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CLINICAL PROBLEM Imaging plays a major role to differentiate interstitial edematous from necrotic pancreatitis and to describe relevant local complications for proper patient management and decision-making in acute pancreatitis. STANDARD RADIOLOGICAL PROCEDURES The revised Atlanta classification 2012 of acute pancreatitis divides patients into mild, moderately severe and severe groups. Computed tomography (CT) and magnetic resonance imaging (MRI) are well established for diagnosis and follow-up of acute pancreatitis and its complications METHODOLOGICAL INNOVATIONS AND ASSESSMENT: Based on the revised Atlanta classification, CT and MRI allow for adequate categorization of interstitial edematous and necrotic pancreatitis. Imaging and standardized reporting nomenclature enable confident differentiation of early and late complications in acute pancreatitis. RECOMMENDATIONS The aim of this review article is to present an image-rich overview of different morphologic characteristics of acute pancreatitis and associated local complications by CT or MRI using case examples.

Imaging plays a major role to differentiate interstitial edematous from necrotic pancreatitis and to describe relevant local complications for proper patient management and decision-making in acute pancreatitis.The revised Atlanta classification 2012 of acute pancreatitis divides patients into mild, moderately severe and severe groups. Computed tomography (CT) and magnetic resonance imaging (MRI) are well established for diagnosis and follow-up of acute pancreatitis and its complications METHODOLOGICAL INNOVATIONS AND ASSESSMENT: Based on the revised Atlanta classification, CT and MRI allow for adequate categorization of interstitial edematous and necrotic pancreatitis. Imaging and standardized reporting nomenclature enable confident differentiation of early and late complications in acute pancreatitis.The aim of this review article is to present an image-rich overview of different morphologic characteristics of acute pancreatitis and associated local complications by CT or MRI using case examples.KLINISCHES PROBLEM: Bildgebend ist die Differenzierung einer interstitiellen ödematösen von einer nekrotisierenden Form der akuten Pankreatitis und ihren lokalen Komplikationen entscheidend für Therapiewahl und den Krankheitsverlauf.Patienten mit der Diagnose einer akuten Pankreatitis werden nach der revidierten Atlanta-Klassifikation von 2012 klinisch einem leichten, mittelschweren oder schweren Verlauf zugeordnet. Bildgebend sind die Computertomographie (CT) und die Magnetresonanztomographie (MRT) in der Diagnostik und Verlaufskontrolle der akuten Pankreatitis und ihrer Komplikationen etabliert.Im Rahmen der revidierten Atlanta-Klassifikation erlauben CT und MRT die sichere Abgrenzung einer interstitiell-ödematösen von einer nekrotisierenden Pankreatitis. Diese Differenzierung geht einher mit der nomenklatorisch korrekten Einordnung der lokalen Früh- und Spätkomplikationen in der CT und MRT. EMPFEHLUNG FüR DIE PRAXIS: Der folgende Beitrag adressiert anhand von Fallbespielen die entscheidenden bilddiagnostischen CT- und MRT-Kriterien für die korrekte Befundeinordnung und -beschreibung der akuten Pankreatitis und ihrer lokalen Komplikationen.

Wir beschreiben den Fall einer retrorektalen Raumforderung, dessen praoperative Diagnostik ein Adenokarzinom ohne Ruckschluss auf einen Primarius ergab. Bei supraanaler Lokalisation musste die Rektumexstirpation erwogen werden. Schleimhautbefund, Palpation und Bildgebung legten jedoch das Vorliegen eines retrorektalen Tumors bzw. die Metastase eines Adenokarzinoms nahe, welche jeweils eine lokale Exzision erfordert hatten. Die Anwendung eines stufenweisen operativen Algorithmus unter Berucksichtigung einer schnellschnitthistologischen Begutachtung ermoglichte eine exakt der Entitat gerechte Therapie.

CDX2 is an epithelial transcription factor that regulates intestinal differentiation and is involved in the development of intestinal metaplasia (IM).To analyse the expression of CDX2 in the gastric mucosa in various locations and its relationship to Helicobacter pylori infection and gastro-oesophageal reflux disease (GORD).69 patients with upper gastrointestinal symptoms were stratified into four groups according to their H pylori and GORD status. Patients without infection and without GORD were the reference group (H pylori(-)/GORD(-)). Biopsies from the antrum, corpus and cardia were assessed by histopathology according to the updated Sydney System. CDX2 transcription levels were determined by quantitative RT-PCR and immunohistochemistry.CDX2 gene expression was significantly up-regulated in antral and cardia mucosa of patients with both H pylori infection and GORD (26- and 100-fold, respectively; p0.05), but remained unchanged in corpus mucosa. If only H pylori infection or GORD was present, CDX2 expression levels were 6- to 11-fold increased in the antrum, but without reaching statistical significance. CDX2 expression correlated positively with the degree of IM (p0.01) and the degree of H pylori induced inflammation (p0.05). Gene expression data were confirmed immunohistochemically by the detection of CDX2 in areas of IM and in focally distributed CDX2-expressing cells in non-metaplastic gastric mucosa.The combined presence of H pylori infection and GORD leads to an up-regulation of CDX2 gene expression in cardia and antral mucosa, but not in the corpus.

Die Refluxösophagitis ist eine Erkrankung, die aufgrund ihrer steigenden Inzidenz und Prävalenz in den industrialisierten Ländern zunehmend an Bedeutung gewinnt. Sie ist gekennzeichnet durch ihre Chronizität und Symptomvielfalt. Hauptsymptom ist das Sodbrennen; sie kann aber auch asymptomatisch verlaufen. Ursache sind vor allem Motilitätsstörungen im oberen Gastrointestinaltrakt. Der Einfluss der Helicobacter pylori Infektion ist Gegenstand der aktuellen Diskussion. Die Einteilung nach Savary-Miller wird zunehmend durch die Los Angeles Klassifikation abgelöst. Neben chronischen Veränderungen wie Ulzera und Strikturen steht das Risiko der Entwicklung eines Barrett-Ösophagus sowie die Ausbildung eines Adenokarzinoms im Vordergrund. Protonenpumpen Inhibitoren stellen die Therapie der Wahl sowohl in der Akuttherapie wie auch in der Redizivprophylaxe dar. Endoskopisch interventionelle Verfahren wie die Thermokoagulation, die photodynamische Therapie und die mukosale Schleimhautresektion zur Therapie des Barrett-Ösophagus mit hochgradigen Dysplasien oder Frühkarzinomen sollten nur im Rahmen kontrollierter Studien eingesetzt werden. Chirurgische Verfahren, wie die Fundoplicatio, sollten nur bei einem selektierten Patientenkollektiv zum Einsatz kommen.

Every duodenal ulcer (DU) associated with H. pylori (HP) infection should be treated with HP eradication therapy. The recommended HP eradication therapy is a short-term triple therapy for 7 or 10 days’ duration, consisting of a protonpump-inhibitor (PPI), or ranitidine bismuth citrate (RBC) and two antibiotics selected among clarithromycin, metronidazole (or tinidazole), and amoxicillin. If possible, any treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued. If continuation of NSAID treatment is necessary, concomitant therapy with a PPI is necessary. HP-negative DUs are treated with one oral standard dose of PPI, although some patients will need higher doses to have the DU healed. Whereas in uncomplicated DU the disappearance of symptoms is a good surrogate marker for DU healing, the healing of bleeding DU must be documented by endoscopy. The role of surgery is to treat complications of DU, such as perforation or uncontrollable bleeding, not to reduce gastric acid secretion.

The current standard of Helicobacter pylori treatment has been confirmed by the studies presented at the Lisbon workshop-that is, one of three one week proton pump inhibitor (PPI) based triple therapies comprising a twice daily standard dose of a PPI in combination with two of the following antimicrobial agents: clarithromycin, amoxycillin, or a nitromidazole. This standard of treatment is also highly efficacious and cost-effective in routine community practice. The current data confirm the equivalence of ranitidine bismuth citrate to PPI, and of azithromycin to clarithromycin. The optimum dose for azithromycin has not yet been defined. There is some evidence that in certain regions treatment for more than one week may be advantageous. The reasons are still not clear. However, microbial resistance may be one important factor, as it has a substantial effect on treatment outcome and the prevalence of resistance varies considerably in different areas. The negative impact of resistance is increased by shortening the treatment time. At present, there is no general necessity to test for resistance before treatment. However, before selection of a second line treatment, testing for resistance is recommended.

We present a case of a retrorectal space occupying lesion diagnosed as an adenocarcinoma of unknown primary origin by preoperative histopathology. Localization slightly above the anal sphincter would have required extirpation of the rectum. Rectal palpation, endosonography and radiological imaging, however, suggested a retrorectal tumor or a metastasis of an adenocarcinoma. Both entities would have required local resection. We applied a surgical algorithm including frozen biopsy allowing a stepwise choice of operative procedure from the spectrum in question. The operation performed was thus tailored to the entity of the tumor.

An increasing rate of infections with Shiga toxin/verotoxin-producing Escherichia coli (STEC/VTEC) O104:H4 has been observed in Germany since May 2011, with unusually high numbers of patients suffering from haemolytic uraemic syndrome (HUS). We report a STEC/VTEC O104:H4 case without HUS, presenting with colonic ischaemia demanding surgery. This atypical clinical presentation of STEC O104:H4 infection might indicate new severe complications associated with this uncommon strain, and highlights the importance of immediate interdisciplinary assessment of STEC/VTEC patients.

An increasing rate of infections with Shiga toxin/verotoxin-producing Escherichia coli (STEC/VTEC) O104:H4 has been observed in Germany since May 2011, with unusually high numbers of patients suffering from haemolytic uraemic syndrome (HUS). We report a STEC/VTEC O104:H4 case without HUS, presenting with colonic ischaemia demanding surgery. This atypical clinical presentation of STEC O104:H4 infection might indicate new severe complications associated with this uncommon strain, and highlights the importance of immediate interdisciplinary assessment of STEC/VTEC patients.

This guideline updates a prior concensus recommendation of the German Society for Digestive and Metabolic Diseases (DGVS) from 1996. It was developed by an interdisciplinary cooperation with representatives of the German Society for Microbiology, the Society for Pediatric Gastroenterology and Nutrition (GPGE) and the German Society for Rheumatology. The guideline is methodologically based on recommendations of the Association of the Scientific Medical Societies in Germany (AWMF) for providing a systematic evidence-based consensus guideline of S 3 level and has also implemented grading criteria according to GRADE (Grading of Recommendations Assessment, Development and Evaluation). Clinical applicability of study results as well as specifics for Germany in terms of epidemiology, antibiotic resistance status, diagnostics and therapy were taken into account.

An adenocarcinoma of the distal esophagus may also be designated as Barrett's carcinoma as it evolves from Barrett's esophagus. Barrett's esophagus currently is defined as a columnar metaplasia of the distal esophagus, as identified by endoscopy, that, upon histopathology, is confirmed to contain intestinal metaplasia. A different histological entity of columnar metaplasia of the distal esophagus is cardia-type mucosa which probably precedes intestinal metaplasia, but lacks goblet cells typical for the latter. The conversion rate from Barrett's esophagus to Barrett's carcinoma amounts to 0.5 to 1 % per year. Patients with reflux symptoms should undergo early endoscopy in order to search for Barrett's esophagus (screening). In those cases where Barrett's esophagus is identified, regular endoscopic controls should be scheduled (surveillance). The intervals for this have been defined by recent consented guidelines. The aim is to detect neoplasia early. Neoplasia confined to the epithelium or mucosal layer can mostly be treated by endoscopic resection. The depth of infiltration, as determined by histopathology of the resected specimen, allows one to estimate the risk of lymph node metastasis, and therefore is crucial for the final judgment as to whether the endoscopic intervention may be considered curative. Individually, the risk of metastasis has to be weighed against the risk of morbidity and mortality conferred by the alternative surgical resection. The rapid increase of the incidence of Barrett's carcinoma in Western countries suggests that life style factors, in particular overweight, having a causal role. Data from interventional trials on prevention are, however, pending.

Liver abscesses in patients with Crohn's disease are rare. We report on a patient with Crohn's disease and a liver abscess of the left lobe caused by an enterohepatic fistula. With treatment of antibiotics and Infliximab the abscess showed complete regression. Percutaneous drainage of the liver abscess was not performed because the abscess was shown not to be completely liquefied at echo-enhanced ultrasound. This case report demonstrates the usefulness of percutaneous conventional and echo-enhanced ultrasound for the diagnosis of liver abscesses. Furthermore, this case also shows that enterohepatic fistulas can be diagnosed precisely with percutaneous ultrasound.

Inflammation of the gastric cardia ('carditis') is a histological diagnosis. It seems reasonable to transfer histological criteria of the updated Sydney classification from the distal stomach to the cardia as long as a special classification of inflammation of the esophagogastric junction is lacking. The two best characterized causes of carditis are Helicobacter pylori infection and gastroesophageal reflux disease (GERD). However, the causal contribution and interference of these two factors are highly controversial, as is the clinical relevance of carditis in terms of eliciting symptoms or conferring an increased cancer risk. Variability of studies on carditis is based on conflicting concepts of the normal anatomy of the esophagogastric junction. Cardia-type mucosa (CM) apparently exists at birth as a tiny circular area, and extends to a larger area in adulthood. This implies that cardia-type mucosa is largely metaplastic. Metaplastic CM may evolve in the lower esophagus as a consequence of GERD. It is a general phenomenon that H. pylori-induced gastritis also involves the gastric cardia, irrespective whether the cardia is lined by fundus-type mucosa or CM. The contribution of GERD to inflammation of CM in H. pylori-negative individuals is, however, highly controversial. Prevalence of carditis in GERD patients fluctuates between 10 and 97%. Hence, because of its high frequency and low specificity, carditis can currently not be considered as a clinical entity. The role of carditis for the increasing incidence of cancer of the esophagogastric junction requires careful studies that include accurate description of the area with adequate biopsy protocols.

Conflicting data regarding new onset or deterioration of gastroesophageal reflux disease (GORD) following eradication of Helicobacter pylori infection have been reported. Successful eradication therapy may influence gastric acid output. The study aimed to to investigate whether patients with pre-existing GORD or peptic ulcer disease may experience deterioration of GORD.75 consecutive patients of a prospective longitudinal study (median age 66 years, n = 45 males) had received successful H. pylori eradication therapy because of the following main diagnosis: peptic ulcer (n = 37), GORD (n = 16), functional dyspepsia (n = 22). Two to three years later, they had an interview regarding the course of their dyspeptic and reflux symptoms. Negative H. pylori status at present was confirmed by (13)C-urea breath test in all patients. Ten patients were excluded because of proton pump inhibitor treatment.Patients with deterioration of GORD (new onset or increasing reflux symptoms) were found significantly more frequently in the group with functional dyspepsia (36 %) compared to pre-existing GORD (16 %) or peptic ulcer disease (5 %). Improvement of pre-existing reflux complaints were reported mostly by patients with peptic ulcer disease. There was no significant impact of initial reflux manifestations like reflux symptoms or reflux oesophagitis on the course.During long-term follow-up after H. pylori eradication, patients experience improvement as frequently as deterioration of reflux symptoms. There is a tendency towards improvement of reflux symptoms if peptic ulcer disease had been the indication for eradication, but towards deterioration in patients with initial functional dyspepsia. A clinical relevant prediction, however, is not feasible.

To study the efficacy of three pantoprazole-based triple therapy regimens for the eradication of Helicobacter pylori infection and gastric ulcer healing.In an open, multi-centre, randomized study, 519 H. pylori-positive patients with active gastric ulcer were randomized to receive pantoprazole (40 mg) (P) and two of three antibiotics: clarithromycin (500 mg) (C), metronidazole (500 mg) (M) or amoxicillin (1000 mg) (A). Triple therapy (PAC, PCM, PAM) was administered twice daily for 7 days, followed by pantoprazole until the ulcer had healed. Antrum and corpus biopsies were taken to determine the pattern of gastritis, to assess the H. pylori status and to determine the strain susceptibility to antibiotics, and from the ulcer margins and base to exclude malignancy. Scores based on the Sydney system were used to categorize the gastritis phenotypically.The H. pylori eradication rates for the per protocol (intention-to-treat) analysis were 89% (67%) for PAC, 83% (68%) for PCM and 76% (60%) for PAM, with a significant difference between PAC and PAM. Healing rates after 4 weeks were 91% for PAM, 90% for PCM and 88% for PAC (per protocol analysis). The eradication rates were lower in patients in whom strains resistant to any antibiotic used in the triple therapies were detected. Successful eradication [odds ratio, 5.2 (3.3; 8.3)] and the ulcer size (15 mm) were significant predictors for healing after 4 weeks. The regimens showed a comparable safety profile and compliance.Pantoprazole-based triple therapies are effective in the eradication of H. pylori infection in gastric ulcer patients, as reported in previous similar sized studies in duodenal ulcer patients. Successful eradication and an ulcer size of15 mm are the best predictors of gastric ulcer healing after 4 weeks.

Re-bleeding of Helicobacter pylori-associated peptic ulcer disease is reduced by H. pylori eradication.To validate a non-invasive test, the Premium Platinum HpSA stool test, in patients with upper gastrointestinal bleeding.Stool samples of consecutive patients with relevant bleeding from gastric or duodenal ulcers or erosions were collected at initial endoscopy and during the following week. Samples were assessed using the HpSA test. H. pylori status was defined by three biopsy-based reference methods: culture, rapid urease test and histology. It was positive if culture was positive or if rapid urease test and histology were positive.One hundred and fourteen patients (mean age, 66 years) were included. In accordance with the definition, 56 (49%) were H. pylori positive. The sensitivity and specificity of the first stool sample were 84% and 90%, respectively. The respective values for two samples from consecutive days were 91% and 86%. In comparison with a serum immunoglobulin G antibody enzyme-linked immunoabsorbent assay, the HpSA test showed superior specificity.The diagnostic accuracy, in particular the sensitivity, of the HpSA stool test is reduced by upper gastrointestinal bleeding. The positive predictive value of 89%, however, justifies the initiation of eradication therapy on the basis of a positive stool test. A negative test result should be confirmed by a further diagnostic method.

Helicobacter pylori eradication marks a historical milestone in the cure of peptic ulcer disease and indications for other H. pylori-associated clinical conditions are now expanding and include also the possible prevention of gastric cancer in selected populations at risk1,2. H. pylori eradication therapies are still complex, and the increased use of these treatments therefore demands careful consideration of factors responsible for treatment failure.

Rapid blood tests for diagnosis of Helicobacter (H.) pylori infection enable to detect antibodies against H. pylori instantly without laboratory equipment. Primary aim: to validate the Helisal Rapid Whole Blood Test (HRBT) with endoscopic bioptic methods as reference. Secondary aim: to compare the HRBT with ELISA IgG serology.The HRBT was performed in 145 consecutive dyspeptic patients (median age 59 years) before undergoing esophagogastroduodenoscopy including biopsies from gastric antrum and corpus. A positive H. pylori status was defined by a positive culture or the combination of a positive rapid urease test and a positive histology. Serum for ELISA IgG testing was available from 92 patients.The H. pylori status was positive in 66% of the patients. The sensitivity of the HRBT resulted at 80%, the specificity at 82%. The sensitivity of the HRBT for a positive ELISA test amounted to 87%, the specificity to 96%.The diagnostic validity of the HRBT is insufficient for clinical application. False test results add up by the general discrepancy between serological and bioptic methods and by diminished sensitivity compared to ELISA serology.

Over the last 15 years several new aspects in the pathogenesis and basic changes in therapeutic strategies for healing of peptic ulcers have been introduced. The discovery of Helicobacter pylori, the possibility of treatment of the infection and consecutive healing of peptic ulcer disease have changed the understanding of the pathophysiology of the peptic ulcer disease. Most gastric or duodenal ulcers are based on Helicobacter pylori infection. Newer therapeutic strategies to cure Helicobacter pylori infection consist of proton pump inhibitor (PPI) based triple therapy, containing in addition two antibiotics chosen from clarithromycin, amoxicillin and metronidazole, administered over 7 days. The other main cause of gastroduodenal ulcers are non-steroidal antirheumatic drugs or aspirin intake. PPI are therapeutic strategies of choice for treatment of such lesions. Main topics of this overview are the principles and the therapeutic proceeding in the management of Helicobacter pylori-associated peptic ulcer disease. The differences between duodenal and gastric ulcer are especially dealt with.

Acid output is related to the gastritis pattern in Helicobacter pylori infection. The hypothesis to be tested is that gastritis in patients with Barrett's esophagus, defined as columnar epithelia lined lower esophagus (CELLO) with intestinal metaplasia (IM), is antrum predominant.Patients undergoing esophagogastroduodenoscopy were investigated for CELLO. The gastritis parameters H. pylori density, activity, and chronicity were graded in biopsy specimens of antrum and corpus. IM was assessed in biopsies from CELLO patients. In a prospective part, 19 patients with CELLO with IM were compared with 38 age-matched control patient with dyspepsia.Of 200 patients with CELLO, 85% had a short segment (3 cm), 15% a segment ofor =3 cm. IM was present in 36% of cases with a short CELLO and in 84% of patients with a long segment. The H. pylori prevalence was 50%, independent of the length of CELLO or the presence of IM. The gastritis phenotype was minimally antrum predominant. The antrum/corpus distribution was not related to the length of CELLO or the presence of IM and not different from controls. The activity in corpus and antrum was lower in patients with CELLO with IM as compared with patients with CELLO without IM or controls.A high proportion of patients with CELLO are H. pylori infected. The pattern of H. pylori gastritis is characterized by a pangastritis with low activity which is not likely to predispose to an increase in acid output after eradication.