Authors: Fixa B, Komarkova O, Prochazkova J.

Summary: Serum lysozyme was reevaluated in inflammatory bowel disease and other gastrointestinal disorders. A total of 109 patients were divided into six groups: ulcerative colitis (28), Crohn's disease (9), simple atrophic gastritis (16), atrophic gastritis and pernicious anemia (23), functional dyspepsia (17), and controls (16).

Elevated levels of lysozyme, compared with control levels, were found not only in ulcerative colitis and Crohn's disease but also in atrophic gastritis with or without pernicious anemia and in functional dyspepsia. The elevation of lysozyme, since it results from the product of granulocytes and macrophages present in increased amounts in the mucosa of inflammatory bowel diseases, is easily explained.

The cellular infiltration in atrophic gastritis may also explain the elevated lysozyme levels. The higher lysozyme levels in some patients with functional dyspepsia could possibly reflect an underlying latent inflammatory process.

Study link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6673061&dopt=Abstract

Authors: Nakajima S, Krishnan B, Ota H, Segura AM, Hattori T, Graham DY, Genta RM.

Institution: Department of Medicine, Veterans Affairs Medical Center, Houston, Texas, USA.

Background and Aims: Mast cells are initiators and regulators of inflammation, but their role in the human stomach remains unclear. Therefore, the extent and distribution of mast cell involvement in gastritis with or without Helicobacter pylori infection was investigated.

Results: Mast cell density was significantly greater in the mucosa with gastritis, with or without H. pylori infection, than in the mucosa of noninfected normal subjects. In the antrum, density was much greater in H. pylori-infected peptic ulcer subjects than in the other gastritis groups. It also correlated significantly with the intensity of inflammation. Mast cell degranulation was demonstrated by electron microscopy in H. pylori-infected mucosa. Mast cell density in ulcer patients decreased significantly after cure of H. pylori infection.

Conclusions: Mast cells may be important effector cells in the pathogenesis of gastritis, especially in H. pylori-associated peptic ulcer.

Study link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9287964&query_hl=106

Authors: Hall W, Buckley M, Crotty P, O'Morain CA.

Institution: Department of Gastroenterology, Adelaide & Meath Hospital, Trinity College, Tallaght, Dublin 24, Ireland, UK.

Background and Aims: Mast cells might be involved in pathogenesis of functional dyspepsia because they can release a wide range of potent mediators, capable of altering gastric nerve and muscle function. This study aimed to determine whether mast cell numbers were increased in the gastric mucosa of patients with functional dyspepsia compared to control subjects.

Results: Mast cells were significantly increased in H. pylori negative functional dyspepsia samples compared to normal control samples in the antrum (230.1 +/- 11.3 vs. 94.8 +/- 8.4, P < 0.001) and corpus (264.1 +/- 27.1 vs. 123.9 +/- 11.5, P = 0.001). Mast cells were also significantly increased in the antrum of patients with H. pylori positive functional dyspepsia compared to asymptomatic control subjects (166.5 +/- 17.0 vs. 94.8 +/- 8.4, P < 0.03). However, there was no significant difference between mast cell numbers in patients with H. pylori positive functional dyspepsia compared to inflammatory control subjects.

Conclusions: Mast cells are increased in functional dyspepsia, independently of inflammation. This might contribute to the pathogenesis of functional dyspepsia by altering signaling in the brain-gut axis.

Study link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15017654&query_hl=94

Author: Spiller RC.

Institution: Division of Gastroenterology, The Wolfson Digestive Disease Centre, University Hospital, Nottingham NG7 2UH, UK. robin.spiller@nottingham.ac.uk

Summary: The term 'Functional diseases' implies symptoms arising from an organ without overt pathology. However this is more apparent than real since inflammation often leaves changes in nerves and mucosal function only apparent with specialised techniques.

Acute onset functional dyspepsia accounts for around 1/5 of functional dyspepsia and is characterised by early satiety, nausea, vomiting and weight loss. Impaired postcibal fundal accommodation may underlie some of these symptoms. Post infectious gastroparesis is much rarer and is associated with markedly delayed gastric emptying and antral hypomotility. Approximately 1/10 of IBS cases describe a post infectious onset.

Post infectious IBS is typically of the diarrhoea-predominant type. Post inflammatory functional diseases tend to be associated with less psychological abnormalities and have a better prognosis than other functional diseases. There are isolated anecdotal reports of symptom response to anti-inflammatory treatments but larger controlled trials are needed.

Study link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15324705&query_hl=94

Authors: Andersen LP, Holck S, Janulaityte-Gunther D, Kupcinskas L, Kiudelis G, Jonaitis L, Janciauskas D, Holck P, Bennedsen M, Permin H, Norn S, Wadstrom T.

Institution: Department of Clinical Microbiology, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. lpa@rh.dk

Summary: Helicobacter pylori is the most important cause of gastritis, peptic ulcers and the development of gastric cancer. The chronic active inflammation is dominated by neutrophils, macrophages, lymphocytes and plasma cells. Several interleukins (IL-8, IL-10 and IFN-gamma) are involved in the inflammatory process in the gastric mucosa. The aim of this study was to investigate the gastric inflammation in patients with functional dyspepsia.

Fifty-three consecutive patients were included and antral biopsies were obtained for histology, culture and immunohistochemistry. The sections were examined for the interleukins IL-4, IL-6, IL-8, IL-10 and IFN-gamma as well as for the cell markers CD4, CD8, CD14, Cd19, CD25 and CD30. Only CD4 and CD19 were significantly increased in patients with increased gastric inflammation and increased density of H. pylori. However, several of the examined markers (IFN-gamma, IL-8, IL-10 and CD14) showed a non-significant trend to be increased in patients with extensive gastric inflammation and high density of H. pylori.

Therefore, an arbitrary index (IM11) for all the 11 immunological markers was made as an average value for each of the four morphological groups. For the four morphologically different groups of patients the values were 0.49, 0.77, 0.86 and 1.25, respectively. Significant increases in the index from none to moderate antral inflammation as well as the density of H. pylori were found (p<0.001).

By using an index of inflammatory markers trends can be summarized and thereby significant which may be of importance when gastric inflammation is investigated in children and patients with functional dyspepsia.

Study link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15866221&query_hl=94