Pathologic Duodenogastric Reflux Research Articles

Принципы диагностики хронического гастрита, ассоциированного с патологическим дуоденогастральным рефлюксом: серия клинических наблюдений

In recent years in the structure of the incidence of chronic gastritis, there has been a decrease in the proportion of Helicobacter pylori-associated gastritis, but the contribution of other etiological factors is increasing. In addition to H. pylori, one of the most frequently diagnosed gastritis in real clinical practice is chemical gastritis, associated with the development of pathological duodenogastric reflux. The increase in prevalence makes the issue of diagnosing biliary gastritis relevant. This publication was prepared with the aim of systematizing and analyzing available data on the incidence, risk factors, mechanisms of formation, as well as clinical, endoscopic and pathomorphological signs of biliary gastritis and is illustrated by a series of observations from real clinical practice.

Biliary gastritis. Pathomorphological features and differential diagnosis

The review article discusses the modern pathogenetic links of biliary gastritis, namely the role of endothelial dysfunction, intestinal metaplasia in inflammation and the influence of Helicobacter pylori infection. The problem of combined damage to the mucous membrane of HP-associated and biliary gastritis remains relevant, since modern foreign studies have not come to a consensus, but most authors state increased carcinogenesis of the stomach with a positive HP status against the background of the course of pathological duodenogastric reflux. The article also presents original materials of histological examination of biliary, HP-associated, autoimmune and hyperplastic gastritis with similar morphological features, thereby demonstrating the difficulties of differential diagnosis.

Diagnostic Principles for Chronic Gastritis Associated with Duodenogastric Reflux.

This article systematizes available data from the literature on biliary gastritis (BG) in order to increase the awareness of specialists about the latest possibilities for diagnosing the disease. BG occurs as a result of pathological duodenogastric reflux. In patients with a preserved duodenogastric junction, the dominant factor is represented by motor disorders of the upper digestive tract (primary biliary gastritis), while in patients recovering from surgical interventions it is represented by structural changes (secondary biliary gastritis). Progressive BG can lead to atrophy of the gastric mucosa, intestinal metaplasia, epithelial dysplasia, and eventually to gastric cancer. Diagnostic methods for BG are carried out to identify risk factors, exclude alarm symptoms and identify persistent motor disorders and pathological reflux (24 h pH-impedancemetry, hepatobiliary scintigraphy, 24 h monitoring of bilirubin content in the reflux using a Bilitec 2000 photometer), as well as to diagnose gastritis itself (esophagogastroduodenoscopy, morphological gastrobiopsy examination). The diagnosis of BG should be based on a multidisciplinary approach that combines a thorough analysis of a patient's complaints, an anamnesis of the disease, and the results of endoscopic and histological research methods.

Potential factors of Helicobacter pylori resistance to clarithromycin.

A comparative dissolution kinetics test (CDKT) and bioequivalence studies of generic proton pump inhibitors (PPIs) do not model pharmacological acid suppression (PAS) and pathological duodenogastric reflux (PDGR). This study aimed to model them in CDKT to assess drugs stability and potential pantoprazole-clarithromycin interactions. In CDKT, PDGR (dissolution medium pH 7.00±0.05, preexposure at pH 1.20±0.05) and PAS (pH 4.00±0.05) were modelled for original pantoprazole (OP) and its generics (GP1-4). In CDKT with high-performance liquid chromatography, dissolution gastric medium in adequate (pH 4.00±0.05) and inadequate (pH 1.20±0.05) PAS were modelled for original clarithromycin (OC) and its generics (GC1-4). After exposure in pH 7.00±0.05, pantoprazole was released from GP1 within 10min in the amount of 68.8%. In рН 4.00±0.05, 83.0% and 81.5% of pantoprazole were released from GP1 and GP4. When OP, GP2 and GP3 were placed in pH 7.00±0.05, pantoprazole was released in amount: 99.4%, 88.0% and 98.2%. Clarithromycin releasing from OC, GC1, GC2, GC3, GC4 in pH 4.00±0.05 was 93.5%, 91.6%, 92.9%, 79.4% and 83.0%. In pH 1.20±0.05: 9.7%, 6.7%, 8.5%, 33.3%, 28.8%. Destruction of enteric coats of some local pantoprazole generics in CDKT-models might be a potential factor for inadequate therapy.

Controversial Points in the Assessment of the Quality of Generic Esomeprazole Formulations

A comparative dissolution kinetics test was performed to model the actions of pathological duodenogastric reflux and therapeutic acid suppression on the stability of esomeprazole formulations from three different manufacturers. After exposure to solutions pH (1.2 ±0.05) or (4.0 ±0.05), formulations were transferred to medium pH (7.0 ±0.05), from which aliquots were collected at 0, 4, 10, 15, 20, 30, 45, and 60 min for estimation of esomeprazole concentrations. The duration of exposure of the medicinal formulation of esomeprazole to pathological duodenogastric refluxate was 4 min. In these test conditions, Generic-1 and Generic-2 were found not to be equivalent to the reference drug (RD); the medicinal formulation of the RD was probably influenced by pathological duodenogastric reflux in the stomach, while Generic-2 was completely degraded in moderately acidic medium pH 4.0, which is evidence of the possible adverse influence of its main antisecretory pharmacodynamic effect of the intragastric stability of the medicinal formulation and the active substance.

Дискуссионные проблемы оценки качества воспроизведенных препаратов эзомепразола

Выполнен тест сравнительной кинетики растворения, моделирующий воздействие патологического дуоденогастрального рефлюкса и лекарственной кислотосупрессии на устойчивость препаратов эзомепразола 3 разных производителей. После экспозиции в растворах с pH (1,2 ± 0,05) или (4,0 ± 0,05) препараты перемещались в среду с pH (7,0 ± 0,05), откуда забирались аликвоты через 0, 4, 10, 15, 20, 30, 45, 60 мин для определения в них концентраций эзомепразола. Время воздействия патологического дуоденогастрального рефлюктата на лекарственную форму эзомепразола равно 4 мин. Показано, что в заданных тестом условиях ВЛС1 и ВЛС2 не являются эквивалентными референтному препарату (РП), лекарственная форма РП, вероятно, подвержена влиянию патологического дуоденогастрального рефлюкса в желудке, ВЛС2 полностью разрушается в умеренно кислой среде с pH 4,0, что свидетельствует о возможном негативном воздействии его основного антисекреторного фармакодинамического эффекта на стабильность в желудке собственной лекарственной формы и действующего вещества.

A Comparative Dissolution Kinetics Test for Omeprazole-Containing Medicines, Reproducing Secretory and Motor-Evacuatory Impairments the Stomach of Patients with Acid-Dependent Diseases

A comparative dissolution kinetics test was used to study the release (dissolution kinetics) of an original and 10 generic formulations of omeprazole from different manufacturers in a medium simulating the moderately acidic conditions in the stomach typical of the state of medication-induced suppression of acidity; tests were also performed in a model of pathological duodenogastric reflux. HPLC was used to measure omeprazole concentrations in aliquots collected at 4, 10, 15, 20, 30, 45, and 60 min in solution with pH 7.0 ± 0.05 after 2 h of exposure at pH 1.2 ± 0.05 or 4.0 ± 0.05. The duration of action of pathological duodenogastric reflux on the therapeutic formulations of omeprazole was 4 min. Not all the study formulations could be completely recognized as equivalents to the original formulation in the in vitro test conditions.

Тест сравнительной кинетики растворения лекарственных препаратов, содержащих омепразол, воспроизводящий секреторные и моторно-эвакуаторные нарушения в желудке больных с кислотозависимыми заболеваниями

С помощью теста сравнительной кинетики растворения изучено высвобождение (кинетика растворения) оригинального и 10 воспроизведенных препаратов омепразола разных производителей в среде, имитирующей умеренно кислую среду желудка, характерную для состояния медикаментозной кислотосупрессии, и в модели патологического дуоденогастрального рефлюкса. Методом ВЭЖХ определяли концентрацию омепразола в аликвотах, отбираемых через 4, 10, 15, 20, 30, 45, 60 мин в растворе с рН (7,0 ± 0,05) после 2 ч экспозиции при pH (1,2 ± 0,05) или (4,0 ± 0,05). 4 мин — время воздействия патологического дуоденогастрального рефлюкса на лекарственную форму омепразола. Показано, что не все изученные препараты могут быть в полной мере признаны эквивалентными оригинальному препарату в изучаемых условиях in vitro.

Pathologic Duodenogastric Reflux and Inhibited Gastric Acid Secretion as Potential Factors Decreasing Omeprazole Stability

Bioequivalence studies are usually conducted with healthy volunteers. However, there are some differences in conditions of enteric-coated acid-labile drug release and absorption between healthy subjects and gastrointestinal patients. Pathologic duodenogastric reflux (PDGR) with high-amplitude changes in gastric pH can lead to destruction of the coating layer, resulting in degradation of the active compounds due to decrease in pH level after a reflux. The pH increasing ≥4 within PPIs administration also promotes dissolution of poor-quality coating. Modified comparative dissolution testing of original omeprazole (OO) and Generics1;2;3;4 proceeded in two stages. At first, we moved drugs from solution with Ph=1.2 (1.2 ± 0.05) to рН=7.0 (7.0 ± 0.05) and examined concentration of omeprazole in solution using high-performance liquid chromatography (HPLC). According to our self-developed formula, pH 7 exposure time of resistance to PDGR for omeprazole is 4 minutes, i.e. the active substance should not be released within 4 minutes at pH 7. The exposure at the second stage was conducted with pH 4 (4.0 ± 0.05), which imitated gastric pH after PPI administration. And then we also moved drugs to pH 7 with the subsequent measurement of omeprazole concentration. Omeprazole concentrations after 4, 10, 15, 20, 30, 45, 60 minutes in pH 7 solution at the first stage (pH 1.2 exposure) were different for OO and generics. For OO, these values were 4,7 ± 0,7%; 41,4 ± 3,0%; 62,8 ± 4,0%; 79,5 ± 2,9%; 83,5 ± 2,9%; 81,6 ± 2,9% (partly degradation of omeprazole); 80,6 ± 4,4%; for Generic1 - 0; 49,3 ± 9,9%; 88,8 ± 2,8%; 90,4 ± 3,7%; 88, 2 ± 2,2%; 87,3 ± 2,0%; 85,9 ± 1,1%; for Generic2 - 0; 30, 6 ± 6,3%; 66,7 ± 8,2%; 76,4 ± 7,4%; 82,8 ± 5,3%; 86,0 ± 3,7%; 84,6 ± 3,3%: for Generic3 - 80,8 ± 3,6%; 83,5 ± 1,9%; 83, 8 ± 3,2%; 83,3 ± 2,7%; 81,9 ± 2,1%; 82,1 ± 2,0%; 82,0 ± 2,4%; for Generic4 - 82,5 ± 1,7%; 84,4 ± 0,8%; 84,2 ± 1,2%; 82, 9 ± 0,9%; 82,9 ± 0,9%; 82,9 ± 0,9%; 82,8 ± 1,1%, respectively. An analysis of the omeprazole concentration in pH 7 solution at the second stage (pH 4 exposure) revealed the following parameters after 4, 10, 15, 20, 30, 45, 60 minutes: for OO - 4,4 ± 0,6%; 40, 5 ± 3,0%; 62,8 ± 2,0%; 80,0 ± 3,1%; 85,4 ± 2,9%; 82,8 ± 3,4%; 80,9 ± 3,5%; for Generic1 – 0; 67,0 ± 7,8%; 89,7 ± 2,3%; 91, 9 ± 4,3%; 89,1 ± 1,6%; 88,3 ± 1,4%; 87,8 ± 1,2%; for Generic2 – 0; 42,2 ± 5,6%; 75,1 ± 7,3%; 81,0 ± 6,0%; 88,4 ± 3,2%; 88, 6 ± 1,3%; 87,9 ± 1,0%; for Generic4 – 85,5 ± 0,5%; 85,6 ± 0,5%; 84,7 ± 0,9%; 82,7 ± 3,0%; 84,4 ± 0,3%; 84,4 ± 0,3%; 84,3 ± 0,4%, respectively. Generic3 release and degradation were completely realized at pH 4. Gastric stability of Generic3 and Generic4 has been decreasing due to PDGR and pharmacodynamic effect of the PPIs themselves.

Cholecystectomy and duodenogastric reflux: interacting effects over the gastric mucosa.

AimsTo evaluate association between duodenogastric reflux and early gastric mucosal changes before and after the cholecystectomy procedure.Materials and methodsPatients were evaluated with preoperative and postoperative endoscopy and endoscopic biopsy. Demographic and clinical characteristics, histological parameters, presence of duodenogastric reflux, and Updated Sydney scores were noted.ResultsA total of fifty patients who obeyed the follow-up were enrolled into the study. Median age of the patients was 43 years (range 25–84). Male–female ratio was 0.51 (17/33). Duodenogastric reflux % and Updated Sydney scores before and after cholecystectomy were 24 (48%) versus 39 (78%) and 2.38 ± 2.21 versus 3.46 ± 3.05, respectively (p = 0.001, p < 0.000). Mucosal inflammation degree showed significant increase in 15 (30%) patients, decrease in 7 (14%) patients and equality in 28 (56%) patients (p = 0.037). Neutrophil activation degree was significantly higher in 21 (42%) patients, lower in 5 (10%) patients after the surgery (p = 0.005). Postoperative glandular atrophy degree was also higher in 13 (26%) patients and equal in 37 (74%) patients (p = 0.001). Pre- and postoperative degree of intestinal metaplasia and H. pylori density did not any show significant difference (p = 0.157, p = 0.248, respectively).There were significant positive correlation between postoperative H. pylori infection and mucosal activity, inflammation, atrophy and intestinal metaplasia.ConclusionCholecystectomy is a potent inducer of pathologic duodenogastric reflux. Early onset of duodenogastric reflux and underlying H. pylori gastritis cause early gastric mucosal injury following cholecystectomy procedure by interacting collectively.

Diagnostic value of combined gastric pH and bilirubin monitoring in pathologic duodenogastric reflux

Diagnostic value of combined gastric pH and bilirubin monitoring in pathologic duodenogastric reflux

Histological features of the gastric mucosa in children with primary bile reflux gastritis

BackgroundBile reflux is one of the primary factors involved in the pathogenesis of gastric mucosal lesions in patients with chronic gastritis; however, little is known about the exact histological features of bile reflux and its contributions to gastric mucosal lesions in this disease, especially in children with primary bile reflux gastritis (BRG). The aim of this study was to investigate the classic histological changes of the gastric mucosa in children with primary BRG.MethodsThe Bilitec 2000 was used for 24 h monitoring of gastric bile in 59 children with upper gastrointestinal symptoms. The histological characteristics of the gastric mucosa were examined and scored.ResultsThirteen of the 59 patients had a helicobacter pylori infection and were excluded; therefore, 46 cases were included in this study. The positive rate of pathological duodenogastric reflux was significantly higher in patients with foveolar hyperplasia than those without foveolar hyperplasia; however, the rate was significantly lower in patients with vascular congestion than those without vascular congestion. The longest reflux time and the total percentage time of bile reflux were significantly lower in patients with vascular congestion than those without vascular congestion. A total of 9 types of histological changes were analyzed using a binary logistic regression. Foveolar hyperplasia and vascular congestion in the superficial layer became significant variables in the last step of the stepwise regression.ConclusionsFoveolar hyperplasia was associated with the severity of bile reflux, suggesting that it is a histological feature of primary BRG in children, while vascular congestion may be a protective factor.

The study on gastric electrical activity and gastric emptying in patients with primary pathological duodenogastric reflux

Objective To explore the etiological factors of primary pathological duodenogastric reflux (DGR) through investigating the relationship between severity of bile refulx,the changes of surface gastric electric rhythm and gastric emptying movement in primary pathological DGR patients.Methods From January 2007 to April 2008 in Qingdao Municipal Hospital,58 cases of outpatients diagnosed as primary pathological DGR and 21 healthy individuals (control group) were collected and underwent 24-hour gastric bilirubin monitoring,gastric endoscopy,gastric electric rhythm,and gastric emptying test.The relationship between gastric electric parameters and gastric emptying,bilirubin reflux,Hp infection was analyzed.Results 1.The main frequency in fasting and postprandial of primary pathological DGR patients [(1.94±0.04) cpm vs (2.93±0.07) cpm; (2.12±0.03) cpm vs (3.35 ±0.05) cpm],the percentage of normal gastric slow wave in fasting and postprandial (74.46± 0.56 vs 85.55 ± 1.06 ; 63.97 ± 0.64 vs 86.13 ± 1.49),and fasting/postprandial power ratio (PR) (1.68±0.02 vs 2.75±0.09) were all lower than those of control group (P＜0.05).The percentage of bradygastria in fasting and postprandial of DGR patients (18.04±0.36 vs 7.76±0.78;23.73±0.91 vs 8.47±0.55),the percentage of tachygastria in fasting and postprandial (8.93±0.26 vs 5.75±0.66;13.02±0.40 vs 7.66±0.27) were higher than that of control group (P＜0.05).2.The main frequency of severe reflux patients in fasting and postprandial [( 1.68 ± 0.07) cpm vs (2.13 ± 0.07)cpm; (2.18±0.09) cpm vs (2.76±0.06) cpm],the percentage of normal gastric slow wave in fasting and postprandial (69.71±0.43 vs 80.35±0.68; 56.36 ±0.85 vs 72.34±0.80),fasting /postprandial PR (1.47±0.04 vs 2.02±0.04) were lower than those of mild-reflux group (P＜0.05).The percentage of bradygastria in fasting and postprandial of severe reflux patients (22.94 ± 0.68 vs 13.47 ± 0.61; 29.61 ± 1.14 vs 17.55 ± 0.51) and the percentage of tachygastria in fasting and postprandial (9.94 ± 0.54 vs 7.02 ± 0.42 ; 17.04 ± 0.70 vs 10.71 ± 0.20) were higher than that of mild-reflux group (P＜0.05).3.There was no significant difference of gastric electrical parameters in fasting and postprandial between Hp-positive and Hp-negative groups (P＞0.05).4.The ratio of gastric emptying in DGR group was significantly lower than that of control group (37.9％ vs 90.5 ％,P＜0.05).The gastric emptying delay in DGR group significantly increased compared with control group (60.3％ vs 9.5％,P＜0.05).There was no significant difference in gastric emptying delay between severe-reflux group and light-reflux group (69.0％ vs 51.7％,P ＞ 0.05).Conclusions There is dysfuntion of gastric myoelectrical activity and gastric motility in primary pathological DGR patients,which may be an important mechanism in pathological DGR. Key words: Duodenogastric reflux; Electrogastrography; Gastric emptying

Diagnostic value of porphobilin staining of gastric mucus for primary pathological duodenogastric reflux

Objective To study the diagnostic value of porphobilin staining of gastric mucus for pfimalt pathologic duodenogastrie reflux （DCR）. Methods A total of 58 DCR patients diagnosed from Janualy, 2007 to April, 2008 were recruited to the study as DGR group, and 21 healthy volunteers as control. All subjects underwent 24-hour intragastric bilimbin monitor and gastroscopy. Bilirubin absorption value of 0. 25 and median reflux time of 23.60% were taken as thresholds to differentiate low reflux group （ reflux time 〈23.60% ） and high reflux group （ reflux time≥23.60% ）. Porphobilin staining of gastric mucosa was quantitatively analyzed. Results Deposition of porphobilin in mucosa of gastric antrum, gastric angle and gastric body in primary pathologi DGR group was significantly higher than those in healthy group （P 〈 0. 05 ）. The occurrence of atrophic and intestinal metaplasia of gastric antrum in high reflux group was significantly higher than that of low reflux group （ P 〈 0. 05 ）. Deposition of porphobilin in mueosa of gastric antrum, gastric angle and gastric body in high reflux group was significantly higher than that of low reflux group （ P 〈 0. 05 ）. The New Sydney system pathological scores of gastric antrum and angle of high reflux group was higher than that of low reflux group （P 〈 0. 05 ）. The deposition uf porphobilin in mueosa of gastric antrum and gastric angle was positively correlated with New Sydney system pathological seores in primary pathological DC, R group （ r = 0. 59, P = 0. 041 and r = 0. 73, P = 0. 038）. Conclusion Porphobilin staining of mucosa in gastric antrum can reflect the severity of bile reflux, and is positively correlated with the extent of gastric mucosal lesion, which may be helpful in diagnosis of primary pathological DGR. Key words: Duodenogastric reflux; Gastric mucosa; Porphobilin staining

Prevalence of pathological duodenogastric reflux and the relationship between duodenogastric and duodenogastrooesophageal reflux in chronic gastrooesophageal reflux disease

The role of duodenogastric reflux in gastrooesophageal reflux disease is still controversial. (i) To determine the prevalence of pathological duodenogastric reflux (DGR) in gastrooesophageal reflux disease patients and (ii) to define the relationship between DGR and duodenogastrooesophageal reflux. We evaluated 92 patients referred for investigation of recurrent reflux symptoms after proton pump inhibitors (PPI) therapy. All the patients filled out symptom questionnaires and underwent endoscopy, oesophageal manometry and combined oesophagogastric pH and bilirubin monitoring. Endoscopy divided the 92 patients into four groups (group I: 25 nonoesophagitis patients, group II: 26 patients with grade A-B oesophagitis, group III: 21 patients with grade C-D oesophagitis and group IV: 20 patients with Barrett's oesophagus. Twenty-four of the 92 patients (26%) showed pathological DGR. Abnormal oesophageal bilirubin exposure was observed in 62 of the 92 patients (67.4%). Of the 62 patients with abnormal oesophageal bilimetry, 15 (24.2%) patients simultaneously showed pathological DGR. The gastric bilirubin exposure in patients with abnormal oesophageal, Bilitec tests did not differ from that in patients with normal oesophageal bilimetry (P>0.05). A weak correlation between oesophageal and gastric bilirubin exposure, both expressed as a percentage of time, was found (r=0.28; P<0.01). Pathological DGR is present in a little more than a quarter of patients with recurrent reflux and dyspeptic symptoms after PPI therapy. Excessive DGR is not a prerequisite for pathological oesophageal exposure to duodenal contents. Gastric bilirubin monitoring may be useful to choose the best surgical treatment for patients with reflux and dyspeptic symptoms refractory to PPI.

Laparoscopic restoration of gastrointestinal continuity after duodenal switch

Biliopancreatic diversion (BPD) with duodenal switch (DS) for morbid obesity was first performed by Hess and Hess [ [1] Hess D.S. Hess D.W. Biliopancreatic diversion with a duodenal switch. Obes Surg. 1998; 8: 267-282 Crossref PubMed Scopus (656) Google Scholar ] in 1988. BPD-DS incorporates two distinct procedures: the BPD, which had been well established by Scopinaro et al. [ [2] Scopinaro N. Gianetta E. Civalleri D. et al. Biliopancreatic bypass for obesity: initial experience in man. Br J Surg. 1979; 66: 618-620 Crossref PubMed Scopus (417) Google Scholar ] in 1976 and the DS, established by DeMeester et al. [ [3] DeMeester T.R. Fuchs K.H. Ball C.S. Albertucci M. Smyrk T.C. Marcus J.N. Experimental and clinical results with proximal end-to-end duodeno-jejunostomy for pathologic duodenogastric reflux. Ann Surg. 1987; 206: 414-424 Crossref PubMed Scopus (173) Google Scholar ]. At 10 years, Hess et al. [ [4] Hess D.S. Hess D.W. Oakley R.S. The biliopancreatic diversion with the duodenal switch: results beyond 10 years. Obes Surg. 2005; 15: 408-416 Crossref PubMed Scopus (213) Google Scholar ] reported excellent long-term results in terms of weight loss, with a percentage of excess weight loss (%EWL) of 75% in 92% of the patients followed up, in addition to high patient satisfaction and low complication rates. Similar long-term results were also reported by Marceau et al. [ [5] Marceau P. Biron S. Hould F.S. et al. Duodenal switch: long-term results. Obes Surg. 2007; 11: 1421-1430 Crossref Scopus (162) Google Scholar ] with a %EWL of 73% ± 19% in 1356 living patients after a mean follow-up of 7.3 ± 3.7 years.

Le reflux biliaire duodéno-gastrique et gastro-œsophagien

This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management. Duodenogastric reflux (DGR) consists of retrograde passage of alkaline duodenal contents into the stomach; it may occur due to antroduodenal motility disorder (primary DGR) or may arise following surgical alteration of gastoduodenal anatomy or because of biliary pathology (secondary DGR). Pathologic DGR may generate symptoms of epigastric pain, nausea, and bilious vomiting. In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma. The treatment of DGR is difficult, non-specific, and relatively ineffective in controlling symptoms. Proton pump inhibitors decrease the upstream effects of DGR on the esophagus by decreasing the volume of secretions; promotility agents diminish gastric exposure to duodenal secretions by improving gastric emptying. In patients with severe reflux resistant to medical therapy, a duodenal diversion operation such as the duodenal switch procedure may be indicated.

Familial adenomatous polyposis predisposes to pathologic exposure of the stomach to bilirubin

The role of duodenogastric reflux in the genesis of gastric polyps in familial adenomatous polyposis (FAP), although suggested by scintigraphy scanning studies, remains unclear. Twenty-four hour intragastric bilirubin monitoring with the Bilitec optoelectronic device was carried out in 25 FAP patients, of whom 19 had gastric polyps (fundic gland in 13, adenomatous in 2, and both histologic types in 4) on endoscopic examination. Gastric exposure to bilirubin was expressed as the percentage of total recording time that absorbance exceeded the threshold of 0.25 and was calculated in reference to values obtained from 25 healthy volunteers. Helicobacter pylori status of the stomach was checked as well. Gastric exposure to bilirubin was pathologic in 14 (56%) patients. Gastric exposure to bilirubin was of longer duration in FAP patients than in healthy volunteers (mean+/-SEM: 19%+/-4% vs 6%+/-2%) (P<.005). It increased from healthy volunteers (6%+/-2%) to FAP patients without gastric polyps (10%+/-3%), and to FAP patients with gastric polyps (22%+/-5%) (P<.004). Bilirubin exposure times were similar in FAP patients with fundic gland polyps only and in those having either adenomatous polyps only or both types of polyps (24%+/-7% vs 17%+/-4%). No patient with pathologic gastric exposure to bilirubin as well as none having gastric polyps, had H. pylori in the antrum. This study shows that gastric exposure to bilirubin is of longer duration in FAP patients than in healthy volunteers, and in FAP patients with gastric polyps than in those without polyps. This study supports the existence of a direct correlation between pathologic duodenogastric reflux (DGR), the absence of H. pylori in the antrum, and the presence of gastric polyps in FAP patients.

Functional evaluation of the intrathoracic stomach as an oesophageal substitute.

A study of duodenogastric reflux and gastric function was undertaken in 16 patients 1-7 years after oesophagectomy and high intrathoracic oesophagogastrostomy for oesophageal carcinoma. All were able to eat satisfactorily; ten complained of mild foregut symptoms and ten had endoscopic mucosal lesions. Biliary excretion scintigraphy demonstrated pathological duodenogastric reflux in 11 patients. The emptying of a semisolid radiolabelled meal from the intrathoracic stomach in the upright position was significantly quicker than in control subjects (P less than 0.01). No gastric motor activity was recorded on manometry, suggesting that the transposed stomach acts like an inert tube. Results of 24-h pH monitoring showed that the area under the curve at pH less than 4 in the stomach was significantly less than in control subjects (P less than 0.001). In addition, patients had a significantly greater oesophageal alkaline exposure (P less than 0.001). The vagotomized intrathoracic stomach therefore empties well in the upright position, but is subjected to reflux of alkaline duodenal contents and can retain the ability to produce acid. The interaction between alkaline and acid contents in the pathogenesis of symptoms and mucosal lesions needs further investigation.

'Bile' in the oesophagus.

Acid gastro-oesophageal reflux occurs when the lower oesophageal sphincter is incompetent, but oesophagitis caused by reflux of duodenal content implies incompetence of both the pyloric and gastro-oesophageal sphincters. The term 'alkaline' reflux oesophagitis was coined long before objective analysis was made of bile in the stomach and oesophagus, and well before pH monitoring was introduced. Surgical procedures to divert bile from the stomach and oesophagus were developed on a clinical basis and gave encouraging results in the management of peptic oesophageal stricture. Alkaline oesophagitis is well recognized after gastric surgery and the entity 'primary pathological duodenogastric reflux', although contested by some, attracts growing support. Recent evidence suggests that the complications of Barrett's oesophagus may be related to duodenogastro-oesophageal reflux. Probes designed to measure gastric and oesophageal bile salts have recently been developed and may give more information in the future.