity and 80% specificity in the detection of patients with stability of disease extent. A ratio of Ca(2+)-independent/Ca(2+)-dependent activities over 0.29 showed 90% sensitivity and 87.5% specificity in the detection of patients with subsequent progression of extent. CONCLUSIONS: Our results show an up-regulation of inducible nitric oxide synthase and a down-regulation of neuronal isoform not only in inflamed mucosa but also in apparently healthy mucosa of patients with ulcerative colitis. The values of activity of both isoforms in apparently healthy mucosa could predict the disease extent after 2 yr follow-up.