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L'infection parHelicobacter pylori de la muqueuse gastrique ne constitue pas par elle-meme un risque d'œsophagite par reflux et meme certaines etudes montrent que Hp peut proteger de l'œsophagite par RGO. Le risque d'œsophagite par reflux augmente apres eradication de Hp. Il existe une correlation negative entre la presence de Hp et le degre de l'œsophagite par reflux de meme qu'entre la prevalence de Hp et le cancer de l'œsophage et du cardia. Differents mecanismes pourraient lier Hp et le reflux, mais jusqu'a present on ne dispose que d'hypotheses. Le mecanismes les plus serieusement envisages pour expliquer l'augmentation de frequence du RGO apres eradication de Hp sont: une secretion acide accrue chez les patients dont la secretion gastrique est inhibee par Hp en raison de l'inflammation de la muqueuse fundique, et les modifications du mode de vie apres eradication de Hp. On ignore tout de l'influence de Hp sur les RTSIO mais la voie reste ouverte aux speculations; nous passons egalement en revuew les roles possibles de la somatostatine, de la gastrine, des prostaglandines et des leucotrienes de l'EGF et du NO. Plusieurs etudes seront encore necessaires pour repondre aux questions posees.

Plusieurs etudes de population, de cas controles, d'etudes de famille, confirment l'association entre infection aHelicobacter pylori (H. pylori) et tumeurs gastriques malignes, carcinomes et maltomes. De facon evidente l'infection aH. pylori precede le developpement des lesions malignes et le micro-organisme a ete mis en evidence a des stades precancereux: il pourrait constituer le «chainon manquant» de la premiere etape du modele de Correa. Selon les etudesin vitro, H. pylori serait implique dans le mecanisme de la carcinogenese, du moins en partie, par induction de l'inflammation chronique et une augmentation de la proliferation cellulaire au niveau de la muqueuse gastrique. La regression du lymphome a cellule B de faible degre de malignite apres eradication deH. pylori prouve le role predominant de cette infection dans cette maladie. Neanmoins, un certain nombre de facteurs jouent un role cle, en particulier dans le carcinome: la virulence des souches deH. pylori, l'action locale de l'ammonium, les facteurs environnementaux et genetiques qui conditionnent la reponse de l'hote. La prevention du carcinome gastrique a travers l'eradication de l'infection aH. pylori est insupportable du point de vue economique mais certains groupes a hout risque ont ete definis et justifient un traitement d'eradication avec un suivi soigneux.

Helicobacter pylori (HP) a ete retrouve au niveau de l’œsophage, uniquement sur un epithelium de type gastrique dans l’œsophage de Barrett, et presque exclusivement chez des patients porteurs d’une contamination gastrique par HP. L’infection de l’œsophage de Barrett par HP n’a aucune influence sur sa severite, ses complications ou son histoire naturelle. La contamination gastrique par HP n’est pas un facteur de risque de reflux gastro-œsophagien et au contraire la presence de HP au niveau gastrique, l’inflammation de la partie fundique et la gastrite atrophique pourraient jouer un role protecteur contre l’œsophagite par reflux. L’eradication de HP chez les patients porteurs d’un ulcere duodenal expose ceux-ci a un risque de developpement d’œsophagite par reflux. HP influence l’efficacite du traitement antisecretoire: les inhibiteurs de pompe a protons et la ranitidine procurent une reduction de l’acidite gastrique superieure chez les sujets contamines par HP par rapport aux sujets HP negatifs. Au cours d’un traitement par inhibiteur de pompe a protons, on constate un deplacement de HP de l’antre vers le fundus. Les traitements prolonges par inhibiteur de pompe a protons provoquent une gastrite atrophique chez les sujets positifs pour Helicobacter pylori, ce qui constitue un argument majeur en faveur de l’eradication de HP chez les patients soumis a une inhibition secretoire acide de longue duree.

De nos jours, le cancer gastrique reste un probleme de sante majeur, malgre la diminution de son incidence. L’histopathogenese a ete decrite dans le modele de Correa, lequel tient compte des influences environnementales impliquees sur l’evolution de la muqueuse gastrique normale vers une gastrite superficielle, ensuite l’atrophie, la metaplasie intestinale, la dysplasie et finalement le carcinome gastrique.Helicobacter pilori est la cause principale de la gastrite chronique active. Lorsque l’atrophie de la muqueuse progresse, la densite bacterienne deH. pylori diminue et dans la gastrite atrophique severe, seuls les anticorps seriques anti-Helicobacter pylori constituent le temoin d’une infection anterieure. Le developpement d’une gastrite atrophique chronique s’accompagne de la presence d’Helicobacter pylori, d’un pH gastrique eleve et d’un abaissement des taux seriques de beta-carotene. La metaplasie intestinale est egalement associee a la presence deH. pylori, a une reduction de la consommation de la vitamine C, a des taux faibles de sa concentration dans le suc gastrique, a un pH gastrique eleve, et a un reflux biliaire. Des taux eleves de prevalence d’H. pylori ont ete observes chez les patients porteurs d’une dysplasie gastrique ou d’un cancer gastrique superficiel. En revanche, les donnees relatives au role deH. pylori dans le cancer gastrique superficiel de type diffus, demeurent contradictoires. Les mecanismes de l’implication deH. pylori dans la carcinogenese gastrique incluent l’inflammation induite parH. pylori, l’augmentation de la proliferation cellulaire gastrique, la production de produits inflammatoires mutagenes;H. pylori permet au sel (NaCl) d’augmenter la proliferation cellulaire gastrique;H. pylori inhibe le maintien de la concentration gastrique en vitamine C; l’ammoniaque, produit par l’urease bacterienne, est capable d’induire une atrophie; enfin la toxine deH. pylori, pour des raisons encore inconnues, constitue un facteur important de la carcinogenese gastrique. On ignore si les lesions precancereuses gastriques sont reversibles. L’effet de l’eradication de deH. pylori chez des patients selectionnes et le role de la vaccination a l’echelle de l’ensemble de la population, restent a evaluer.

We analyzed the rates of antimicrobial resistance of Helicobacter pylori strains isolated from patients from 1990 to 2009 and identified risk factors associated with resistance. Gastric biopsy specimens were collected from several digestive disease centers in Brussels, Belgium. We routinely performed antimicrobial susceptibility testing for clarithromycin (CLR), metronidazole, amoxicillin, tetracycline, and ciprofloxacin. Evaluable susceptibility testing was obtained for 9,430 strains isolated from patients who were not previously treated for Helicobacter pylori infection (1,527 isolates from children and 7,903 from adults) and 1,371 strains from patients who were previously treated (162 isolates from children and 1,209 from adults). No resistance to amoxicillin was observed, and tetracycline resistance was very rare (

SUMMARYThe prevalence ofHelicobacter pyloriinfection is decreasing in developed countries. In this study we included 22 612 patients in whom a first culture of gastric biopsy (routinely performed in our medical centres) yielded an interpretable result over a 20-year period (1988–2007) in Brussels. The effects of patients' age, gender and ethnic background were analysed. The overall proportion ofH. pylori-infected patients was 37·7%, with a progressive decline over time (P−5). A gender effect was observed in adults. The lowest infection rate was observed in Western European patients (n=11 238) with respectively 36·2% and 15·2% infected subjects in 1988 and 2007, compared to 71·7% and 40% in North African patients (n=3200) (P−5). However, no trend of decline was observed over time in North African children aged ⩽9 years. These data show the effects of time, age and ethnicity on the prevalence ofH. pyloriinfection, and its complex heterogeneity in the same cosmopolitan urban area.

The SOSTAR-X project has developed a demonstrator dedicated to the surveillance of both fixed and moving targets on large coverage areas, target activity analysis on dedicated areas and classification on designated targets. In this project, The Netherlands contribution has been in the areas of Spectral Classification (SPC mode), SAR SPOT mode autofocus, antenna harness, and ground target coordination during the flight campaign in the Netherlands. This paper focuses on the topic of Spectral Classification. The so-called SPC mode is a dedicated mode activated on a designated target, which classifies the target as wheeled, tracked (treaded), rotary wing, or rotating antenna. This is achieved by producing a high resolution Doppler profile, containing modulations caused by moving parts of the vehicle, and classifying on the basis of this profile. The SPC mode has been designed, implemented in the sensor and the Radar Processing Unit, and validated during extensive flight trials, in the Netherlands, Germany, and France.

The Authors describe a case of presacral hemorrhage after a colonoscopy in a patient taking anticoagulation. Surgical treatment was necessary to stop the hemorrhage.

Cutaneous Paget's disease (PD) is a rare entity, predominantly involving the breasts. Anal involvement is rather exceptional, and can be associated with underlying malignancies, among which prostate and rectal adenocarcinoma. We report the case of a 71-year-old man suffering from a long history of anal itching, associated with an erythematosquamous lesion of the right buttock extending up to the anus. The diagnosis of perianal PD (PAPD) was confirmed by histopathological demonstration of Paget's cells from a biopsy performed after ineffective topical treatment. Radiological and further clinical inspections allowed us to exclude any synchronous malignancy. A first-step surgery consisted in coelioscopic diverting sigmoid colostomy, along with multiple perianal, anal and rectal biopsies revealing an anal canal involvement. Coelioscopic abdominoperineal surgery and a wide cutaneous excision were then performed. Histopathological analysis revealed positive posterior margin, requiring further excision. No adjuvant therapy was prescribed, and to this day, after a one-year and a half follow-up, the patient remains disease-free. Our case report and review of PAPD stress that appropriate management is required to improve the poor prognosis of this rare affection.

The article gives an overview of the current status of treatment of AP. The different therapeutical strategies are described and compared. The basic treatment for severe AP remains a medical therapy in an Intensive Care Unit. Surgical therapy is indicated in case of infection of necrotizing areas or other severe complications. The potential benefit of antiprotase agents and other new molecules is discussed.

Acute pancreatitis is an unusual complication of systemic lupus erythematosus but can also stem from immunosuppressive therapy. Although abnormal liver tests are commonly seen in SLE, peliosis hepatis is very rarely described. We report here the first case of SLE associating a severe acute pancreatitis with peliosis hepatis who responded well to the immunosuppressive therapy. As suggested by the favourable outcome in this case, the presence of peliosis hepatis in SLE cannot not be held as a strong argument against an aggressive immunosuppressive therapy.

A putative pathogenetic role has been ascribed to Helicobacter pylori in several extradigestive diseases, including vascular (atherosclerosis and ischaemic heart disease, primary Raynaud phenomenon, primary headache), autoimmune (Sjögren's syndrome, Henoch-Schönlein purpura, autoimmune thyroiditis, idiopathic arrythmias, Parkinson's disease, nonarterial anterior optic ischemic neuropathy), and skin diseases (chronic idiopathic urticaria, rosacea, alopecia areata), sideropenic anemia, growth retardation, late menarche, extragastric MALT lymphoma, diabetes mellitus, hepatic encephalopathy, sudden infant death syndrome, and anorexia of aging. We examine critically the strength of the evidence linking these diseases to Helicobacter pylori, using ischaemic heart disease as an example of epidemiological techniques, and skin diseases as an example of treatment studies. By the standards of evidence-based medicine, studies have been often of low quality. The best evidence usually is not indicative of a role for Helicobacter pylori in these diseases.

Currently, the first therapeutic attempt to eradicate Helicobacter pylori fails in one case out of six in intention to treat analysis. The main causes of failure are bad compliance, partly because of side effects that are severe in 1 to 4% of cases, absence of local validation of the treatment scheme, since some differences do exist between regions and countries, primary and secondary resistance of the strain (stable for Imidazole-derivates, but increasing for Macrolides), and, to a lesser extent, smoking and pre-treatment with proton pump inhibitors. Moreover, in routine medicine, inappropriate treatment cocktails are still prescribed, even by gastroenterologists. Obviously, there is a need for careful medical education and information both as far as concerns doctors and patients, for well-designed prescription, based on local experience and the precise previous history of every patient, as well as for continuous monitoring of the bacterial resistance to antibiotics. Culture of the strain is recommended after eradication failure with the classic one-week triple therapy, but if reliable culture and resistance testing are not available, the quadruple therapy as a second-line treatment is, so far, the best choice.

"HP testing must be regarded as ONE of the important elements of the proper diagnostic work-up of a DISEASE, managed in close cooperation between GP's and specialists": that's the key message of the national consensus meeting held in CHU Brugmann on February 6th and 7th 1998. HP testing (usually by 2 direct methods: RUT-histology) and eradication treatment (ER), in infected patients, are strongly recommended in: 1. Past or current GDU (absolute indication), regardless of activity, complication(s), NSAID intake; 2. Low-grade MALT Lymphomas (Stage IE1) unequivocally diagnosed, managed and followed-up in specialised centers; 3. Post endoscopic resection of EGC. ER is advisable in HP carriers with a family history of gastric cancer. Chronic atrophic-, lymphocytic-, giant folds gastritis and hyperplastic polyps are acceptable indications for ER as well as scheduled long-term NSAID treatment in individuals with known HP status. Systematic ER in HP+ patients with fully investigated NUD is not indicated but could be considered in individual patients. Extra alimentary disorders and auto immune gastritis are no indication and there was no consensus for a "test and treat" policy in patients under 45 yrs old without alarm symptoms. Systematic screening of asymptomatic individuals is not recommended. A correct monitoring of eradication after treatment is recommended, mainly by UBT. In severe or refractory PUD, symptom recurrence and follow-up of EGC and Maltomas, endoscopic follow-up with HP testing is mandatory. The recommended first line treatment course (except known allergy or intolerance) is PPI full dose bid, Clarithromycin 500 mg bid Amoxycillin 1000 mg bid (7 days minimal 10 days maximal). RBC-based schemes must be locally validated and quadruple therapy is proposed when retreatment is needed. Culture, optional after the first treatment failure, is strongly recommended after a second failure. Overall, ER therapies are safe and neither the decreased efficacy of acid-lowering drugs, nor the possible increased risk of peptic oesophagitis are considered as contra-indications to eradicate. ER is cost-effective and cost-beneficial in PUD and adjusted number of pills delivered would cut costs. No clear economic data are currently available for a potential benefit of ER in GC prevention or NUD management. A national monitoring of HP resistance (Macrolides and Imidazoles) must be organized by specialised centers.

HP infection of the stomach is not a risk factor for reflux oesophagitis, and may even protect against reflux oesophagitis. HP eradication may lead to an accelerated development of GERD in duodenal ulcer disease patients. It is unknown whether this is also true for HP positive patients who do not suffer from duodenal ulcer disease. HP eradication may decrease the efficacy of acid secretion lowering drugs such as Proton Pump Inhibitors and H2-Receptor Antagonists. It is unclear whether this has any practical consequences, but it cannot be excluded that some patient may need an increased dose of acid secretion lowering drugs after HP eradication for control of symptoms and lesions of GERD. There are conflicting data on the possibility that long-term proton pump inhibitor treatment may accelerate the development of atrophic gastritis in Helicobacter pylori positive patients. The possible acceleration of atrophic gastritis development in HP positive patients using strong acid secretion inhibitors is the strongest argument in favour of eradicating HP in patients receiving long term potent acid inhibition, especially GERD patients. In view of the uncertainty concerning these data, both eradicating and non eradicating HP in patients with GERD can be defended.

After a decade of research, Helicobacter pylori eradication is still a problem because of the steady increase of bacterial resistance (imidazole, macrolides), pH-dependent efficiency of antibiotics, poor compliance of patients and frequent side effects of the therapies. After the failure of various monotherapies and the unefficiency of Amoxicillin-Imidazole combination for Imidazole-resistant strains, the two weeks ¿Oral Triple Therapy' with a 85% mean eradication rate, was abandoned because of a mean 35% side effects rate. The current goal is to obtain 90% eradication rate and the excellent results of german studies with a 2 weeks regimen combining a Proton Pump Inhibitor (PPI) with Amoxicillin have not been confirmed elsewhere in Europe. PPI plus Clarithromycin (two weeks) gave a mean 72% eradication rate on an ITT basis. The short, low-dose combination PPI-Clarithromycin-Imidazole for one week proposed by Bazzoli is very efficient in a population where Imidazole resistant strains are rare. The recent result of one week with (Omeprazole 20-Clarithromycin 250-Tinidazole 500) BID or (Omeprazole 20-Clarithromycin 500-Amoxi 1000) BID reached a 95% eradication rate but these very promising results are not confirmed in Belgium in an on-going study including 147 patients.

We performed a literature search as well as a review of our own results to evaluate HP serology as a screening method in young dyspeptic patients, prior to endoscopy. This strategy has been proposed by various teams in order to decrease the endoscopy workload. We analysed the results that could be obtained when not performing endoscopy in seronegative patients, in terms of avoided endoscopies and missed lesions. We found that too many lesions would remain undiagnosed, and thus untreated, regarding our reimbursement system, if the strategy was used without a strict selection of patients. The screening might be advisable among highly selected patients, but the percentage of avoided endoscopies would then decrease regarding the total number of endoscopies performed. Our conclusion is that HP serology as a screening method in young dyspeptic patients cannot be advised in Belgium for the time being.

To compare the efficacies of omeprazole-based antimicrobial therapies in Helicobacter pylori-positive patients.We report the results of seven therapeutic trials combining omeprazole, clarithromycin, amoxycillin, colloidal bismuth subcitrate and tinidazole in 198 patients (peptic ulcer disease/non-ulcerative dyspepsia, 137/61) to eradicate H. pylori infection. The diagnosis of infection was performed by Sydney system biopsies, compliance was checked after a pill count at the end of the treatment and eradication was assessed at least 4 weeks after the end of the treatment either by the Sydney system for peptic ulcer disease or the urease breath test for non-ulcerative dyspepsia.When results were analysed on a protocol basis, the only significant difference in eradication (P = 0.006) was found between the total population of patients treated with amoxycillin-based combinations (27 eradications out of 48 patients) and those given a treatment that included clarithromycin (84 eradications out of 108). Forty-two patients (21%) dropped out either because of side effects (10 among patients taking clarithromycin and two taking amoxycillin) or because they were lost to follow-up (27 patients). Out of 64 patients with active ulcers, 43 (67%) were both H. pylori-negative and ulcer-free 4-8 weeks after the end of therapy, 12 out of 64 (19%) were ulcer-free but remained H. pylori-positive and nine out of 64 (14%) were H. pylori-positive and had active ulceration.

Gastric cancer is the world's overall second most common cancer, and carries a bad prognosis. In the Correa model of gastric carcinogenesis, environmental factors (salt, nitrate, a lack of vitamin C and beta-carotene, bile reflux, bacterial overgrowth in atrophic gastritis with nitrosamine formation) are related to the evolution from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma. The incidence of H. pylori decreases with progressing preneoplastic lesions. In several studies, the prevalence of H. pylori was elevated in patients with gastric cancer, with a trend for a higher prevalence in intestinal type gastric cancer vs diffuse type. Family members of patients with gastric adenocarcinoma have a higher H. pylori prevalence than controls; patients infected with H. pylori have more family members with gastric cancer. Several epidemiological studies showed a higher H. pylori prevalence in regions or populations with high gastric cancer risk vs low-risk populations. Large-scale studies in China and Europe showed a correlation between H. pylori seroprevalence and gastric cancer incidence and mortality. Three prospective nested case-control studies showed that infection with H. pylori increased the risk of further development of gastric adenocarcinoma, showing that H. pylori infection precedes the development of gastric cancer. Several pathways can be identified explaining the association between H. pylori and gastric adenocarcinoma. We showed that gastric cell proliferation is increased in parallel with inflammation. The ascorbic acid concentrating mechanism is abolished in gastritis. Ammonia, generated by H. pylori's urease, gives rise to gastric mucosal atrophy. We showed that salt increases the gastric cell proliferation only in H. pylori-infected individuals. The organism's toxin may play a role in gastric cancer. Besides H. pylori, other environmental factors are important in determining the gastric cancer risk. For instance, we showed that in Belgium, Maghreb immigrants have a high prevalence of H. pylori infection but a low prevalence of intestinal metaplasia and gastric cancer. Gastric lymphoma is rare (about 5% of all gastric tumours), but its incidence is steadily increasing. It was shown that H. pylori also increases the risk for low-grade as well as high-grade gastric lymphoma. Eradication of H. pylori has been shown to cure several cases of unequivocally proven gastric low-grade lymphoma.(ABSTRACT TRUNCATED AT 400 WORDS)

Proton pump inhibitors (PPIs) might soon become the most prescribed drugs in reflux esophagitis and peptic ulcer disease (PUD). In many comparative clinical trials, they were shown to heal ulcerous lesions more rapidly than H2-receptor antagonists. They are so far the most potent non-surgical means to suppress gastric acidity, long recognized as a key factor in PUD. Their possible role in the treatment of the other key factor in PUD, Helicobacter pylori (HP) infection, is a very attractive field in clinical research. So far, few papers have been published about this topic, and this review deals mainly with personal experience, letters to editors and abstracts (out of 32 references, only 5 are full papers). We summarize our current knowledge about the potential role of PPIs in the treatment of HP infection. So far, this crucial (and sometimes very emotional) question has no definite answer. There is a mixing of facts, hopes, and wishes, and while reading this chapter one must remember that what is true today will often be wrong tomorrow.

The incidence of gastric cancer is rapidly declining in the Western world, but it remains high in the Third World and in Japan. Systematic screening for gastric cancer has been undertaken in Japan, where barium X-ray is used in people over the age of 40. Evaluation data suggest a benefit in reduced mortality, but biases cannot be ruled out. A similar screening programme has been started in Venezuela. Currently, stomach cancer screening programmes cannot be recommended as public health policy, except in high-risk areas where they have already started. The Correa model of gastric carcinogenesis states that environmental influences cause a normal gastric mucosa to undergo successive stepwise changes, through superficial gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, carcinoma and, finally, invasion. Incriminated environmental influences include irritant, antibodies, gastrectomy, nutritional deficits, intake of nitrogen compounds and Helicobacter pylori. These bacteria cause a chronic superficial gastritis, which may develop into atrophic gastritis. H. pylori is less frequently found in advancing preneoplastic lesions, and seldomly in gastric carcinoma tissue (it may, however, be identified more readily in the surrounding non-cancerous tissue). Several lines of evidence suggest that H. pylori may play an important role in human gastric carcinogenesis. We found that in some patients with H. pylori infection and without preneoplastic lesions, the gastric cell turnover was increased; this was correlated with the intensity of the inflammatory changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Both juxtapapillary duodenal diverticula and colon diverticula are acquired lesions, the pathogenesis of which is believed to involve the influence of high intraluminal pressure on loci minoris resistentiae in the gastrointestinal wall. We wanted to investigate whether juxtapapillary duodenal diverticula and colon diverticula occur independently, or whether they are part of a hypothetical general "gastrointestinal diverticular disease". 239 patients with juxtapapillary duodenal diverticula were identified in 2231 patients undergoing ERCP. Complete radiology data were available in 119/239 patients. Double contrast barium enema had been performed in 28/119 patients. In these patients, colon diverticula were present in 9/20 women and 1/8 men. The frequency of colon diverticula in these patients was compared with randomly chosen age- and sex-matched controls, for whom barium enema results were available. In these controls, 9/20 women and 1/8 men also had colon diverticula (n.s.). We conclude that after stratification for age and sex, the occurrence of colon diverticula is not higher in patients with juxtapapillary duodenal diverticula than in the general population. Juxtapapillary duodenal diverticula and colon diverticula thus occur independently. These data are not in favor of the existence of a general gastrointestinal diverticular disease.

Adherence of pathogenic bacteria to their target cells is a key event in the pathogenesis of bacterial infection (Beachey 1981).

In a comparative, histologically controlled study, no significant difference was found in the accuracy of conventional fiberendoscopy and videoendoscopy in the diagnosis of upper gastrointestinal tract lesions. Both techniques permitted accurate description of focal and/or ulcerative lesions, but videoendoscopy did not provide better sensitivity than fiberendoscopy in the diagnosis of superficial, non-ulcerative, inflammatory changes. The same results were obtained on checking the reproducibility of the macroscopic diagnosis by a delayed review of recorded videotapes.

In order to explore the relationship between duodenal diverticula and biliary stone disease, we reviewed 2231 endoscopic retrograde cholangio-pancreatography procedures. We found at least one juxtapapillary diverticulum per 239 patients (10.8%). The occurrence of duodenal diverticula increases with age. Patients with duodenal diverticula were older, had more gallbladder stones, more common bile duct stones, had undergone cholecystectomy more frequently, and experienced more frequently common bile duct stone recurrence after cholecystectomy. We thus confirm an association between the presence of diverticula of the second part of the duodenum, and biliary stone pathology, including gallbladder stones, common bile duct stones, and recurrent stones after cholecystectomy. We discuss the aetiopathogeny of this affection.

In a retrospective study of 702 consecutive colonoscopies, the authors observed 185 cases of diverticulosis or moderate diverticulitis. They studied the colonic diseases associated with the presence of diverticula (78 cases) and discussed the role of endoscope in the approach of colonic diverticulosis.

Worldwide Campylobacter pylori is a major cause of active chronic gastritis in man. This curved spiraled microorganism can readily be detected within the mucusgel especially in the antrum, in particular in patients suffering from peptic ulcer disease or non-ulcer dyspepsia, rarely in individuals with normal gastroduodenal mucosa. Increasingly arguments are being presented in support of a pathogenetic role of C. pylori in non-ulcer dyspepsia and in peptic ulcer disease. There is a striking discordance between in vitro antibiotic sensitivity, and in vivo efficacy with respect to suppression or eradication of the organism. At present the combination of colloidal bismuth subcitrate and amoxicilline or tinidazole appears to be encouraging with respect to longterm eradication of this peculiar microorganism. Eradication by antibacterial treatment ultimately may result in histologic normalization of the gastric mucosa. To what extent peptic ulcer disease. There is a striking discordance between in vitro antibiotic sensitivity, and in.

The efficacy of various antimicrobial and anti-ulcer agents on the eradication of Campylobacter pylori in patients with antral gastritis or duodenal ulcers was investigated by several open studies or double-blind, placebo-controlled protocols. Among the anti-ulcer agents, ranitidine, cimetidine or sucraflate had no effect on C. pylori. Colloidal bismuth subcitrate achieved clearance of C. pylori in 40% of treated patients at the end of therapy but a high relapse rate (14/16 patients) was observed after a 6-month follow-up period. The antibacterial agents doxycycline, minocycline, ofloxacin, clindamycin, paromomycin and nifuroxazide failed to eradicate C. pylori in most patients. By contrast, short term elimination of C. pylori could be achieved in more than 90% of patients treated with amoxycillin. However, relapse occurred as a rule in all amoxycillin-treated patients within one month after therapy. Overall, we observed no correlation between the in-vitro activity of the different antibacterial agents and their in vivo efficacy. Development of resistance during therapy does not seem to account for this discrepancy since it occurred only with ofloxacin. On the basis of these results, we conclude that long term eradication of C. pylori from the gastric antrum cannot be achieved after monotherapy either with antibiotics or with bismuth salts.

The logic of this question comes from the knowledge of the three essential pathophysiological data about reflux esophagitis (R.E) To each of these data corresponds potential pharmacological effects of prostaglandins (PG).