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Does the treatment and healing of esophagitis influence the pathophysiology of reflux disease The proton pump inhibitors (PPI), omeprazole and lansoprazole, have improved radically our ability to achieve healing and symptomatic relief in patients suffering from reflux esophagitis.

This has necessitated a re evaluation of the roles of medical and surgical therapy in the short and long term management of gastroesophageal reflux disease (GERD). Evidence that treatment with PPIs may influence the pathophysiology of reflux disease can, in principle, be garnered from several sources. However, since there are only limited data concerning the effects of PPIs on esophageal function, some of the potential influences must be inferred from data available regarding the consequences To address the question posed in the title, one may ask whether treatment with PPIs is associated with a decreased relapse rate once treatment has stopped. One may also examine whether reduction of esophageal exposure to acid or healing of esophagitis, by whatever means, is associated with a change in any of the parameters considered to be indicative of impaired esophageal function in GERD. These questions will be addressed on the basis of three hypotheses discussed below. PPI therapy produces lower relapse rates than other therapies The pre eminent effect of PPIs is to reduce the secretion of gastric acid [1] and thereby, to reduce esophageal acid exposure [2,3]; there are no data to indicate that PPIs produce healing of reflux esophagitis by any direct mechanism other than the reduction of esophageal mucosal exposure to acid. However, one may postulate that effective medical therapy breaks the vicious cycle whereby reflux induced esophageal damage impairs esophageal function, such that esophageal exposure to acid is increased and damage is exacerbated still further. If this postulate held true, the recurrence rate would be lower after PPI therapy provided that PPI therapy resulted in more complete esophageal healing than did less effective medical therapy. In the absence of maintenance treatment, at least half of the patients in clinical trials have relapsed within 6 months of stopping treatment (Fig. 1, [4 14]) and if anything, the relapse rates michael kors purses handbags after PPI therapy are higher than those observed after healing with other medications [13,14]. However, the recurrence rate after omeprazole was not higher than that observed after ranitidine [13] and the higher relapse rates seen after omeprazole are thought to be due to the fact that it produces healing in patients who would not otherwise have healed. In consequence, patients who have severe esophagitis resistant to therapy other than omeprazole are likely to relapse rapidly once treatment stops [15]. Such patients may not be representative of patients with less severe disease in whom motility changes may arguably be reversed by omeprazole. However, there is no evidence that PPIs produce lower relapse rates, after cessation of therapy, than do other therapeutic regimens. Lower esophageal sphincter (LES) function improves during or after antisecretory therapy There are numerous reports that LES function is impaired in GERD; the majority have shown that patients with reflux esophagitis have a decreased resting LES pressure [16 18] whilst Dent [19,20] first implicated transient relaxations of the lower esophageal sphincter (TLESRs) in the pathogenesis of GERD. However, it is not immediately obvious which abnormality is the most important in any individual patient. Manometric studies suggest that resting LES pressure is not a major Figure 1. The pooled relapse rate (with 95% confidence intervals), in the absence of active treatment, is shown as the total. pathogenetic factor in children with reflux esophagitis [21]; the results of another study in adults indicate that TLESRs are equally frequent in controls and patients with reflux esophagitis but that a higher proportion of TLESRs are associated with reflux in patients with reflux esophagitis. However, despite these data and the finding [22] that LES function is poorer in patients with complicated reflux esophagitis (strictures, ulceration or Barrett's esophagus), there are no clear data that LES dysfunction is a consequence rather than a cause of GERD. Certainly, there are no reports that PPIs can improve LES function, although it has been reported that omeprazole therapy does not produce the diminution in LES pressure seen under some circumstances during H2 RA therapy [23,24]. The notion that LES function might improve with healing of esophagitis receives some support from animal studies showing that acid perfusion of the esophagus or induction of experimental esophagitis are associated with a decrease in basal, resting LES pressure [25,26], It is clear that LES resting pressure increases in most (Fig. 2A) [27 30] but not all [31] patients following surgery; to a large extent, this is a direct and intended consequence of michael kors hand wallet the surgical procedure, although it is conceivable that the consequent resolution of esophageal inflammation may also contribute to the improvement in LES pressure. An initial case report did indeed report that LES pressure increased after esophagitis had been healed after treatment with cimetidine and antacids in two patients [32]. However, with the exception of a report that esophagitis healing was followed by an increase in LES pressure during the postprandial period [33], the effect of healing, achieved with acid antisecretory agents, including omeprazole [34], on resting LES pressure has been negligible (Fig. 2B) [2,28,32,33,35 39]. Esophageal body function improves during or after antisecretory therapy It has been shown in animal studies that esophageal body function is impaired following acid perfusion of the esophagus [40] or induction of experimental esophagitis [41]. Furthermore, there are many reports that esophageal motor function is impaired in patients with GERD [17,18,22,30,35,38,42 44]. However, the exact nature michael kors handbags outlet of the defect or defects remains controversial. Impaired esophageal clearance of luminal contents is presumed to be the consequence of esophageal dysmotility; this Figure 2. The data presented are from studies cited in the reference section. has been demonstrated using a swallowed radiolabeled bolus [45 47] and also, most elegantly, by Kahrilas and colleagues using manometry and simultaneous videofluoroscopy of a swallowed barium bolus [48]. The latter group showed that failure to clear barium from the distal esophagus was associated with manometric features of failed primary peristalsis or hypotensive peristalsis in the distal esophagus, previously noted in a substantial minority of patients with peptic esophagitis. One or more features of impaired esophageal body function, including reduced contraction amplitude, reduced contraction duration, reduced propagation velocity of peristaltic contractions and a higher proportion of nonpropagated or incompletely propagated contractions, have been reported to be more prevalent in patients with reflux esophagitis [16 18,22,33, 48 50]. However, it is still not clear which, if any, is the predominant abnormality. More controversial yet, is the nature of the relationship between esophagitis and dysmotility. This has been taken to support the hypothesis that esophageal body dysmotility is a consequence of GERD [22] although the alternative hypothesis, that esophageal dysmotility is the primary disorder in GERD, also has its proponents [46,51,52]. The concept that dysmotility is a secondary phenomenon is consistent with the postoperative increases in esophageal contraction amplitude (Fig. 3A) and in the percentage of propagated contractions (Fig. 4A) reported 3 to 30 months after patients have undergone fundoplication [27,29,30]. Improved esophageal motility after surgery is not, however, universal suggesting either that dysmotility is, in some cases, a primary phenomenon which predates the development of GERD or that it is a secondary occurrence which becomes irreversible if inflammation persists or progresses unchecked [22]. If esophageal body dysmotility is, indeed, secondary one might expect that effective medical therapy, leading to healing of reflux esophagitis, would produce improvements in motility comparable to those observed after surgery. The previously mentioned increase in LES pressure following successful medical treatment of reflux esophagitis was accompanied by increases in contraction amplitude and in the percentage of propagated contractions [32]. However, no subsequent papers have reported a clear improvement in esophageal body function as judged by contraction amplitude (Fig. 3B) or by the percentage of contractions which propagate normally (Fig. 4B) following michael kors bag small black medical therapy, either with omeprazole [34,39,53] or with other antisecretory agents [28,32,33,37,38]. Despite case reports that improved esophageal function follows healing of esophagitis by medical means [32], subsequent studies have failed to show any change in resting lower esophageal sphincter pressure, in esophageal body contraction amplitude, duration and velocity or in the proportion of esophageal body contractions which is propagated normally. There are limited data on the changes produced by omeprazole, but they do not seem to differ significantly from those seen after treatment with Figure 3. The data presented are from studies cited in the reference section. histamine H2 RAs. Thus, despite their ability to decrease profoundly the secretion of gastric acid, PPIs do not seem to affect the changes in esophageal motility produced by surgery. As mentioned previously, an increase in LESP is to be expected since this is one of the main aims of surgery. However, the major, longer term effect of surgery is to reduce esophageal exposure to acid, similar to the effect of PPIs. It may be argued that surgery also prevents the reflux of acid unrelated gastric contents which may be as injurious under some circumstances as acid and pepsin. However, since there is a clear relationship between gastric acid suppression and the degree and rate Figure 4. The data presented are from studies cited in the reference section. of healing seen with medical therapy in esophagitis [1] and since, furthermore, the majority of patients with esophagitis will heal after treatment with a PPI, it seems probable that acid exposure is the major pathogenetic factor leading to esophageal damage. One possible explanation for the discrepancy between sequelae of surgery and those of PPI therapy is the difference in duration of treatment prior to esophageal testing in the two groups. In the medical treatment studies, the mean duration of treatment was approximately 2.5 0.1 months, similar to that noted for the four omeprazole treatment groups combined (2.4 0.1 months) [2,34,39,53]. However, the mean time elapsed between surgery and esophageal testing in the studies discussed here is 17 1.1 months. Grande and colleagues [29] showed a clear and steady increase in esophageal contraction amplitude and LES pressure with a progressive increase from pretreatment levels to those seen at 6 months and a further rise between 6 and 12 months (Fig. 5). Thus, the failure to record an effect of medical therapy on esophageal function and hence on the pathophysiology of GERD may be attributable to medical treatment periods which are too short to allow any change to occur. Healing of the esophageal mucosa does not necessarily indicate normalization of esophageal function [35]. Another possible explanation for the increase in esophageal contraction amplitude seen after surgery is that fundoplication produces a degree of obstruction which stimulates esophageal contractility. These changes may be analogous to the increased contraction amplitudes observed in patients with "vigorous" achalasia although the contractions which occur in vigorous achalasia are generally simultaneous [54,55] whilst fundoplication is followed by an increase in the proportion of peristaltic contractions (Fig. 4A). However, it is highly likely that many other factors also influence the differential, long term responses of reflux esophagitis to medical and surgical treatment. The pathophysiology of GERD is multifactorial, involving any one or more of the factors shown in Table 1. Barlow et al. [56] found, in a study of 75 patients with an abnormal 24 h pH metry, that gastric hypersecretion was more common in patients with a normal LES (10/22, 48%) than in patients with impaired LES function (11/54, 20%; p = 0.0244). Thus, in some GERD patients, LES dysfunction is the predominant defect, whereas in other patients gastric hypersecretion is more important.

The importance of esophageal body dysmotility remains unclear but, as with other pathogenetic factors, it is unlikely to be the only factor in many patients. Furthermore, a defect in esophageal body motility may be primary in some patients [46,57] but secondary to reflux induced damage [22,57] in other patients. If this is the case.

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