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OESO©2015
 
Volume: The Esophageal Mucosa
Chapter: Epidemiology
 

What factors are predictive of esophageal ulceration in GER?

G. Cadiot, J. Vatier, M. Mignon (Paris)

There are many differences between gastroesophageal reflux (GER) patients with esophagitis and those without esophagitis, when considering the patients as a group. However, to our knowledge, none of these differences can predict the occurrence of esophageal erosions, when considering a given individual with GER disease (GERD).

Those differences are the characteristics of the patients (sex, age) [1], the existence of exogenous factors (tobacco, alcohol, NSAID) [2], the clinical characteristics of GERD (quantitative extent of reflux [3], nycterohemeral periods of reflux [3-5], duration of disease [2]) and finally, the pathophysiological factors of GERD. Among the latter, the abnormalities of esophageal clearance, which determines the duration of the contact between refluxate and esophageal mucosa, the composition of the gastroesophageal refluxate and the esophageal mucosal resistance are probably the most significant factors of esophagitis.

Esophageal clearance of the refluxate is determined by secondary esophageal peristalsis and salivary secretion (neutralization of acid by salivary bicarbonates) [6]. The association of esophageal clearance abnormalities to lower esophageal sphincter (LES) incompetence and to gastric emptying delay, suggests that GERD is a primary motor disorder of the esophagus [7], whose origin might be vagal for some authors [8]. The fact that esophageal peristalsis and clearance abnormalities are not modified after esophagitis healing, is in favor of the existence of a primary motor disorder [9]. Our group showed, using a multifactorial approach with a logistic regression, that esophageal clearance abnormalities, reflected by the number of refluxes lasting more than 5 min, was one among the three significant factors differentiating GER patients without esophagitis from those with esophagitis [10]. However, when considering a given individual, measuring esophageal clearance (by scintigraphy [11] or pH-metry) did not predict the occurrence of esophageal erosions since there was a big overlap

of the individual values between the two groups of patients. Esophageal motor perturbances (aperistalsis, low amplitude contraction waves) and LES hypotonia are correlated with esophagitis grade [12]. However, when considering a given individual, they also do not allow prediction of the occurrence of esophagitis [12].

Esophagitis is more frequent when hiatal hernia is present; in our experience hiatal hernia was present in 73% of patients with esophagitis, as compared to 39% in the patients without esophagitis [10]. Hiatal hernia favors esophageal clearance abnormalities, especially when it is irreducible [13]. However, its presence cannot allow prediction of the occurrence of esophageal erosions.

It is reasonable to anticipate that the composition of the refluxate, which in turn depends upon that of the gastric juice, is a factor of esophagitis. However, this remains a matter of debate in spite of evidence obtained in animals and humans [14-16]. We have shown that 25% of GER patients without esophagitis and 31% of those with esophagitis had gastric acid hypersecretion [15]. These percentages did not differ significantly. However, pentagastrin-stimulated peptic outputs were significantly higher in the patients with esophagitis than in the others [15]. Nevertheless, secretory parameters were not significant after multifactorial analysis [10]. The importance of a high concentration of pepsin in the refluxate has been recently emphasized by Gotley et al., but only in high grade esophagitis [17]. The relevance of duodenogastric reflux remains debatable.

The other major pathophysiological factor of esophagitis is probably the esophageal mucosal resistance. Modifications of mucosal resistance might explain why esophagitis develops in some patients when it does not in others who do not have significantly different GERD, both from quantitative and qualitative points of view. Esophageal mucosal resistance includes pre-epithelial, epithelial and postepithe-lial defense mechanisms and also mucosal regenerative factors [18]. However, to our knowledge, none have studied modifications of these different mechanisms in patients with esophagitis as compared to patients without esophagitis.

It is theoretically possible to determine, after multifactorial analysis, a mathematical equation which allows prediction of the risk of esophagitis in a given patient. However, taking into account the high number of potential factors to study and the high number of patients necessary to obtain a good statistical analysis, such a study is difficult to realize. Our multifactorial analysis, imperfect since some pathophysiological factors of esophagitis were not studied (especially mucosal resistance), aimed to determine the factors significantly associated to esophagitis [10]. The number of refluxes lasting more than 5 min, the amplitude of the esophageal contraction waves and male sex were the three factors which were significant after logistic regression [10].

In conclusion, if numerous factors or parameters are most often present or abnormal in cases of esophagitis, when considering the patients as a group, it is difficult to predict the occurrence of esophageal erosions when deliberating a given individual.

References

1. Wienbeck M, Barnert J. Epidemiology of reflux disease and reflux esophagitis. Scand J Gastroenterol 1989;24(suppl 156): 7-13.

2. Dedieu P, Gaillard F, Lavignolle A et al. Oesophagite par reflux: aspects epidemiologiques, anatomopathologiques et evolutifs (123 cas). Gastroenterol Clin Biol 1981;5:266-274.

3. DeMeester TR, Wang CI, Wernly JA, Pellegrini CA, Little AG, Klementschitsch P, Bermudez G, Johnson LF, Skinner DB. Technique, indications, and clinical use of 24 hour esophageal pH monitoring. J Thorac Cardiovasc Surg 1980;79: 656-670.

4. DeCaestecker JS, Blackwell JN, Pryde A, Heading RC. Daytime gastro-oesophageal reflux is important in oesophagitis. Gut 1987;28:519-526.

5. Freidin N, Fisher MJ, Taylor W, Boyd D, Surratt P, McCallum RW, Mittal RK. Sleep and nocturnal acid reflux in normal subjects and patients with reflux oesophagitis. Gut 1991 ;32:1275-1279.

6. Katzka DA, DiMarino AJ. Pathophysiology of gastroesophageal reflux disease: LES incompetence and esophageal clearance. In: Castell DO (ed) The Esophagus. Boston: Little, Brown and Company, 1992:449-461.

7. Castell DO. Gastroesophageal reflux disease is a motility disorder. In: Scarpignato C (ed) Advances in drug therapy of gastroesophageal reflux disease. Front Gastrointest Res, Basel: Krager 1992:20:11-16.

8. Cunningham KM, Horowitz M, Riddell PS et al. Relations among autonomic nerve dysfunction, oesophageal motility and gastric emptying in gastro-oesophageal reflux disease. Gut 1991 ;32:1436-1440.

9. Singh P, Adamopoulos A, Taylor RH, Colin-Jones DG. Oesophageal motor function before and after healing of oesophagitis. Gut 1992:33:1590-1596.

10. Cadiot G, Bruhat A, Hetzel D et al. Multivariate analysis of pathophysiological factors of gastroesophageal reflux and peptic esophagitis in 74 patients. Gastroenterology 1992;102:A46(abstract).

11. Stanciu C, Bennett JR. Oesophageal acid clearing: one factor in the production of reflux oesophagitis. Gut 1974:15:852-857.

12. Kahrilas PJ, Dodds WJ, Hogan WJ, Kern M, Arndorfer RC, Reece A. Esophageal peristaltic dysfunction in peptic esophagitis. Gastroenterology 1986;91:897-904.

13. Sloan S, Kahrilas PJ. Impairment of esophageal emptying with hiatal hernia. Gastroenterology 1991:100:596-605.

14. Goldberg HI, Doods WJ, Gee S, Montgomery C, Zboralske FF. Role of acid and pepsin in acute experimental esophagitis. Gastroenterology 1969;56:223-230.

15. Sekera E, Cadiot G, Poitevin C, Vallot T, Vatier J, Mignon M. Gastric proteolytic content in gastroesophageal reflux and esophagitis. Gastroenterol Clin Biol 1992;16:141-147.

16. Hirschowitz BI. A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis. Gastroenterology 1991:101:1149-1158.

17. Gotley DC, Morgan AP, Ball D, Owen RW, Cooper MJ. Composition of gastro-oesophageal refluxate. Gut 1991:32:1093-1099.

18. Orlando RC. Pathophysiology of gastroesophageal reflux disease: Esophageal epithelial resistance. In: Castell DO (ed) The Esophagus. Boston: Little, Brown and Company, 1992;463-478.


Publication date: May 1994 OESO©2015