Tamara Madácsy

Analysis of research activity in gastroenterology: Pancreatitis is in real danger

Objective Biomedical investment trends in 2015 show a huge decrease of investment in gastroenterology. Since academic research usually provides the basis for industrial research and development (R&D), our aim was to understand research trends in the field of gastroenterology over the last 50 years and identify the most endangered areas. Methods We searched for PubMed hits for gastrointestinal (GI) diseases for the 1965–2015 period. Overall, 1,554,325 articles were analyzed. Since pancreatology was identified as the most endangered field of research within gastroenterology, we carried out a detailed evaluation of research activity in pancreatology. Results In 1965, among the major benign GI disorders, 51.9% of the research was performed on hepatitis, 25.7% on pancreatitis, 21.7% on upper GI diseases and only 0.7% on the lower GI disorders. Half a century later, in 2015, research on hepatitis and upper GI diseases had not changed significantly; however, studies on pancreatitis had dropped to 10.7%, while work on the lower GI disorders had risen to 23.4%. With regard to the malignant disorders (including liver, gastric, colon, pancreatic and oesophageal cancer), no such large-scale changes were observed in the last 50 years. Detailed analyses revealed that besides the drop in research activity in pancreatitis, there are serious problems with the quality of the studies as well. Only 6.8% of clinical trials on pancreatitis were registered and only 5.5% of these registered trials were multicentre and multinational (more than five centres and nations), i.e., the kind that provides the highest level of impact and evidence level. Conclusions There has been a clear drop in research activity in pancreatitis. New international networks and far more academic R&D activities should be established in order to find the first therapy specifically for acute pancreatitis.

Pancreatic epithelial fluid and bicarbonate secretion is significantly elevated in the absence of peripheral serotonin

We read the manuscript by Sonda et al 1 recently published in Gut with great interest. The authors elegantly demonstrated that lack of peripheral serotonin (5-HT) in tryptophan hydroxylase 1 knockout (TPH1−/−) mice remarkably limited pancreatic damage and leucocyte infiltration during the early phase of cerulein-induced acute pancreatitis (AP) and identified 5-HT as an important regulator of zymogen secretion in acinar cells. Although the study was very comprehensive, the ductal function of TPH1−/− mice was not investigated, which might be another key player in this protection. Notably, 5-HT was shown to inhibit fluid and HCO3− secretion of pancreatic ductal epithelial cells,2 which play a pivotal role in pancreatic physiology and can influence the severity of AP.3 Thus, we investigated the possible alterations of pancreatic ductal secretion in TPH1−/− mice. To achieve our aim, intralobular/interlobular pancreatic ducts were isolated from the pancreas of wild-type (TPH1+/+) and TPH1−/− mice. HCO3− secretion was measured by three different, but complementary methods using …