[雙語翻譯]--（節(jié)選）外文翻譯--賁門炎癥、腸上皮化生和食管胃接合部癌（原文）

1、European Journal of Cancer Pre?ention 2001, 10, 483?487REVIEWCarditis, intestinal metaplasia and adenocarcinoma of oesophagogastric junctionM Conio1, R Filiberti2, S Blanchi1, A Giacosa1( ) Recei?ed 7 August 2001; accept

2、ed 29 August 2001Barrett’s oesophagus is a precancerous condition in which the normal squamous epithelium is replaced by ( ) intestinal metaplasia IM . IM can then progress through increasingly severe dysplasia to oesoph

3、ageal ( ) ( ) adenocarcinoma EAC . In the gastric cardia the normal gastric mucosa, when inflamed carditis , can be ( ) replaced by IM and can then progress to gastric adenocarcinoma GAC . The same histopathological sequ

4、ence can take place on either side of the oesophagogastric junction. Since the location of that junction can be uncertain this can result in confused diagnosis between EAC and GAC. In this review, the diagnostic criteria

5、, incidence and risk factors for Barrett’s oesophagus and carditis are discussed, together with the factors determining the risk of progression to adenocarcinoma of the oesophagus or cardia. The risk factors include fami

6、lial? ? ? ? ?genetic, environmental and dietary characteristics. Finally, these risk factors are discussed within the context of cancer prevention. ? 2001 Lippincott Williams Weston et al., 1996; Cameron, 1997; Morales

7、. et al., 1997b; Caygill et al., 1999; Hirota et al., 1999 . BO patients should undergo regular endoscopic and bioptic follow-up, as it is believed that there is a step-wise neoplastic progression from low- to high- ? gr

8、ade dysplasia Sampliner, 1998; van Sandick et al., . 1998; Rudolph et al., 2000; Conio et al., 2001 . The present definition of BO includes any upward metaplastic extension identifiable by endoscopy, with histologically

9、proven IM. The incidence of ? . oesophageal adenocarcinoma EAC in BO patients ranges between 1?52 to 1?441 patient-years and ? those over 50 years old are at major risk Cameronet al., 1985; Spechler and Goyal, 1986; Achk

10、ar and Carey, 1989; Hameeteman et al., 1989; Van der . Veen et al., 1989; Williamson et al., 1991 . BO patients have a 30?125 times increased risk of devel- ? oping EAC than the general population Cameron . et al., 1985

11、. The incidence of EAC has increased progressively over the last decades while that of antral carcinoma ? has progressively declined Powell and McConkey, . 1992 . The absolute increase of EAC is greater than ? that of an

12、y other neoplasia Blot et al., 1991; Blot et . al., 1993a . The incidence of EAC is higher in ? . patients with long-segment BO ?3 cm . Menke- ? . Pluymers et al. 1993 reported that a doubling of segment length was assoc

13、iated with a 1.7-fold in- crease in the risk of EAC. However, a recent report has suggested that the risk of neoplastic progression in patients with short-segment BO is not lower than ? that in patients with longer exten

14、sions Rudolph et . al., 2000 .1Department of Gastroenterology and Clinical Nutrition; 2Department of En?ironmental Epidemiology and Biostatistic, National Cancer Research Institute, Largo R Benzi, 10, 16132 Geno?a, Italy

15、. Correspondence to: M Conio.0959-8278 ? 2001 Lippincott Williams Zhang et al., 1997b; Chow et al., 1998a; Lagergren et al., 1999a,b; Romero and Locke, 1999; Wilson et al., . 1999 . The presence of a family history of r

16、eflux symp- toms would seem to be a risk factor in the develop- ment of Barrett’s oesophagus. A high frequency of BO and EAC was observed in several members of ? . the same family Romero et al., 1997 . Trudgill et al. ?

17、. 1999 observed a greater frequency of reflux symp- toms in relatives of patients with gastroesophageal ? . reflux disease GERD and an increase in the expo- sure of the oesophagus to acidity. Relatives with reflux sympto

18、ms are more liable to BO than the general population. It is not clear why some subjects with chronic reflux develop Barrett’s oesophagus. Alterations of ? . the lower esophageal sphincter LES and the oesophageal peristal

19、sis are necessary. The degree of mucosal damage is greater when gastric juice is mixed with that of the duodenum. Other factors present in gastroesophageal reflux could also be involved in the occurrence of IM. Studies o

20、f gastric cancerogenesis have shown that a high consumption ? of certain nutrients, such as methionine and its . metabolite, 2-chloro-4-methylthiobutanoic acid , nitrites and salt, is associated with a high risk of ? . g

21、astric adenocarcinoma La Vecchia et al., 1997 . However, the role of N-nitroso compounds in gastric cancerogenesis has not been definitely clarified. ? . Botterweck et al. 2000 reported an inverse corre- lation between t

22、he consumption of vitamin C and gastric cancer. The reduction of concentration of vitamin is correlated to the pH of the gastric juice, the severity and extension of gastritis and to the H. ? pylori type CagA-positive in

23、fection Zhang et al., . 1998 . The European Cancer Prevention Organisation ? . ECP has a double-blind factorial designed study in progress in which the H. pylori will be eradicated from half the patients. Both the eradic

24、ated and the control group have been randomized to 3 years of interventions with vitamin C or placebo. The study ? . will be completed within 2001 Hill, 1995 . A reduced amount of antioxidant and an excess of free radica