Correspondence (letter to the editor): Incomplete picture.

A review article can be expected to provide a critical appraisal of published scientific evidence, especially if the bibliography is updated to include 2011. This was not done to a sufficient degree in all subchapters on the diagnostic evaluation and treatment of gastroenteropancreatic neuroendocrine tumors (GEP-NET) (1). The enormous importance of surgical resection undertaken with a curative intent, including surgery to lymph nodes and hepatic metastases in combination with microparticle liver embolization (transcatheter arterial embolization, TAE) and/or radiopeptide therapy in mostly metastasized NET was dealt with to an unsatisfactory extent. Such complex planning is currently the main task of an interdisciplinary NET center and preferably coordinated by an endocrinologist. Current data on the basis of recent studies do not allow any conclusions about the mean progression time, mean progression-free survival, prolonging the median progression-free interval, and the median time to renewed progression (1). On this background, prolonging the progression-free interval by only six months by means of new molecular therapies (2) is highly unsatisfactory and would presumably hardly be what the authors intended. The diagnosis of insulinoma in 2011 is based on the biochemical analysis of the unmistakable insulin secretion profile (3). This is recorded for 3–12 hours after glucose loading until neuroglucopenia. Without a secretion profile that is typical for an insulinoma, neuroglucopenia subsequently requires a selective intraarterial calcium injection test (SACI) (4). The 72 hour fasting test or C-peptide suppression test hardly helps to distinguish between patients with insulinoma and patients with pancreatic islet cell hyperplasia. Pathologists often refer to the latter as nesidioblastosis, whereas clinicians prefer the term non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS). Measuring proinsulin is vital, in contrast to measuring C-peptides. Testing for sulfonylureas is uncecessary; it implies that insulinoma patients are dissembling and also means that the indication was not clearly defined. In 30 years’ practice, we have never seen any reason to measure sulfonylureas, although we have diagnosed insulinoma in patients with a false-positive glibenclamide test result.