Esophageal Mast Cell Infiltration in a 32-Year-Old Woman with Noncardiac Chest Pain
0
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Noncardiac chest pain (NCCP) is one of the most common esophageal symptoms and lacks a clearly defined mechanism. The most common cause of NCCP is gastroesophageal reflux disease (GERD). One of the accepted mechanisms of NCCP in a patient without GERD has been altered visceral sensitivity. Mast cells may play a role in visceral hypersensitivity in irritable bowel syndrome. In this case, a patient with NCCP and dysphagia who was unresponsive to proton pump inhibitor treatment had an increased esophageal mast cell infiltration and responded to 14 days of antihistamine and antileukotriene treatment. We suggest that there may be a relationship between esophageal symptoms such as NCCP and esophageal mast cell infiltration.
Abstract
Noncardiac chest pain (NCCP) is one of the most common esophageal symptoms and lacks a clearly defined mechanism. The most common cause of NCCP is gastroesophageal reflux disease (GERD). One of the accepted mechanisms of NCCP in a patient without GERD has been altered visceral sensitivity. Mast cells may play a role in visceral hypersensitivity in irritable bowel syndrome. In this case, a patient with NCCP and dysphagia who was unresponsive to proton pump inhibitor treatment had an increased esophageal mast cell infiltration and responded to 14 days of antihistamine and antileukotriene treatment. We suggest that there may be a relationship between esophageal symptoms such as NCCP and esophageal mast cell infiltration.
참고문헌 (26)
- Fass R, "The clinical and economic value of a short course of omeprazole in patients with noncardiac chest pain", Gastroenterology, 115, pp.42~49 (1998)
- Van Handel D, "The pathophysiology of non-cardiac chest pain", J Gastroenterol Hepatol, 20(3), pp.S6~S13 (2005)
- Fass R, "Noncardiac chest pain", J Clin Gastroenterol, 42, pp.636~646 (2008)
- Traver E, "Mucosal mast cells mediate motor response induced by chronic oral exposure to ovalbumin in the rat gastrointestinal tract", Neurogastroenterol Motil, 22, pp.e34~e43 (2010)
- Miner PB Jr, "The role of the mast cell in clinical gastrointestinal disease with special reference to systemic mastocytosis", J Invest Dermatol, 96(3), pp.40S~43S (1991)
- Jakate S, "Mastocytic enterocolitis: increased mucosal mast cells in chronic intractable diarrhea", Arch Pathol Lab Med, 130, pp.362~367 (2006)
- Lee H, "Heterogeneity of mucosal mast cell infiltration in subgroups of patients with esophageal chest pain", Neurogastroenterol Motil, 26, pp.786~793 (2014)
- O’Sullivan M, "Increased mast cells in the irritable bowel syndrome", Neurogastroenterol Motil, 12, pp.449~457 (2000)
- Weston AP, "Terminal ileal mucosal mast cells in irritable bowel syndrome", Dig Dis Sci, 38, pp.1590~1595 (1993)
- Akhavein M A, "Allergic mastocytic gastroenteritis and colitis: an unexplained etiology in chronic abdominal pain and gastrointestinal dysmotility", Gastroenterol Res Pract, 2012, pp.950582~ (2012)
- Park SW, "Esophageal mucosal mast cell infiltration and changes in segmental smooth muscle contraction in noncardiac chest pain", Dis Esophagus, 28, pp.512~519 (2015)
- Ford AC, "Meta-analysis: the epidemiology of noncardiac chest pain in the community", Aliment Pharmacol Ther, 34, pp.172~180 (2011)
- Richter JE, "Esophageal chest pain: current controversies in pathogenesis, diagnosis, and therapy", Ann Intern Med, 110, pp.66~78 (1989)
- Fass R, "Differential effect of long-term esophageal acid exposure on mechanosensitivity and chemosensitivity in humans", Gastroenterology, 115, pp.1363~1373 (1998)
- Klooker TK, "The mast cell stabiliser ketotifen decreases visceral hypersensitivity and improves intestinal symptoms in patients with irritable bowel syndrome", Gut, 59, pp.1213~1221 (2010)
- Deiteren A, "Histamine H4 and H1 receptors contribute to postinflammatory visceral hypersensitivity", Gut, 63, pp.1873~1882 (2014)
- Cenac N, "Potentiation of TRPV4 signalling by histamine and serotonin: an important mechanism for visceral hypersensitivity", Gut, 59, pp.481~488 (2010)
- Amadesi S, "Protease-activated receptor 2 sensitizes the capsaicin receptor transient receptor potential vanilloid receptor 1 to induce hyperalgesia", J Neurosci, 24, pp.4300~4312 (2004)
- Sadofsky LR, "Transient receptor potential vanilloid-1-mediated calcium responses are inhibited by the alkylamine antihistamines dexbrompheniramine and chlorpheniramine", Exp Lung Res, 34, pp.681~693 (2008)
- Hellbom E, "Chlorpheniramine, selective serotonin-reuptake inhibitors (SSRIs) and over-the-counter (OTC) treatment", Med Hypotheses, 66, pp.689~690 (2006)
- Dickman R, "The role of pain modulators in esophageal disorders: no pain no gain", Neurogastroenterol Motil, 26, pp.603~610 (2014)
- Yu Y, "Alterations of mast cells in the esophageal mucosa of the patients with non-erosive reflux disease", Gastroenterol Res, 4, pp.70~75 (2011)
- Siegert SI, "Are gastrointestinal mucosal mast cells increased in patients with systemic mastocytosis?", Am J Clin Pathol, 122, pp.560~565 (2004)
- Straumann A, "Idiopathic eosinophilic esophagitis is associated with a T(H)2-type allergic inflammatory response", J Allergy Clin Immunol, 108, pp.954~961 (2001)
- Abonia JP, "Involvement of mast cells in eosinophilic esophagitis", J Allergy Clin Immunol, 126, pp.140~149 (2010)
- Liacouras CA, "Eosinophilic esophagitis: updated consensus recommendations for children and adults", J Allergy Clin Immunol, 128(e6), pp.3~20 (2011)
