Correlation of mast cell density and histological parameters in helicobacter pylori-associated gastritis

Pathology ◽  
2010 ◽  
Vol 42 ◽  
pp. S75-S76
Author(s):  
Mana Taweevisit ◽  
Nareumon Wisedopas
2007 ◽  
Vol 2 (1) ◽  
pp. 14 ◽  
Author(s):  
Fatemeh E Mahjoub ◽  
Behnam Hassanbeglou ◽  
Zahra Pourpak ◽  
Fatemeh Farahmand ◽  
Nasim Kashef ◽  
...  

Cephalalgia ◽  
2013 ◽  
Vol 33 (5) ◽  
pp. 323-329 ◽  
Author(s):  
Jung Sook Yeom ◽  
Myung Bum Choi ◽  
Ji-Hyun Seo ◽  
Ji Sook Park ◽  
Jae-Young Lim ◽  
...  

Background Although many patients with functional dyspepsia experience headache concurrently with dyspeptic symptoms, studies suggesting mechanisms underlying this phenomenon are limited. Herein, we explore the relationship between gastrointestinal inflammatory cells and presence of headache associated with dyspeptic symptoms in children with Helicobacter pylori-negative functional dyspepsia. Methods Fifty-six patients with H. pylori-negative functional dyspepsia underwent upper endoscopy with biopsy to investigate recurrent epigastric pain or discomfort. Patients were divided into two groups according to self-reported presence of headache associated with dyspeptic symptoms. Inflammatory cells including mast cells, and enteroendocrine cells in the gastroduodenal mucosa were evaluated. Associations between headache presence and cellular changes in the gastroduodenal mucosa were examined. Results Headache was not associated with the grade of lymphocytes, neutrophil infiltration, or enteroendocrine cell density in the gastroduedenal mucosa. However, headache was significantly associated with high mast cell density in the body (27.81 ± 8.71 vs. 20.30 ± 8.16, p < 0.01) and duodenum (23.16 ± 10.40 vs. 14.84 ± 5.88, p < 0.01). Conclusions Presence of headache associated with dyspeptic symptoms is strongly related to mucosal mast cell density in pediatric patients with H. pylori-negative functional dyspepsia. Thus, our results may help clinicians understand and treat headache during dyspeptic symptoms in such pediatric patients.


2011 ◽  
Vol 5 (1) ◽  
pp. 163-167 ◽  
Author(s):  
Mana Taweevisit ◽  
Naruemon Klaikaew

Abstract Background: Helicobacter pylori (H. pylori) are a major cause of chronic gastritis and peptic ulcer. This organism plays a role in gastric carcinoma and B-cell lymphoma. However, the exact pathogenesis of gastric inflammation is still unclear. Mast cells, the important inflammatory cells for allergic process, may participate in the pathogenesis of gastritis related to H. pylori infection. Objective: Analyze the relationship between mast cell density, H. pylori intensity, histological alterations, and their severity of biopsy proven gastritis. Methods: One hundred eleven biopsied specimens were collected from Thai patients who were diagnosed H. pylori-associated gastritis of the antrum at King Chulalongkorn Memorial Hospital between 2002 and 2005. All biopsied specimens were examined according to the Updated Sydney System. Mast cell density was evaluated by 0.1% toluidine-stained sections. Results: The higher mast cell density was correlated with increased neutrophilic infiltration (r = 0.220, p = 0.020), chronic inflammatory cell infiltration (r = 0.381, p <0.001), and lymphoid aggregation (r = 0.271, p = 0.004). No relationship was found between mast cell density and intensity of H. pylori, glandular atrophy, or intestinal metaplasia. Conclusion: Mast cells might take part in the pathogenesis of H. pylori gastritis.


1970 ◽  
Vol 1 (1) ◽  
pp. 34-36
Author(s):  
SR KC ◽  
GL Amatya

Background: Helicobacter pylori infection is associated with mixed inflammatory cell infiltrate consisting of neutrophils, eosinophils, lymphocytes and plasma cells. Helicobacter pylori lead to mast cell degranulation and release of active chemical compounds in in-vitro conditions. The objective of this study was to find out the association of mast cell density and Helicobacter pylori in the antral mucosa of the stomach. Materials and Methods: A total of 150 endoscopic biopsies were included in the study. In addition to routine Hematoxylin and Eosin stained slides, Giemsa stain was done in each case for the evaluation of Helicobacter pylori and mast cell density in the gastric mucosa. Results: Out of 150 gastric biopsies with histopathological diagnosis of chronic gastritis, 36 cases (24%) were positive for Helicobacter pylori. In the antral mucosa, mast cell density was significantly higher in the Helicobacter pylori-positive group than in the Helicobacter pylori-negative group (P<0.01). Conclusion: Mast cells may play a role in the development of Helicobacter pylori gastritis. Keywords: Gastritis; Mast Cell; Helicobacter pylori DOI: 10.3126/jpn.v1i1.4448 Journal of Pathology of Nepal (2011) Vol.1, 34-36


2005 ◽  
Vol 99 (1) ◽  
pp. 20-25 ◽  
Author(s):  
John K. Chan ◽  
Alessandra Magistris ◽  
Vera Loizzi ◽  
Fritz Lin ◽  
Joanne Rutgers ◽  
...  

1977 ◽  
Vol 42 (2) ◽  
pp. 174-178 ◽  
Author(s):  
A. Tucker ◽  
I. F. McMurtry ◽  
A. F. Alexander ◽  
J. T. Reeves ◽  
R. F. Grover

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19–48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30–500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.


Author(s):  
Joanne L. Van Der Velden ◽  
Donna Barker ◽  
Garry Barcham ◽  
Emmanuel Koumoundouros ◽  
Stuart Hirst ◽  
...  

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