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Background: Recently, single photon emission computed tomography (SPECT) scanning was described as a non-invasive technique to assess fundic accommodation. However, in contrast with the barostat, no intragastric distending force is applied during SPECT scanning. We hypothesised that in the absence of a barostat balloon, SPECT scanning largely detects the volume effect of the ingested meal and is a rather insensitive tool to detect fundic relaxation. Methods: After an overnight fast, healthy volunteers underwent a barostat study and SPECT scanning on two separate days to assess: (1) meal induced fundic accommodation (Nutridrink, 200 ml, 300 kcal); and (2) gastric relaxation to 1 mg intravenous glucagon. Results: Fasting fundic volumes (145 (8) v 280 (32) ml; p = 0.001) and average postprandial volume (329 (10) v 571 (53) ml; p = 0.001) were significantly lower measured with SPECT compared with the barostat study. Meal induced fundic relaxation (183 (10) v 289 (46) ml; p = 0.050) and the postprandial/fasting volume ratio (2.32 (0.10) v 2.27 (0.29); p = 0.892) did not differ significantly between SPECT scanning and the barostat. However, no correlation could be determined between accommodation volumes measured by both techniques. In contrast with meal induced relaxation, the glucagon induced increase in fundic volume (19 (5) v 406 (56) ml; p = 0.007) and post/pre glucagon ratio (1.16 (0.03) v 3.02 (0.54); p = 0.046) were significantly lower when measured by SPECT scanning compared with the barostat. Conclusion: SPECT scanning detects changes in postprandial volume but is less suitable than the gastric barostat in detecting changes in gastric tone. Our study therefore questions its role as a tool to detect impaired accommodation and warrants further validation of this technique.

IgG4-associated cholangitis (IAC) is a recently defined disease entity which shares a number of clinical, biochemical, and radiological features with primary sclerosing cholangitis (PSC). In contrast to PSC, IAC responds to immunosuppressive treatment, is not associated with inflammatory bowel disease, and mainly affects elderly men above the age of 60 years. Today, IAC is regarded as one variant of IgG4-related systemic disease (ISD) of which autoimmune pancreatitis (AIP) is the best studied organ manifestation. The diagnosis of IAC is based on biochemical, radiological and histologic features, among which elevated serum levels of IgG4, extra- and intrahepatic biliary strictures as visualized by cholangiography, multifocal IgG4-rich lymphoplasmacytic sclerosing infiltrations in liver and bile duct tissue, and association with AIP are of key importance. This review aims at summarizing clinical features, diagnostic criteria, therapeutic strategies and most recent insights in the pathophysiology of IAC and other organ manifestations of ISD.

SUMMARYSeveral important pathophysiological mechanisms have been identified in functional dyspepsia, however a complete understanding of these mechanisms and beneficial therapeutic strategies are still lacking. Based on the currently available literature we aimed at providing a critical view on one of these pathophysiological mechanisms, impaired accommodation.Although impaired gastric accommodation is identified as a major pathophysiological mechanism, the clinical evidence supporting its role as an important therapeutic target is currently still lacking. Treatment with fundic relaxant drugs has shown conflicting results and has been rather disappointing in general.These negative findings could be explained by the fact that impaired fundic accommodation is part of a more complex disorder involving other regions of the proximal gut or by the increasing insight that central mechanisms may play an important role. Future studies of impaired accommodation should take these considerations into account.

Distal oesophageal acid exposure has been shown to increase visceral sensitivity of the proximal oesophagus via central sensitization. Here we evaluated whether acidification of the distal oesophagus also affects the sensorimotor function of the proximal stomach. A gastric barostat study combined with a 30-min acid (HCl 0.15 mol L(-1)) or saline infusion in the distal oesophagus was performed in 18 healthy volunteers. Gastric and cutaneous sensitivity was assessed before and up to 2 h after the start of infusion. Directly after acid infusion, but not after saline, the threshold for discomfort decreased (-6.4 +/- 1.7 vs 0.4 +/- 0.4 mmHg; P = 0.028) and distension-induced symptoms increased significantly compared with the baseline (122 +/- 49% vs -3 +/- 9%). Cutaneous sensitivity remained unaffected by acid infusion. In contrast, when the infused liquid was aspirated 3 cm more distally, at the level of the lower oesophageal sphincter, the effect of acid infusion on gastric sensitivity was abolished and the increase in distension-induced symptoms was reduced (61 +/- 24%). Distal oesophageal acid infusion induces visceral hypersensitivity without affecting somatic sensitivity arguing against a similar mechanism of central sensitization as observed in non-cardiac chest pain. As reduction of the acid load to the stomach prevented this effect, our findings indicate that either gastric and/or duodenal acidification is involved. It should be emphasized though that aspiration from distal oesophagus may have attenuated the effect by reducing the acid-exposed area or by reducing the contact time.