Retention Esophagitis as a Significant Clinical Predictor of Progression to Esophageal Cancer in Achalasia
2
조회
0
다운로드
2
인용
0
참고문헌
키워드
초록
Background/Aims: Chronic liquid and/or food stasis caused by retention esophagitis (RE) in achalasia is a notable endoscopic findingbecause of the presence of a thickened or whitish esophageal mucosa and histologically altered squamous hyperplasia. We aimed toidentify the clinical features of RE associated with achalasia and to clarify the clinical definition of RE in achalasia as a precancerouslesion identified by analyzing biomarker expressions. Methods: From 2006 to 2015, we retrospectively reviewed 37 patients with achalasia without previous treatment. Among them, 21patients had diagnostic findings of RE (RE+) and 16 patients had no diagnostic findings of RE (RE–). Immunohistochemical stainingof p53, p16, and Ki-67 was performed on the endoscopic biopsy tissues from the patients with achalasia and 10 control patients withnon-obstructive dysphagia. Results: The symptom duration and transit delay were significantly longer in the RE+ group than in the RE– group. We foundparticularly high p53 positivity rates in the RE+ group (p<0.001). The rate of p16 expression was also significantly higher in the RE+group than in the other two groups (p=0.003). Conclusions: A high p53 expression rate was more frequently found in the RE+ group than in the other two groups. RE could be ameaningful clinical feature of achalasia for predicting esophageal carcinogenesis.
Abstract
Background/Aims: Chronic liquid and/or food stasis caused by retention esophagitis (RE) in achalasia is a notable endoscopic findingbecause of the presence of a thickened or whitish esophageal mucosa and histologically altered squamous hyperplasia. We aimed toidentify the clinical features of RE associated with achalasia and to clarify the clinical definition of RE in achalasia as a precancerouslesion identified by analyzing biomarker expressions. Methods: From 2006 to 2015, we retrospectively reviewed 37 patients with achalasia without previous treatment. Among them, 21patients had diagnostic findings of RE (RE+) and 16 patients had no diagnostic findings of RE (RE–). Immunohistochemical stainingof p53, p16, and Ki-67 was performed on the endoscopic biopsy tissues from the patients with achalasia and 10 control patients withnon-obstructive dysphagia. Results: The symptom duration and transit delay were significantly longer in the RE+ group than in the RE– group. We foundparticularly high p53 positivity rates in the RE+ group (p<0.001). The rate of p16 expression was also significantly higher in the RE+group than in the other two groups (p=0.003). Conclusions: A high p53 expression rate was more frequently found in the RE+ group than in the other two groups. RE could be ameaningful clinical feature of achalasia for predicting esophageal carcinogenesis.
참고문헌 (22)
- Moonen A, "Current diagnosis and management of achalasia", J Clin Gastroenterol, 48, pp.484~490 (2014)
- Vaezi MF, "ACG clinical guideline: diagnosis and management of achalasia", Am J Gastroenterol, 108, pp.1238~1249 (2013)[DOI]
- Fehmi Ates, "The Pathogenesis and Management of Achalasia: Current Status and Future Directions", Gut and Liver, 9(4), pp.449~463 (2015), 거트앤리버 소화기연관학회협의회
- Boeckxstaens GE, "Achalasia", Lancet, 383, pp.83~93 (2014)[DOI]
- Streitz JM Jr, "Achalasia and squamous cell carcinoma of the esophagus: analysis of 241 patients", Ann Thorac Surg, 59, pp.1604~1609 (1995)[DOI]
- Dunaway PM, "Risk and surveillance intervals for squamous cell carcinoma in achalasia", Gastrointest Endosc Clin N Am, 11, pp.425~434 (2001)
- Leeuwenburgh I, "Long-term esophageal cancer risk in patients with primary achalasia: a prospective study", Am J Gastroenterol, 105, pp.2144~2149 (2010)[DOI]
- Chino O, "Clinicopathological studies of esophageal carcinoma in achalasia: analyses of carcinogenesis using histological and immunohistochemical procedures", Anticancer Res, 20, pp.3717~3722 (2000)
- Shields TW, "General thoracic surgery" (2009), Lippincott Williams & Wilkins
- Crookes PF, "Gastroesophageal reflux in achalasia. When is reflux really reflux?", Dig Dis Sci, 42, pp.1354~1361 (1997)[DOI]
- Kiraly A, "Gastroesophageal reflux disease progressing to achalasia", Dis Esophagus, 18, pp.355~358 (2005)[DOI]
- Goldblum JR, "Histopathologic features in esophagomyotomy specimens from patients with achalasia", Gastroenterology, 111, pp.648~654 (1996)[DOI]
- Goldblum JR, "Achalasia. A morphologic study of 42 resected specimens", Am J Surg Pathol, 18, pp.327~337 (1994)[DOI]
- Lehman MB, "Squamous mucosal alterations in esophagectomy specimens from patients with end-stage achalasia", Am J Surg Pathol, 25, pp.1413~1418 (2001)[DOI]
- Minami H, "New endoscopic indicator of esophageal achalasia: "pinstripe pattern"", PLoS One, 10, pp.e0101833~ (2015)[DOI]
- Leeuwenburgh I, "Expression of p53 as predictor for the development of esophageal cancer in achalasia patients", Dis Esophagus, 23, pp.506~511 (2010)[DOI]
- Sikkema M, "Aneuploidy and overexpression of Ki67 and p53 as markers for neoplastic progression in Barrett's esophagus: a case-control study", Am J Gastroenterol, 104, pp.2673~2680 (2009)[DOI]
- Meijssen MA, "Achalasia complicated by oesophageal squamous cell carcinoma: a prospective study in 195 patients", Gut, 33, pp.155~158 (1992)[DOI]
- Belsey R, "Functional disease of the esophagus", J Thorac Cardiovasc Surg, 52, pp.164~188 (1966)
- Raymond L, "Inflammatory aetiology of primary oesophageal achalasia: an immunohistochemical and ultrastructural study of Auerbach's plexus", Histopathology, 35, pp.445~453 (1999)[DOI]
- Sherr CJ, "Cancer cell cycles", Science, 274, pp.1672~1677 (1996)[DOI]
- Boller D, "Lugol chromoendoscopy combined with brush cytology in patients at risk for esophageal squamous cell carcinoma", Surg Endosc, 23, pp.2748~2754 (2009)[DOI]
