Erosive Esophagitis and Barrett's Esophagus in Taiwan (A Higher Frequency than Expected)

In contrast to Western countries, erosiveesophagitis has been considered less common, Barrett'sesophagus presumed less frequent, and hiatal herniaextremely uncommon in the Orient. However, accelerated modernization and adoption of Western customshave resulted in marked life-style changes in manyAsians in the Orient that may potentially affect thefrequency of erosive esophagitis and Barrett's esophagus in this population. Our aim was to determinethe current frequency of erosive esophagitis, Barrett'sesophagus, and other gastroesophageal reflux diseasecomplications in self-referred Chinese patients undergoing upper gastrointestinal endoscopy inTaipei, Taiwan. Between July 1991 and June 1992, 464consecutive patients underwent endoscopy for a varietyof upper gastrointestinal symptoms at a major medical center. The presence of erosive esophagitis,strictures, Barrett's esophagus, and hiatal hernia wasrecorded. The extent of mucosal injury was determined byusing the Savary-Miller grading system. Sixty-six (14.5%) patients were found to have erosiveesophagitis, 9 (2%), Barrett's esophagus, and 32 (7%)hiatal hernias. Erosive esophagitis showed amale-to-female preponderance of 3.1:1. Disease severityincreased with age and peaked during the sixth andseventh decades. We concluded that in contrast toprevious experience, the Chinese population in Taiwanappears to have a higher frequency of erosiveesophagitis, Barrett's esophagus, and hiatal hernia.Increased fat consumption, aging, and other possiblefactors are suggested as possible mechanisms.     

Histological Esophagitis (Clinical and Histological Response to Omeprazole in Children)

Many children with esophagitis demonstratehistological changes without gross evidence ofesophagitis by esophagoscopy. The effect of omeprazoleon the histological healing of esophagitis in childrenis unknown. Therefore, the aim of this study wasto determine the effect of omeprazole on refractoryhistological esophagitis in pediatric patients. Eighteenpatients with histological evidence of esophagitis and recurrent symptoms despite therapy withH₂-receptor antagonists and prokinetic agentswere prospectively treated with omeprazole. Dosing wasadjusted by monitoring intragastric pH, andesophagoscopy was repeated after 8-12 weeks of omeprazoletreatment. Two patients did not complete the study dueto either worsening symptoms or hypergastrinemia. Of theremaining patients, 76% were asymptomatic with omeprazole treatment and 24% reportedimprovement in their symptoms. Approximately 40%demonstrated complete histological healing of theiresophagitis. Three patients (17%) had persistentelevations in serum gastrin levels while on omeprazoletreatment, which was associated with both youngerpatient age and higher omeprazole dosing; however, allelevated gastrin levels returned to normal afterdiscontinuation of the medication. All patients had recurrenceof their symptoms after completing a course ofomeprazole, even patients with complete histologicalhealing. Omeprazole is efficacious in treating children with esophagitis refractory toH₂-receptor antagonist and prokinetic agents.However, none of the patients were able to discontinueacid suppressive therapy even after documented healingof their esophagitis.     

Helicobacter pylori Infection Has No Role in the Pathogenesis of Reflux Esophagitis

In a prospective study of consecutive patientswith reflux esophagitis and/or hiatal hernia andBarrett's esophagus, the prevalence of Helicobacterpylori was assessed. Antral biopsy specimens werestudied and a serum sample for detection of IgGantibodies against Helicobacter pylori was taken. As areference group patients presenting with a normalesophagus, stomach, and duodenum were taken. Refluxesophagitis was diagnosed in 118 patients, hiatal herniawithout esophageal inflammation in 109, and Barrett'sesophagus in 13. Helicobacter pylori was present in 74(30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacterpylori was significantly lower in all groups comparedwith the reference group (P < 0.001). There was nodifference when patients with esophagitis, Barrett'sesophagus, or hiatal hernia were compared. Patients withesophagitis and Helicobacter pylori in their antrum aresignificantly older than esophagitis patients withoutconcomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). Itis concluded that the prevalence of Helicobacter pyloriinfection in patients with gastroesophageal refluxdisease is significantly lower than in the reference group, irrespective of the severity ofesophagitis. Helicobacter pylori infection has no rolein the pathogenesis of reflux esophagitis.     

Prevalence of Upper Gastrointestinal Lesions and Helicobacter pylori Infection in Crohn's Disease

Crohn's disease can affect the upper gut withreported variable frequency, although concurrentHelicobacter pylori infection has been reported to below. We prospectively investigated the prevalence of esophageal, gastric, and duodenal lesions andHelicobacter pylori infection in 67 Crohn's disease, 41ulcerative colitis patients, and 43 controls. Symptoms,esophagogastroduodenoscopy, and multiple biopsies were performed on all patients consecutively.Endoscopic lesions were found in 63% of Crohn's diseasepatients, with a Helicobacter pylori prevalence of 28%. Granulomas were found in three patients. Twenty-two percent of the ulcerative colitis patients hadlesions, with a 29% prevalence of Helicobacter pyloriinfection. Half of the controls had pathologicalendoscopy, and Helicobacter pylori was positive in 40% of the cases. Subjective symptoms did notpredict the presence of endoscopic lesions orHelicobacter pylori infection in inflammatory boweldisease patients. Chronic gastritis and duodenitis arecommon in Crohn's disease patients, and the majorityare not associated with Helicobacter pyloriinfection.     

The Place of Upper Gastrointestinal Tract Endoscopy Before and After Vertical Banded Gastroplasty for Morbid Obesity

In industrialized countries, surgicalgastroplasty is performed more and more frequently inpatients with morbid obesity. The aims of thisprospective study were to determine the incidence ofupper gastrointestinal lesions in obese patients and to assess theplace of digestive endoscopy in symptomatic patientsafter gastroplasty. A consecutive group of 159 obesepatients were studied before and after vertical banded gastroplasty. In the preoperative evaluation,reflux esophagitis and gastroduodenal lesions wereendoscopically observed in 31% and 37% of the patients,respectively. Interestingly, the majority of the obese patients with upper gastrointestinallesions were asymptomatic. In the postoperativefollow-up period, 55 of the 159 patients complained ofupper gastrointestinal symptoms such as vomiting (72%), esophageal reflux (17%), and epigastric pain(3%). Stenosis of the outlet of the gastric pouch wasdescribed in 40 of the 55 symptomatic patients.Esophagitis was observed in 60% of these patients.Endoscopic dilation using Savary bougies or TTS balloonwas successfully performed in all the patients withsymptomatic stenosis of the gastric outlet. Foodimpaction was endoscopically removed in four patients.Thus, we recommend performing an uppergastrointestinal endoscopy in obese patients who arecandidates for surgical gastroplasty because of the highincidence of upper gastrointestinal peptic lesions.Endoscopy is also helpful in patients with digestivedisorders occurring after gastroplasty in order todefine and to treat the lesions.     

Manometric Study of Hiatal Hernia and Its Correlation with Esophageal Peristalsis

The pathogenesis of gastroesophageal refluxdisease (GERD) is considered multifactorial, butalterations of the esophagogastric junction (EGJ) andhiatal hernia play a prominent role. The correlationsbetween hiatal hernia and the other pathogeneticfactors are as yet unclear, and they need to beinvestigated by a methodological approach based on newanatomic and functional criteria. Our aim was to study,by stationary manometry, the relationships betweensmall reducible hiatal hernia, identified by endoscopy,and esophageal peristalsis, in patients with and withoutGERD. According to the absence or presence of esophagitis (E), and the absence or presenceof hiatal hernia (H), 58 subjects were divided into fourgroups: controls 10; H 14; E 10; and HE 24. Stationarymanometry was performed by the rapid pull-through (RPT) technique, with catheter water perfused,to study the lower esophageal high pressure zone [loweresophageal sphincter (LES) and diaphragmatic crura] andthe parameters of esophageal peristalsis. In patients with hiatal hernia, the variouscombinations of peak and/or deflection of manometricline pressure identified five EGJ profiles, only one ofwhich reveals (by one-peak profile due to superimposed LES and diaphragmatic crura) the reducibilityof the hernia. The frequency of the five profiles wascalculated in the HE and H groups: a two-peak profilewas significantly more prevalent in these patients, although less so in the group with esophagitis.In E patients the distal amplitude and the distalpropagation of esophageal waves were significantly lowerthan in the other three groups (P < 0.05 vs controls and group HE; P < 0.01 vs group H).Furthermore, the distal amplitude was significantlyhigher in the group H than in the HE (P < 0.01). Ourresults show a better definition of hiatal hernia morphology, via the RPT technique, disclosingfive pressure profiles. In addition, a significant linkwas found between small reducible hiatal hernia withoutGERD and wave amplitude of the distal esophagus. The amplification of peristaltic clearing maybe considered the initial protective process againstacid reflux; the breakdown of this mechanism may triggerthe pathological sequence of GERD.     

Empirical Therapy versus Diagnostic Tests in Gastroesophageal Reflux Disease (A Medical Decision Analysis)

Our objective was to describe the conditionsthat determine the costs of empirical therapy ingastroesophageal reflux disease (GERD). Our design wasa threshold analysis using a decision tree. The costs of medications were estimated from the averagewholesale prices. The costs of diagnostic procedureswere expressed as the sum of physician and facilitycosts. A decision tree was modeled to calculate the threshold probability of GERD, for whichempirical therapy became the preferred managementstrategy. Bayes' formula was used to transform thesensitivity and specificity of various symptoms and thejoint occurrence of multiple symptoms into diseaseprobabilities. The decision in favor of empiricaltherapy is influenced by four factors: the probabilityof GERD, the duration or costs of GERD therapy, the costs of erroneous empirical therapy inpatients with diagnosis other than GERD, and the costsof diagnostic procedures. In general, the expectedbenefit of saving the costs of a diagnostic procedureoutweighs the costs of occasional erroneous empiricaltherapy. However, if surgical therapy is considered orantisecretory therapy is administered for a time periodof 10 or more years, diagnostic confirmation of GERD should be sought. In the long run, thefailure to differentiate between peptic ulcer and GERDresults in the highest cost associated with erroneousempirical therapy. In patients with multiplecharacteristic symptoms of GERD, the diagnosis can beascertained with sufficient confidence to warrantempirical therapy.     

Adaptation of Esophageal Mucosa to Acid- and Pepsin-Induced Damage (Role of Nitric Oxide and Epidermal Growth Factor)

To study whether the esophageal mucosa was ableto elicit mucosal adaptation, we induced esophagealdamage by perfusing acidified pepsin in rabbits. Mucosaladaptation was induced by preexposing the esophageal mucosa to a mild irritant (acidified saline)for 60 min prior to acidified pepsin (strong irritant).Macroscopic and microscopic esophageal injury, cellproliferation, and mucosal barrier function(H⁺, K⁺, hemoglobin flux rates)were studied. Preexposure of the esophageal mucosa toacidified saline significantly decreased both themucosal damage and the mucosal barrier dysfunctioninduced by acidified pepsin. The development of this phenomenon wasnondependent on cell proliferation. Concomitanttreatment with either the nitric oxide synthaseinhibitor, N^G-nitro-L-arginine, or theperfusion of immunospecific EGF-receptor antibodies or tyrphostin-25, aninhibitor of the tyrosine kinase activities ligated tothe intracytoplasmatic domain of the EGF receptor,during the preexposure period completely reversed the protection induced by acid. We conclude thatthe rabbit esophageal mucosa shows mucosal adaptation toacid and pepsin. The development of this phenomenon isfast, not dependent on cell proliferation, and dependent, at least in part, on nitric oxideand EGF-receptor-mediated mechanisms.     

Effects of Omeprazole on Mechanisms of Gastroesophageal Reflux in Childhood

Prolonged recordings of esophageal motility haveshown that dynamic changes of lower esophageal sphincter(LES) pressure such as transient LES relaxation and LESpressure drifts are the most common mechanisms underlying gastroesophageal reflux (GER). Thecoexistence of a delayed gastric emptying has also beenreported in a high proportion of patients with refluxdisease. However, not much information is available on the effects of antireflux therapy on thepathogenetic mechanisms of GER. The purpose of thisstudy was to determine in a group of children withsevere reflux disease the effect of omeprazole therapy on motor changes of LES underlying GER as wellas on gastric emptying time. Twenty-two children (medianage: 6.6 years) with GER disease, refractory to combinedranitidine and cisapride administration, entered into an eight-week omeprazole course.Ten subjects with moderate GER disease served ascontrols (median age: 6.0 years). Before and afteromeprazole administration, the following variables were assessed: esophagitis grading, fasting and fedsimultaneous prolonged recording of distal esophagealsphincter pressure (with a sleeve catheter) andintraesophageal pH, LES and esophageal peristalsisamplitude, and gastric emptying time of a mixedsolid-liquid meal (measured with gastric ultrasound). Ascompared to controls, patients showed a higher rate oftransient LES relaxation and LES pressure drift (P <0.01), a reduced amplitude of basal sphincter pressure(P < 0.01) and peristalsis (P < 0.05), and a moreprolonged gastric emptying time (P < 0.05). Afterending omeprazole, there was no significant change inany of the motor abnormalities of the esophagus and ingastric emptying time despite a marked improvement ofsymptoms and esophagitis in all patients. Sixteenpatients were symptomatic when reevaluated on a clinical basis two months after ending therapy. Weconclude that in children with severe GER disease, anabnormally high rate of both transient LES relaxationand LES pressure drift and slow gastric emptying are not affected by omperazole treatment, eventhough esophageal mucosal damage is markedly improved orcured. These abnormalities represent a primary motordisorder and can be implicated in the refractoriness of reflux disease.