Based on several case-control studies, it has been estimated that familial aggregation and genetic susceptibility play a role in up to 10% of patients with pancreatic cancer, although conclusive epidemiologic data are still lacking. Therefore, we evaluated the prevalence of familial pancreatic cancer and differences to its sporadic form in a prospective multicenter trial. A total of 479 consecutive patients with newly diagnosed, histologically confirmed adenocarcinoma of the pancreas were prospectively evaluated regarding medical and family history, treatment and pathology of the tumour. A family history for pancreatic cancer was confirmed whenever possible by reviewing the tumour specimens and medical reports. Statistical analysis was performed by calculating odds ratios, regression analysis with a logit-model and the Kaplan-Meier method. Twenty-three of 479 (prevalence 4.8%, 95% CI 3.1-7.1) patients reported at least 1 first-degree relative with pancreatic cancer. The familial aggregation could be confirmed by histology in 5 of 23 patients (1.1%, 95% CI 0.3-2.4), by medical records in 9 of 23 patients (1.9%, 95% CI 0.9 -3.5) and by standardized interviews of first-degree relatives in 17 of 23 patients (3.5%, 95% CI 2.1-5.6), respectively. There were no statistical significant differences between familial and sporadic pancreatic cancer cases regarding sex ratio, age of onset, presence of diabetes mellitus and pancreatitis, tumour histology and stage, prognosis after palliative or curative treatment as well as associated tumours in index patients and families, respectively. The prevalence of familial pancreatic cancer in Germany is at most 3.5% (range 1.1-3.5%) depending on the mode of confirmation of the pancreatic carcinoma in relatives. This prevalence is lower than so far postulated in the literature. There were no significant clinical differences between the familial and sporadic form of pancreatic cancer.

Although this small study appears to show that DBE has a clinically higher diagnostic yield than spiral enteroscopy, larger studies are needed to confirm this preliminary finding.

This large prospective survey shows that propofol sedation in gastrointestinal endoscopy is a safe procedure with a low potential of risk in daily routine. However, high risk patients (ASA ≥ 3) should be identified, especially before emergency endoscopies and managed by additional persons for NAAP and under intensive care surveillance.

We examined 39 samples of metaplastic specialized epithelium (SE), 27 of low-grade dysplasia (LGD), 27 of high-grade dysplasia (HGD), and 46 of adenocarcinoma (CA) derived from Barrett esophagus for c-erb-b2 gene amplification using differential polymerase chain reaction and for overexpression of c-erb-b2 protein using immunohistochemical analysis. Amplification of the c-erb-b2 gene was as follows: SE, 0.0%; LGD, 0.0%; HGD, 11.1%; and CA, 13.6%; and protein overexpression was as follows: SE, 0.0%; LGD, 7.4%; HGD, 18.5%; and CA, 21.7%. In 8 (89%) of 9 samples, c-erb-b2 gene amplification correlated with protein overexpression. The reverse was true in 8 (47%) of 17 samples: c-erb-b2 protein overexpression was proved with simultaneous gene amplification. Amplification of c-erb-b2 is a late event in the carcinogenesis of Barrett esophagus. In contrast, protein overexpression appears more often and earlier Besides gene amplification, other mechanisms to induce protein overexpression must exist.

Background Eosinophilic esophagitis (EoE) is detected frequently in dysphagia and noncardiac chest pain. Management of patients with EoE may be complicated because EoE is associated frequently with esophageal motility disorders. We present the rare case of esophageal achalasia (EA) associated with eosinophilic infiltration and a literature review. Material and methods A patient with dysphagia and eosinophilic infiltration referred to our clinic underwent standardized diagnostic work-up including symptom questionnaire, esophagogastroduodenoscopy (EGD) with esophageal biopsies, barium swallow, high-resolution esophageal manometry, and combined intraluminal 24-hour pH-impedance testing (pH/MII). Results The patient had an Eckardt score of 8. EGD and mucosal biopsies showed typical EoE with > 15 eosinophil leucocytes per high-power field. Barium swallow revealed typical sign of achalasia. HREM indicated EA type 2 according to the Chicago classification. PH/MII was normal. Oral and systemic corticoid therapy were without effect. After successful treatment by pneumatic dilation of the cardia, symptoms relieved and eosinophilic infiltration returned to normal. Conclusion The results suggest that the patient had primary EA associated with eosinophilic infiltration and that the combined occurrence of these rare diseases is not just a coincidence.