[Collagenous gastritis and ileo-colitis occurred in autoimmune context: report of a case and review of the literature]. / Gastrite collagène et iléocolite collagène survenant dans un contexte dysimmunitaire: à propos d'un cas et revue de la littérature.

Collagenous colitis belongs to the group of microscopic colitis. The aetiology and pathogenesis are unknown but different pathogenic hypothesis, autoimmune, infectious, alimentary and medicinal being are advanced, the last one being the most frequent aetiology. The collagenous gastritis is a rare entity and its association with collagenous colitis was exceptionally reported, only six cases being published. We report the seventh case of collagenous gastritis, ileitis and colitis in a 75-year-old woman with chronic diarrhea and important weight loss. This thickened subepithelial collagen band was appeared in an autoimmune injury context with antecedent of Hashimoto's thyroiditis and probably chronic atrophic Biermer's gastritis. The clinical and histological evolution was favourable with budesonide.

High prevalence of small intestinal bacterial overgrowth in patients with morbid obesity: a contributor to severe hepatic steatosis.

BACKGROUND: With the increasing prevalence of obesity, non-alcoholic fatty liver disease (NAFLD) has become a major cause of liver diseases. Small intestinal bacterial overgrowth (SIBO) could be related to NAFLD. Our aim was to determine the prevalence of SIBO and its relationship with liver lesions in morbidly obese patients. METHODS: A glucose hydrogen (H(2)) breath test (positive if fasting breath H(2) concentration > 20 ppm and/or an increase of > 10 ppm over baseline within the first 2 h) was performed in obese patients referred for bariatric surgery (body mass index [BMI] > 40 kg/m(2) or > 35 in association with comorbidities) and in healthy non-obese subjects. In obese patients, a surgical liver biopsy was performed. RESULTS: One hundred and forty-six patients (129 women, age [mean+/-SE]: 40.7 +/- 11.4 years) were prospectively included in the study. The mean BMI was 46.1+/-6.4 kg/m(2). A liver biopsy was available in 137 patients and a breath test in 136. The frequency of positive breath tests was higher in obese patients (24/136, 17.1%) than in healthy subjects (1/40, 2.5%; P=0.031). In the univariate analysis, SIBO was not associated with clinical variables, but tended to be associated with more frequent severe hepatic steatosis (26.3 vs. 10.3%, P=0.127), whereas the frequency of sinusoidal or portal fibrosis, lobular necrosis and non-alcoholic steatohepatitis (NASH) were not different. In the multivariate analysis, SIBO (P=0.005) and the presence of a metabolic syndrome (P=0.006) were independent factors of severe hepatic steatosis. CONCLUSION: In morbidly obese patients, bacterial overgrowth prevalence is higher than in healthy subjects and is associated with severe hepatic steatosis.

The V249I polymorphism of the CX3CR1 gene is associated with fibrostenotic disease behavior in patients with Crohn's disease.

OBJECTIVES: CX3CR1, the receptor of CX3CL1/fractalkine, is involved in regulation of inflammatory response and the CX3CR1-I249-M280 naturally occurring mutants are associated with altered binding to the ligand. Our aim was to evaluate the frequency of CX3CR1 V249I and T280M polymorphisms and NOD2/CARD15 mutations in Crohn's disease patients and to search for a relationship with phenotype. METHODS: Clinical data were retrospectively collected. V249I and T280M polymorphisms of CX3CR1 gene and NOD2/CARD15 mutations (R702W, G908R, 3020InsC) were identified. RESULTS: Two hundred and thirty-nine patients (140 females, 39.7+/-14.1 years) were included. About 37.4% were heterozygous and 8.8% were homozygous for the V249I CX3CR1 polymorphism, 18.1% were heterozygous and 1.3% homozygous for the T280M CX3CR1 polymorphism and 35.9% had at least one of the three mutations of NOD2/CARD15. The T280M CX3CR1 polymorphism was not associated with any phenotype. In univariate analysis, stenosis was significantly associated with both V249I CX3CR1 polymorphism and 3020InsC NOD2/CARD15 mutations. In smoker patients carrying the CX3CR1 allele I249, there was a significant increase in the frequency of fibrostenosing disease [P=0.005, odds ratio (OR): 3.25] whereas this relationship disappeared in the group of nonsmokers (P=0.72). In multivariate analysis, 3020InsC NOD2/CARD15 mutations and the V249I CX3CR1 polymorphism were independent risk factors for intestinal stenosis (P=0.046, OR: 1.8 and P=0.044, OR: 2.4, respectively). CONCLUSION: In Crohn's disease, V249I CX3CR1 polymorphism is associated with intestinal strictures, particularly in smokers. This association is independent of CARD15 mutations.

Relationship between obstructive sleep apnea and liver abnormalities in morbidly obese patients: a prospective study.

BACKGROUND: Morbid obesity is a risk factor of nonalcoholic steatohepatitis (NASH). Obstructive sleep apnea (OSA) could also be an independent risk factor for elevated liver enzymes and NASH. The relationships between liver injuries and OSA in morbidly obese patients requiring bariatric surgery were studied prospectively. METHODS: Every consecutive morbidly obese patient (BMI > or =40 kg/m2 or > or =35 kg/m2 with severe comorbidities) requiring bariatric surgery was included between January 2003 and October 2004. Polygraphic recording, serum aminotransferases (ALT, AST), gamma-glutamyltransferase (GGT) and liver biopsy were systematically performed. OSA was present when the apnea-hypopnea index (AHI) was >10/h. RESULTS: 62 patients (54 F; age 38.5 +/- 11.0 (SD) yrs; BMI 47.8 +/- 8.4 kg/m2) were included. Liver enzymes (AST, ALT or GGT) were increased in 46.6%. NASH was present in 34.4% and OSA in 84.7%. Patients with OSA were significantly older (P = 0.015) and had a higher BMI (P = 0.003). In multivariate analysis, risk factors for elevated liver enzymes were the presence of OSA and male sex. The presence of NASH was similar in patients with or without OSA (32.7% vs 44.4% of patients, P = 0.76). CONCLUSION: In this cohort of morbidly obese patients requiring bariatric surgery, one-third of patients had NASH, a prevalence similar to previous studies. OSA was found to be a risk factor for elevated liver enzymes but not for NASH.

Gastro-esophageal reflux and esophageal motility disorders in morbidly obese patients before and after bariatric surgery.

BACKGROUND: Obesity is a predisposing factor to gastro-esophageal reflux disease (GERD), but esophageal function remains poorly studied in morbidly obese patients and could be modified by bariatric surgery. METHODS: Every morbidly obese patient (BMI > or =40 kg/m2 or > or =35 in association with co-morbidity) was prospectively included with an evaluation of GERD symptoms, endoscopy, 24-hour pH monitoring and esophageal manometry before and after adjustable gastric banding (AGB) or Roux-en-Y gastric bypass (RYGBP). RESULTS: Before surgery, 100 patients were included (84 F, age 38.4 +/- 10.9 years, BMI 45.1 +/- 6.02 kg/m2), of whom 73% reported GERD symptoms. Endoscopy evidenced hiatus hernia in 39.4% and esophagitis in 6.4%. The DeMeester score was pathological in 53.3%; 69% of patients had lower esophageal sphincter (LES) pressure <15 mmHg and 7 had esophageal dyskinesia. BMI was significantly related to the DeMeester score (P = 0.018) but not to LES tone or esophageal dyskinesia. Postoperative data were available in 27 patients (AGB n = 12/60, RYGBP n = 15/36). The DeMeester score (normal < 14.72) was significantly decreased after RYGBP (24.8 +/- 13.7 before vs. 5.8 +/- 4.9 after; P < 0.001) but tended to increase after AGB (11.5 +/- 5.1 before vs. 51.7 +/- 70.7 after; P = 0.09), with severe dyskinesia in 2 cases. CONCLUSION: GERD and LES incompetence are highly prevalent in morbidly obese patients. Preliminary postoperative data show different effects of RYGBP and AGB on esophageal function, with worsening of pH-metric data with occasional severe dyskinesia after AGB.

MDR3 mutations associated with intrahepatic and gallbladder cholesterol cholelithiasis: an update.

BACKGROUND: The recurrent microlithiasis represents one of the most frequent clinical forms of lithiasis of the bile ducts. This affection is characterized by the presence of cholesterolic microgallstones on hepatic canaliculars, and belongs to a heterogeneous group of autosomal recessive liver disorders. Radiological diagnosis can be confirmed by analysis of MDR3 gene, coding a protein involved in physiologic translocation of phospholipids in bile. Discovery of MDR3 mutations is of particular interest, since normally associated with good effectiveness of medication by ursodesoxycholic acid. AIM: To review MDR3 mutations in humans associated with recurrent cholesterol microlithiasis and to suggest a practical approach for MDR3 gene analysis. RESULTS: 48 mutations of MDR3 gene have been reported in humans to date, from which 43 (89.5%) in the coding region, and 5 splice site mutations have been associated to cholesterol cholelithiasis. 21 (43.8%) of the 43 precited mutations are located in only 8 exons on 28, near transmembrane or nucleotide binding domains of the protein. From the 22 remaining described mutations, 9 (18.8%) are restricted to exon 14. We suggest therefore to start analysis of MDR3 gene by screening exons 6, 7, 9, 10, 12, 14, 17, 23 and 24 with an appropriate protocol in this diagnosis associated with effective treatment. In conclusion such therapeutic orientation is valuable, since recurrent cholesterolic microlithiasis occurs relatively early in life, and by the fact that recurrence of symptoms may occur despite cholecystectomy, or shock-wave therapy.

[Acute pancreatitis after treatment by celecoxib]. / Pancréatite aiguë survenant après la prise de celecoxib.

Drug-induced pancreatitis injury due to celecoxib, a first generation Cox-2 inhibitor, has been rarely reported. We describe one case of severe pancreatitis after treatment with celecoxib for 3 months in a woman. No aetiology has been found for pancreatitis. The role of celecoxib in the etiology of colitis was considered probable. This report and a few other cases in the literature suggest to seek a pancreatitis in the event of pains abdominal when there is a catch of the cyclooxygenase-2 selective non-steroidal anti-inflammatory drug inhibitor.

Incidence and severity of non alcoholic and non biliary pancreatitis in a gastroenterology department.

AIMS: Etiological investigations proposed for patients with acute pancreatitis have been evolving considerably these past few years, significantly limiting the number of cases labeled idiopathic. The aim of this study was to determine the incidence of non alcoholic non biliary pancreatitis and identify causes, comparing severity by etiology. PATIENT AND METHODS: This retrospective analysis included 108 patients managed from October 1996 to April 2005. Standar-dized extensive etiological investigations were performed. The following criteria of severity were recorded: peak CRP value, Ranson score, Balthazar score, duration of hospital stay and pseudocyst occurrence. RESULTS: The cause of acute pancreatitis was alcohol (N=45), gallstones (N=50), obstruction (N=10), unknown (N=10), drugs (N=9), auto-immunity (N=4), infections (N=3), post-operative (N=2), post-ERCP (N=2), trauma (N=1), hypertriglyceridemia (N=1), genetic (N=1). The main criteria of severity were significantly different between non alcoholic non biliary pancreatitis and the other causes (CRP>120 mg/L, Ranson score>3 and Balthazar score > or =D) while other criteria (pseudocyst occurrence and duration of hospitalisation) were similar. Mean peak CRP was 79.5 mg/L for the overall population and varied significantly by etiology: peak CRP for drug-induced acute pancreatitis (4.6 mg/L) was significantly lower than for the other causes (P<10(-6)). CONCLUSION: This study shows that non alcoholic non biliary causes account for one third of the cases of acute pancreatitis, usually with a mild to moderate presentation. As the mean peak CRP value is significantly lower in drug-induced acute pancreatitis, careful search for an adverse drug reaction is appropriate in patients with acute pancreatitis of unknown cause and a low peak CRP level.

Prevalence and predictive factors of non-alcoholic steatohepatitis (NASH) in morbidly obese patients undergoing bariatric surgery.

BACKGROUND: In patients with morbid obesity selected for bariatric surgery, previous studies have shown a prevalence of NASH varying from 2.6% to 91%. The prevalence of NASH and extensive fibrosis were studied in a prospective cohort of patients with morbid obesity requiring bariatric surgery, to identify predictive factors of NASH. METHODS: From July 01 to Sept 02, every patient requiring bariatric surgery had a liver biopsy. The diagnosis of NASH was established using Lee's criteria. RESULTS: 92 patients (85 women, age 38 +/- SEM 11 years) were analyzed. Mean BMI was 45.7 +/- 5.1 kg/m2. 35 patients had lobular inflammation. 9 patients had steatosis associated with lobular necrotic and inflammatory foci and ballooning degeneration or pericellular fibrosis. No cirrhosis or extensive fibrosis was evidenced. The prevalence of NASH in this population was 9.8%. Waist/hips ratio and BMI were independent predictors of lobular inflammation, but only BMI was an independent factor of NASH in multivariate analysis. CONCLUSION: In this prospective cohort of patients at bariatric surgery, the prevalence of NASH was 9.8%. BMI was the only predictive factor for NASH.

Mesenteric adenitis and portal vein thrombosis due to Fusobacterium nucleatum.

We report the first description of portal and mesenteric vein thrombosis associated with suppurative mesenteric adenitis in a 71-year-old woman. The bacterium detected in mesenteric lymph nodes was Fusobacterium nucleatum, an anaerobic Gram-negative bacillus. Our patient had a clinical syndrome of pharyngitis and fever preceding portal vein thrombosis. Abdominal symptoms improved with antibiotics and anticoagulant therapy. This location of F. nucleatum in mesenteric lymph nodes provides an interesting insight into the occurrence of septic thrombosis in the portal vein following pharyngo-tonsillar infection.