[Progress in 2008 for acid related diseases]. / Maladies peptiques.

The treatment of reflux disease did not change in the review period. PPI therapy remains the first line treatment and surgery the second line approach. Endoscopic anti-reflux procedures should be only performed in controlled studies. Beside the classic triple therapy, sequential treatment of Helicobacter pylori infection can today be considered as a first line therapy. PPI are effective in the prevention of gastroduodenal lesions and in the treatment of dyspeptic symptoms induced by NSAIDs treatment. Only patients younger then 65 years and without any risk factors do not need a preventive PPI prescription during classic NSAIDS treatment.

[Peptic diseases]. / Maladies peptiques.

The therapeutical acquisitions of the year 2004 are: 1. The sequential treatment of the Helicobacter pylori infection reaches an eradication rate of 95%. 2. The use of COX-2 inhibitors reduced significantly the gastrointestinal side effects of anti-inflammatory treatments. Since cardiac averse effects of certain COX-2 inhibitors had been reported, the treatments with COX-2 inhibitors came widely into question. In the case of patients with risk of NSAID induced gastrointestinal toxicity, the alternative is to return to a treatment with non specific NSAID associated to an prophylactic PPI treatment.

The effects of omeprazole on healing and appearance of small gastric and duodenal lesions during dosing with diclofenac in healthy subjects.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with gastrointestinal mucosal damage. Omeprazole prevents the formation, and accelerates the healing, of NSAID-induced ulcers. AIM: To test whether omeprazole accelerates healing of standardized gastroduodenal lesions in the presence of diclofenac. METHODS: In a double-blind, double-dummy, placebo-controlled, crossover study, 12 healthy volunteers received consecutive, 2-week courses of omeprazole (40 mg o.d.) and placebo, in random order, with an intervening, 4-week washout period; diclofenac (50 mg t.d.s.), was given for the second week of each course. Five endoscopies were performed, one at the outset and the others before and after each course of diclofenac. Biopsies were taken from the endoscopically normal mucosa of the corpus, antrum and duodenum and also from any new mucosal lesion that developed after diclofenac. The sites of biopsies taken before each course of diclofenac were evaluated endoscopically after each course to assess the extent of healing according to a predetermined healing score scale. RESULTS: The healing scores observed after administration of placebo/diclofenac (median=0; range 0-6) and after omeprazole/diclofenac (median=0; range 0-6; P=0.17) did not differ. Small gastroduodenal lesions developed de novo in six subjects during placebo/diclofenac and in seven during omeprazole/diclofenac. Focal chemical gastropathy was observed only in close proximity to macroscopic lesions. CONCLUSIONS: In healthy subjects, omeprazole does not accelerate the healing of pre-existing mucosal lesions or prevent the development of small diclofenac-induced mucosal lesions.

Effects of misoprostol on healing and prevention of biopsy-induced gastroduodenal lesions occurring during the administration of diclofenac to volunteers.

AIM: To determine whether misoprostol promotes the healing of non-steroidal anti-inflammatory drug-induced gastroduodenal lesions in a human experimental model. METHODS: Mucosal damage and healing of mucosal biopsy sites were assessed endoscopically in 10 healthy, Helicobacter pylori-negative volunteers with a normal initial endoscopy: they were enrolled in a double-blind, double-dummy, placebo-controlled cross-over study. They received 2-week courses of misoprostol (200 micrograms b.d.) or placebo; a water-soluble non-steroidal antiinflammatory drug diclofenac 50 mg t.d.s., was given during the second week of each dosage regimen after three endoscopic biopsies had been taken from each of the duodenum, antrum and corpus. RESULTS: The number of unhealed biopsy sites was not different after misoprostol or placebo, although the number of healed biopsy sites was greater in the corpus and duodenum than in the antrum. Misoprostol did not prevent the appearance of diclofenac-induced erosions and petechiae. Epigastric discomfort was related to the intake of diclofenac and was reduced by misoprostol. Bloating and flatulence occurred more frequently with misoprostol alone and with misoprostol plus diclofenac, than with placebo alone or placebo plus diclofenac. CONCLUSION: Misoprostol does not prevent new mucosal lesions induced by diclofenac in healthy volunteers and it does not accelerate the healing of the biopsy sites. Misoprostol decreases the frequency of diclofenac-induced epigastric discomfort, but it increases gas bloating and flatulence.

[Anal fissure: conservative treatment]. / Fissure anale: traitement conservateur.

Anal fissure is a common and painful disorder. Conservative treatment must be reserved for acute forms. Hygiene rules, stool softeners and topical local anaesthetic agents are the mainstays of treatment. Healing often takes long time. Recurrences can be prevented with chronical prescription of stool softeners. Surgical treatment is indicated for chronic fissures, acute fissures refractory to 2 monthes conservative treatment and persistent painful forms.

Endoscopic features of Helicobacter pylori-related gastritis.

BACKGROUND AND STUDY AIMS: It is still controversial whether certain endoscopic features can be used to diagnose Helicobacter pylori (Hp)-related gastritis. To clarify this issue, we performed two consecutive prospective studies. PATIENTS AND METHODS: In the first study, we tried to identify endoscopic criteria associated with Hp-related gastritis from a total of 66 predefined gastric features on endoscopy. These features were selected by a stepwise logistic regression analysis in 101 patients. The validity of these features gained from this first study was then evaluated in a second study in 86 patients (40 with Hp gastritis, 8 with Hp-unrelated gastritis and 38 with normal gastric mucosa). RESULTS: Three features, namely an abnormal antral surface texture, a mammillated corpus surface, and white antral erosions, were identified in the first study as independent predictors of Hp-related gastritis. However, the sensitivity and specificity of these three criteria, as assessed in the second study, were only 75% and 63% respectively. CONCLUSIONS: We conclude that it is not possible to diagnose Hp-related gastritis on the basis of the endoscopic appearance alone. The diagnosis should be based on other criteria, such as a rapid urease test, or a histological examination of gastric biopsies, or both.

[The value of enteroscopy in recurrent digestive hemorrhages of undetermined origin]. / Intérêt de l'entéroscopie pour les hémorragies digestives itératives d'origine indéterminée.

conventional endoscopic procedures do not allow direct visual access to the small bowel. Small bowel bleeding can be investigated by enteroclysis, radionuclide bleeding scan and angiography of the mesenteric artery. However, localization of the bleeding can only be determined with these diagnostic tools in 15% of cases. A case of small bowel bleeding diagnosis by enteroscopy is presented, followed by an overview of the literature related to this novel endoscopic technic.

[Gastric rupture secondary to barotrauma in the framework of a diving accident. Apropos of a case report and literature review]. / Rupture gastrique secondaire à un barotraumatisme dans le cadre d'un accident de plongée. A propos d'une observation et revue de la littérature.

Gastric perforation secondary to barotrauma is rare. The case of a diver suffering from gastric rupture due to a decompression accident is presented here. This rupture was a linear one, localized on the lesser curvature and responsible for a large pneumoperitoneum. Rupture occurs with an excluded stomach, a condition implying cardio-pyloric occlusion. The expansion of intra-gastric air, further worsened by accelerated surfacing provokes excessive gastric dilatation leading to partial or complete rupture (by virtue of the Boyle-Mariotte law: Pressure x Volume = constant). The lesion is always on the lesser curvature. However, it is often difficult to locate, even when peroperative gastroscopy is performed.

Human Co115 colon carcinoma cells potentiate the degradation of laminin mediated by tissue-type plasminogen activator.

The plasminogen activation (PA) system of human Co115 colon carcinoma cells was investigated. Analysis at the levels of protein and mRNA of cultured cells and of histozymography of tumor xenografts in nude mice showed that Co115 cells produce only tissue type PA (t-PA) and no urokinase (u-PA). Also, mRNA for the u-PA receptor and for PA inhibitor type 2 (PAI-2), but not for PAI-1, were detected. We developed a quantitative degradation assay using glutaraldehyde-immobilized 125I-laminin to investigate the capacity of Co115 cells to degrade laminin. Laminin degradation by Co115 cells was completely inhibited by 100 micrograms/ml of polyclonal anti-t-PA IgG, by the plasmin inhibitors aprotinin (100 micrograms/ml) or epsilon-aminocaproic acid (EACA; at 0.3 M), but not by antibodies against u-PA or u-PAR nor by nonimmune IgG. Cycloheximide-treated Co115 cells were unable to degrade laminin but increased laminin degradation induced by conditioned medium of Co115 cells or recombinant t-PA. No potentiation was observed when Co115 cells and laminin were kept separated by Transwell inserts. Our results suggest that Co115 human colon carcinoma cells degrade laminin by potentiating t-PA-mediated plasminogen activation at the cell surface which requires close contact between tumor cells and laminin substrate.

Importance of substrate competition in the mechanism of insulin resistance in man.

Carbohydrate (CHO) oxidation induced by a glucose or fructose (0.5 g/kg X h) infusion over two hours was compared for 160 minutes by means of continuous indirect calorimetry in seven normal subjects without or with a concomitant infusion of Intralipid, a neutral fat emulsion. The glucose infusion was accompanied by a rise over basal values in both glucose (99 +/- 10 mg/dL) and insulin (36 +/- 7 microU/mL) plasma levels, with a further rise of both curves during the Intralipid infusion (140 +/- 7 mg/dL and 53 +/- 12 microU/mL). By contrast, plasma glucose and insulin rose only minimally during the fructose infusion (3.5 +/- 2.9 mg/dL and 5.3 +/- 1.4 microU/mL, respectively, without Intralipid, and 10.6 +/- 2.1 mg/dL and 9.6 +/- 2.0 microU/mL with Intralipid). During the two-hour sugar infusion, a mean quantity of 68.7 g glucose or fructose was infused. The total CHO oxidation was 15.6 +/- 1.2 g for glucose and 21.6 +/- 2.6 for fructose infusion for the 160 minutes of the test. During the Intralipid infusion, CHO oxidation was inhibited with values of 5.9 +/- 1.3 g for glucose (P less than .005) and 13.8 +/- 1.8 g (P less than .05) for fructose infusion. Lipid oxidation was increased in both cases during the Intralipid infusion. These results show that the lipid-induced inhibition of CHO oxidation observed with glucose infusion also occurs to some extent with fructose, suggesting that insulin might not be primarily involved. They suggest a metabolic origin for insulin resistance during elevated fat metabolism.

Comparative study of maltitol and sucrose by means of continuous indirect calorimetry.

The metabolism of the hydrogenated disaccharide maltitol was compared to that of sucrose in a group of eight normal subjects. On two separate days, with an interval of at least one week each subject ingested a load of 30 g of either substance. The evolution of the levels of plasma glucose, insulin, and free fatty acids was followed during the 6 hr following the oral load. Carbohydrate and lipid oxidation rates were assessed simultaneously by continuous indirect calorimetry during the 6 hr following the oral load. Plasma glucose and insulin peaks occurred 30 min after ingestion of the load for both sugars. The peak of the delta glucose concentration was significantly smaller after maltitol than after sucrose (21 +/- 4 vs 38 +/- 4 mg/100 ml, p less than 0.02), as was the peak of the delta insulin concentration (9.3 +/- 2.7 microU/ml after maltitol vs 25.5 +/- 5.0 microU/ml after sucrose, p less than 0.001). The peak of the stimulation of glucose oxidation occurred 60 min after the load of sucrose and 90 min after the load of maltitol. The delta glucose oxidation was significantly lower with maltitol than with sucrose during the first 90 min after the ingestion of the load. It was slightly higher (although not significantly) with maltitol than with sucrose starting from the 210th min. Maltitol resulted in a cumulated suprabasal glucose oxidation which amounted to 40% that obtained with sucrose after 180 min.