Obstructive jaundice can have various causes, and both neoplastic and non-neoplastic lesions have to be considered. In cases of malignant disease, the tumors are usually located in the extrahepatic bile ducts, the pancreatic head, or the ampulla of Vater [1]. In rare cases, the causative lesion originates from the duodenum [2] [3].

Pyloric gland adenoma is a peculiar tumor which mainly occurs within the stomach. Rarely, the tumor has been documented to originate from the duodenum and from other extragastric sites [1] [2] [3] [4].

Peripheral nerve sheath tumors (PNST) form the third commonest group of mesenchymal tumors within the gastrointestinal tract. They occur with a frequency of approximately 5 %, which compares with 50 % for gastrointestinal stromal tumors (GIST) and 30 % for smooth-muscle neoplasms [1]. In 2008, Liegl et al. described 10 cases of microcystic reticular schwannoma as a distinct variant with predilection for visceral sites [2]. Herein, we present two additional tumors that were detected upon screening colonoscopy in asymptomatic patients.

Giardia lamblia is the most common human parasite with a worldwide distribution and fecal-oral way of transmission. Diagnostic procedures include stool examination and gastroduodenoscopy with biopsy or secret aspiration. In most cases histology reveals a dense accumulation of the parasites on the surface of the duodenal mucosa with no or only slight inflammation. In rare cases, a dense inflammatory infiltrate with severe mucosal atrophy and increased count of intraepithelial lymphocytes may be seen. If in such cases the amount of parasites is low, the histological picture may mimic celiac disease. The two presented cases demonstrate the close morphological relationship and show the importance of considering giardiasis in the differential diagnosis in patients with suspected celiac disease.

To the Editor: Opportunistic infections are infections caused by organisms that take advantage of compromised host immunity. In patients with inflammatory bowel diseases (IBD) they may be linked to an inherent lack of appropriate immune response and/or to the use of immunomodulatory drugs. The majority of opportunistic infections are caused by viruses, such as herpes and cytomegalovirus, and they predominantly affect extraintestinal sites. Gastrointestinal bacterial infections in patients with IBD, which, in general, are not referred to as opportunistic, are commonly associated with symptomatic relapse of disease and may be detected by stool microscopy or culture in 10% of patients. Therein the majority of infections are due to Clostridium difficile and less frequently caused by other pathogens such as Salmonella or Campylobacter species. The prevalence of opportunistic bacterial infections, however, especially those affecting the gastrointestinal tract is unclear. We recently dealt with a 33year-old woman with ulcerative colitis diagnosed 1 year before, who reported upper abdominal pain, nausea and vomiting for the last 5 days. The stool frequency and consistency were normal. At time of consultation the patient was on azathioprine (AZA/6MP; 50 mg per day) as single medication. On clinical examination, deep palpation showed tender areas in the epigastrium. White blood cell count and C-reactive protein were within normal limits. Abdominal ultrasound was unremarkable. Esophagogastroduodenoscopy (EGD) showed mild erythema of the gastric mucosa with accentuation in the body. Similar mucosal changes were present in the duodenal bulb. Testing for Helicobacter pylori was negative using a C urea breath test as well as biopsy urease test. Microscopic examination of the gastric biopsy specimens revealed neutrophilic cryptitis with multiple crypt abscesses and a mixed inflammatory infiltrate within the stroma (Fig. 1). Staining for H. pylori was negative. The occurrence of multiple crypt abscesses with cystic dilation of crypt lumina is not typical for IBD-related changes within the upper gastrointestinal (GI) tract. In fact, histology was similar to acute infectious-type colitis, thus prompting diagnosis of presumably infectious gastritis. A second EGD performed 10 days later showed identical endoscopical as well as histological findings. Microbiological culturing of biopsy specimens identified Lancefield group C streptococcus as a causative pathogen. Following diagnosis, the patient was put on proton pump inhibitor (PPI) therapy (pantoprazole; 40 mg per day) and mesalazine (4 g per day) in addition to AZA/6MP. Treatment with respect to a microbial sensitivity test was discussed, but was refused by the patient. Our case corresponds well with the definition of opportunistic infections in IBD patients presented by Toruner et al, who reported the use of AZA/6MP to increase the risk of opportunistic infection 2–3-fold. Opportunistic gastric bacterial infections in IBD patients under AZA/6MP treatment remain poorly recognized. This may be due to overlapping signs and symptoms with acute exacerbation of the underlying disease as well as limited specificity of histological diagnosis. Focally enhanced gastritis, characterized by foveolae and/or glands surrounded by inflammatory cells consisting mainly of lymphocytes and histiocytes, and, occasionally, neutrophil granulocytes, is common in patients with Crohn’s disease. Gastroduodenitis associated with ulcerative colitis (GDUC), however, has only recently been recognized as a distinct clinical

A 51-year-old woman presented with acute epigastric pain after ingestion of a rice meal. The patient’s history was unremarkable apart from a long-term habit of ingestion of hot peppermint candies and nicotine misuse (20 cigarettes per day). Examination of the oral cavity revealed patchy leukoplakia. Laboratory tests were unremarkable apart from positive antinuclear antibody (ANA) (1 : 320) and positive anti-dsDNA antibodies. Gastroscopy disclosed a 6 cm long, incomplete rupture extending into the muscularis propria of the middle third of the esophagus ([Fig. 1 a]). The surrounding mucosa appeared thickened and showed areas of diffuse keratinization, thus acquiring a ”crackleware“ appearance. On histological examination, extensive hyperkeratosis was noted ([Fig. 1 b]). Biopsy specimens taken from the gastroesophageal junction revealed mild reflux disease. Further investigations with respect to esophageal involvement in collagenosis-associated motility disorders (including oesophageal manometry), however, were negative.