The columnar-lined mucosa at the gastroesophageal junction may contain an inflammatory infiltrate, commonly referred to as carditis (or cardia gastritis). The etiology of carditis is not entirely clear since published data are conflicting. Some authors believe it to be secondary to gastroesophageal reflux disease (GERD) and others to Helicobacter pylori gastritis. This prospective study aims at clarifying the relationship between carditis and the histological, clinical, and endoscopic findings of GERD, in a large cohort of individuals negative for H. pylori infection. Eight hundred and seventy-three individuals (477 females and 396 males, median age 53 years) participated in this study. Biopsy material was systematically sampled from above and below the gastroesophageal junction. Reflux-associated changes of the esophageal squamous epithelium were assessed according to the Esohisto consensus guidelines. Grading of carditis was performed according to the Updated Sydney System, known from the histological evaluation of gastritis. In total, 590 individuals (67.5%) had chronic carditis. Of these, 468 (53.6%) had mild chronic inflammation, with 321 individuals (68.6%) showing no or minimal changes on endoscopic examination (Los Angeles Categories N and M). The presence of chronic carditis was associated with several GERDrelated parameters of the esophageal squamous epithelium (P < 0.0001), and data retained statistical significance even when analysis was restricted to individuals with mild chronic carditis and/or endoscopically normal mucosa. Chronic carditis was also associated with the presence of intestinal metaplasia (P < 0.0001). In addition, chronic carditis had a statistically significant association with patients' symptoms of GERD (P = 0.0107). This observation remained valid for mild chronic carditis in all patients (P = 0.0038) and in those with mild chronic carditis and normal endoscopic mucosa (P = 0.0217). In conclusion, chronic carditis appears to be the immediate consequence of GERD, correlating with patients' symptoms and endoscopic diagnosis. These results are valid in individuals with nonerosive reflux disease, which indicates a higher sensitivity of histological diagnosis. Our findings may impact the routine assessment of reflux patients.

Pseudomaligne Läsionen im Gastrointestinaltrakt stellen für den Pathologen eine besondere Herausforderung dar. Bei Patienten mit Refluxösophagitis kann die regenerative Hyperplasie des Plattenepithels des distalen Ösophagus erhebliche Atypien zeigen und somit Malignität vortäuschen. So genannte „bizarre Stromazellen“ stellen einen weiteren diagnostischen Fallstrick dar. Wir präsentieren den Fall einer 46-jährigen Patientin mit den Symptomen einer Refluxösophagitis, bei der wir einen gutartigen inflammatorischen Polypen des Ösophagus diagnostizierten. Die Histologie zeigte irreguläre („bizarre“) deutlich polymorphe Zellen im Stroma des Polypen, die durch nukleäre Hyperchromasie und Zellvergrößerung gekennzeichnet waren. Mitosen wurden nicht beobachtet. Die atypischen Zellen waren positiv für Vimentin. Die Ki67/MIB-1-Proliferationsrate war gering. Das morphologische Erscheinungsbild, einschließlich hilfreicher Merkmale für die Differenzialdiagnose und die Ätiologie bzw. Pathogenese der bizarren Stromazellen werden diskutiert.

In the gastrointestinal tract an accurate diagnosis of tumor-like lesions can be challenging. In patients with reflux disease regenerative hyperplasia of esophageal squamous epithelium may show marked pleomorphism and atypia thereby simulating malignancy. Bizarre stromal cells are another diagnostic pitfall. We present the case of a 46-year-old patient with symptoms of reflux disease who was diagnosed with a benign inflammatory polyp at the distal end of the esophagus. Histology revealed bizarre cells within the stroma of the polyp characterized by nuclear hyperchromatism and enlargement. Mitoses were not observed. The atypical cells were positive for vimentin. The Ki67/MIB-1 proliferation rate was low. The morphology and etiology of bizarre stromal cells, including helpful features for differential diagnosis are thoroughly discussed.

We present the case of a 58-year-old woman with a long-standing history of systemic lupus erythematosus (SLE) who developed a cytomegalovirus (CMV) infection with colonic perforation and subsequent purulent peritonitis whilst using combined immunosuppressive therapy. The pathogenesis and the clinical presentation of this unique case is discussed in detail. Opportunistic infection should always be kept in mind in SLE patients presenting with fever. Viral serology should be routinely performed in these patients, especially when immunosuppressive therapy is given, to avoid delay in instituting adequate management and therapy.

Hereditary diffuse gastric cancer is an autosomal dominant cancer syndrome with approximately 70%-80% penetrance. The cumulative lifetime risk of clinically detected gastric cancer is 63%-83% for women and 40%-67% for men. The average age at diagnosis is 40 years. Approximately 25%-40% of patients carry a germline mutation of the CDH1 gene. This gene encodes the transmembrane protein E-cadherin which plays a central role in cell adhesion and signal transduction. Classified according to Laurén, patients develop multifocal diffuse signet-ring cell carcinoma and, in late stages, linitis plastica. In the foveolar neck region, the site of gastric stem cells, in situ signet-ring cell carcinoma has been identified as a precursor lesion of invasive cancer. Therein, pagetoid spread of tumour cells below the preserved epithelium within the basal membrane represents the characteristic morphology. PAS staining may facilitate detection of tiny lesions.The present article provides detailed information on this cancer syndrome from the point of view of the pathologist as well as the human geneticist, focussing on the multidisciplinary management of affected patients.

Beim hereditären diffusen Magenkarzinom handelt es sich um ein autosomal-dominant vererbtes Tumorsyndrom mit 70–80%iger Penetranz. Das Lebenszeitrisiko, an einem klinisch manifesten Magenkarzinom zu erkranken, beträgt bei Frauen 63–83%, bei Männern 40–67%. Das Durchschnittsalter bei Diagnosestellung ist 40 Jahre. Betroffene Patienten besitzen in etwa 25–40% der Fälle eine Keimbahnmutation im CDH1-Gen. Dieses Gen kodiert für das Transmembranprotein E-Cadherin, das eine Schlüsselfunktion in der Zelladhäsion und in der Signaltransduktion einnimmt. Klassifiziert nach Laurén haben die Patienten ein multifokales diffuses Magenkarzinom mit Siegelringzellen und in späten Stadien eine Linitis plastica. Als Vorläuferläsionen kann ein siegelringzelliges In-situ-Karzinom in der Drüsenhalsregion, dem Sitz gastraler Stammzellen, gefunden werden. Charakteristisch sind Läsionen mit pagetoider Anordnung der Siegelringzellen unterhalb erhaltenem nichtneoplastischem Epithel. Die Anwendung einer PAS-Färbung erleichtert die Entdeckung kleinster Tumorherde. Der vorliegende Beitrag beleuchtet den Blickwinkel des Pathologen und den des Humangenetikers sowie das komplexe multidisziplinäre Management der Patienten.