Evaluation of gastric acid secretion at endoscopy with a modified Congo red test

BACKGROUND: Markedly decreased or absent gastric acid production is associated with a number of clinically significant conditions, and identification of patients with hypo/achlorhydria may be important. However, current methods of assessing impaired acid secretion are unreliable, time-consuming, and/or complex. The aim of this prospective study was to evaluate a modified endoscopic Congo red test for the diagnosis of hypo/achlorhydria by correlation with a standard gastric acid secretory test. METHODS: One hundred six consecutive outpatients with or without dyspeptic symptoms referred for endoscopy were evaluated by using a modified endoscopic Congo red test and a standard test of gastric acid secretion. The modified endoscopic Congo red test suggested hypo/achlorhydria when there was no color shift or a shift of small extent (less than one third of fundic mucosa). Hypo/achlorhydria by the standard gastric acid secretory test was defined as a maximal acid output of less than 6.9 mmol/hour in men and 5.0 mmol/hour in women. RESULTS: The accuracy of the modified endoscopic Congo red test for the diagnosis of hypo/achlorhydria was 0.98 (95% CI [0.93, 0.99]). The sensitivity was 1.0 (95% CI [0.92, 1.00]) and specificity 0.96 (95% CI [0.88, 0.99]). All patients tolerated the modified endoscopic Congo red test well. CONCLUSION: The modified endoscopic Congo red is an accurate, simple, fast, inexpensive, and well-tolerated chromoendoscopic method for identification of patients with hypo/achlorhydria during routine upper endoscopy.     

Gastrectomy Has No Effect on Bone Regeneration in Rats Despite a Decrease in Bone Mass

Objective. Acid secretion produced by a heterotopic gastric mucosal patch (HGMP) in the proximal esophagus, instead of gastric acid, may be responsible for laryngopharyngeal reflux (LPR), passing the upper esophageal sphincter. The aim of this study was to investigate the prevalence of HGMP in the proximal esophagus in patients with posterior laryngitis indicating the presence of LPR in comparison with a control group and to elucidate the possible role of this lesion in the pathogenesis of LPR. Material and methods. A total of 36 consecutive patients with posterior laryngitis diagnosed on laryngoscopic examination were enrolled in the study. Esophagoscopy and ambulatory 24-h intra-esophageal dual-probe pH monitoring were performed in all patients. During endoscopy, special attention was paid to the proximal part of the esophagus, and the proximal electrode for pH monitoring was placed in this region under endoscopic view. The control group comprised 660 consecutive patients who had undergone upper gastrointestinal endoscopy for the usual indications. When HGMP was found, biopsies were taken for histological confirmation. Results. HGMP was detected in 5 out of 36 patients. One out of five patients with patches was excluded from the study because the histopathology of this patient's patch revealed antral-type mucosa, which is not capable of acid secretion. Thus a total of 35 patients were included in the study, yielding a HGMP prevalence of 11.4% (4/35). Compared with the prevalence of the control group (1.6%), a significant difference was observed (p<0.005). pH monitoring showed that 45.4% of the patients had abnormal proximal acid reflux. All of four HGMP (+) patients with posterior laryngitis revealed significantly higher abnormal proximal reflux compared to the patients without patches (p<0.05). Conclusions. This first preliminary study may suggest that HGMP in the cervical esophagus could play a role in the pathogenesis of LPR, at least in a minor group of patients with posterior laryngitis, depending on its capability to produce acid in situ, although isolated proximal reflux could not be demonstrated. This finding may need to be supported by further studies with larger patient populations and using acid stimulation tests.     

食管高位胃黏膜异位与Barrett食管的对比研究

目的 探讨食管高位胃黏膜异位（HGM）与Barrett食管（BE）患者在症状、内镜下表现、组织病理学、Hp感染以及细胞角蛋白染色方面的差异。方法选择对2004年2月-2005年9月明确诊断的BE患者152例（BE组）、食管高位HGM患者52例（食管高位HGM组）,收集两组患者临床资料,总结各组患者的症状特点、各型黏膜的常规内镜下和放大内镜下特点;比较各型黏膜的组织病理学结果,快速尿酶法及Warthin—Starry银染检测病灶部位及胃窦部Hp感染情况,免疫组化法检测细胞角蛋白CK7、CK20、CK13及CK19的表达情况。结果BE组有反流症状者占64．5％（98／152）,显著高于食管高位HGM组的（13．5％,7／52）（X^2=40．36,P〈0．01）。放大内镜下BE黏膜小凹表现为点状46例、条纹状65例、绒毛状41例,而食管异位胃黏膜的小凹全表现为条纹状。组织病理学分型上,152例BE患者中属胃底型56例、交界型39例、特殊肠化型57例;而52例食管高位HGM患者中31例为胃底型、16例为交界型、5例为胃窦腺型,无一例发现有杯状细胞。BE黏膜中中、重度炎症细胞浸润所占比例为63．2％（96／152）,显著高于食管异位胃黏膜的28．8％（15／52）（P〈0．01）;而两组胃窦部中、重度炎症细胞浸润所占比例分别为44．7％（68／152）、51．9％（27／52）,差异无统计学意义（P〉0．05）。BE黏膜Hp检出率为32．2％（49／152）,BE组胃窦部黏膜Hp检出率为48．0％（73／152）;食管异位胃黏膜Hp检出率为44．2％（23／52）,食管高位HGM组胃窦部黏膜Hp检出率为40．4％（21／52）;两组Hp感染检出率差异均无统计学意义（P〉0．05）。细胞角蛋白免疫组化检测中,食管异位胃黏膜以及正常的食管鳞状上皮中无CK7的阳性表达,而BE黏膜的3种类型的上皮中均有表达;CK20和CK19在BE黏膜和食管异位胃黏膜中均有阳性表达;CK13     

Motility-Related Cyclic Fluctuations of Interdigestive Gastric Acid and Bicarbonate Secretion in Man: A Source of Substantial Variability in Gastric Secretion Studies

The relationship between interdigestive gastric motility and secretion was studied in eight healthy volunteers. Acid and bicarbonate output rates were measured with a high time resolution, using a perfusion system based on continuous registration of pH and Pco₂ of gastric effluent. Antral pressure was measured by manometry. The total duration of the interdigestive motility cycle (time between two phase-Ill complexes) was 96 ± 12min (mean ± SE). In late migrating motor complex phase II, acid output, bicarbonate output, and bile reflux increased significantly. Acid secretion reached a peak in association with motor phase III. The gastric lumen was then rapidly alkalinized; this phenomenon was due to a simultaneous decrease in acid secretion and a short-lasting (15 ± 2min, mean ± SE) phasic increase in bicarbonate output, which was not associated with bile reflux (bilirubin). After these phase-III-related events both acid and bicarbonate output rates reached a relatively stable level during phase I and early phase II. This period of stability constituted 47 ± 3% (acid) and 41 ± 6% (bicarbonate, means ± SE), respectively, of the cycle. The peak to base line output ratio was 6.6 ± 1.2 (p < 0.001) for acid and 2.8 ± 0.3 (p < 0.001) for bicarbonate (means ± SE). The results show a marked variability in acid and bicarbonate output rates during the interdigestive motility cycle. The magnitude of this variability has previously been underestimated owing to poor time resolution of the secretion measurements. If not taken into account, these ‘spontaneous’ secretory variations may constitute a considerable source of error in gastric secretion studies.     

Symptomatic ectopic gastric epithelium of the cervical esophagus

Four patients were found with patches of gastric fundal type epithelium just distal to the cricopharyngeus, separated from the gastroesophageal junction by 15–20 cm of normal squamous epithelium. Three of the four had symptoms of dysphagia localized to the area of the esophagus containing the epithelium. Congo red dye (a pH indicator) applied to the mucosa during endoscopy revealed acid production by the mucosa after stimulation with pentagastrin. Interestingly, the patients' symptoms decreased during treatment with cimetidine only to return on cessation of therapy.     

Clinical study of 31 patients with primary gastric mucosa-associated lymphoid tissue lymphoma

BACKGROUND: The purpose of the present paper was to investigate the clinical, endoscopic and histological features of 31 patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma to enable correct, early stage diagnosis. METHODS: A retrospective study was undertaken of 31 patients with gastric MALT lymphoma. The cases were examined immunohistologically with anti-CD(20CY) and CD(45RO) antibodies for further diagnosis. Helicobacter pylori infection was also detected with modified Giemsa staining. RESULTS: Patients with MALT lymphoma were aged between 22 and 73 years (mean, 45.0 years), and the male:female ratio was 11:20. The patients presented with non-specific symptoms, but chronic epigastric pain was the common symptom in a large proportion of the cases. The gastric smaller curvature was involved in 83.9% of cases (26/31) and in 13/31 cases (41.9%) it was confined the antrum. Under endoscopy, large and deep ulcers were similar to cancers in the majority of patients. Only 29.0% of patients were diagnosed by endoscopy on first examination. CD(20CY) were expressed in all cases and CD(45RO) expressed in only one case among 10 cases of indefinite diagnosis. Helicobacter pylori infection was found in 87.1% of patients. CONCLUSIONS: These findings suggest that primary gastric MALT lymphoma has unique clinical, endoscopic and histological features. The diagnosis for primary gastric MALT lymphoma was delayed not only due to the non-specific symptoms but also due to lack of attention to its features. Endoscopy and submucosal multiple biopsy were the principal diagnostic tools in patients with gastric MALT lymphoma. CD(20CY) and CD(45RO) immunological staining are recommended, especially for patients with indefinite diagnosis of gastric MALT lymphoma.     

Gastric Electrical Stimulation Does Not Significantly Affect Canine Gastric Acid Secretion and 24-Hour Gastric pH

Gastric electrical stimulation (GES) was shown to improve symptoms in patients with gastroparesis. However, the underlying mechanisms remain unclear. This study assessed the influence of various patterns of GES on fasting and postprandial gastric acid secretion and 24-hr gastric pH. Eight healthy dogs were studied and we found that in the fasting state, low-frequency, long-pulse (6/12-cpm, 375-msec, 4-mA) GES at the proximal stomach significantly inhibited the secretion of gastric juice (P < 0.05). No such effect was observed during GES (6/12 cpm) at the distal stomach. In the postprandial period, low-frequency, long-pulse GES at both proximal and distal sites and at both frequencies did not significantly affect gastric acid secretion. High-frequency, short-pulse GES, investigated for obesity (21 Hz, 8 mA, and 250 microsec, with 2 secs on, 3 sec off), at the proximal and distal stomach did not significantly affect the 24-hr gastric pH profile. In conclusion, GES with various stimulation parameters, and at various sites, has little effect on gastric acid secretion. The clinical effects induced by GES at these parameters may not be related to their effect on gastric acid homeostasis.     

Gastroösophageale Refluxerkrankung

Gastroesophageal reflux disease (GERD) is present when the passage of gastric contents into the esophagus causes symptoms or mucosal damage. Potent suppression of gastric acid secretion with proton pump inhibitors (PPIs) is an effective and safe treatment for many patients with this condition; however, acid suppression has not solved the problem of GERD. The relationship between reflux symptoms, endoscopic findings, and esophageal acid exposure is not straightforward. Some patients fail to respond to PPIs; at endoscopy, the esophagus is often normal, and pH studies may not reveal the cause of symptoms. It is clear that, although gastric acid secretion can be suppressed, we are far less successful at managing reflux itself. Apart from ?typical” reflux symptoms, other complaints, including dysphagia, noncardiac chest pain, and chronic cough, have been linked to GERD, but it can be difficult to identify those patients who will benefit from antireflux treatment. This is relevant because the risk of esophageal adenocarcinoma is elevated in patients with reflux symptoms, in particular those with Barrett’s esophagus.     

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients

BACKGROUND AND AIM: Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis. METHODS: Helicobacter pylori infection was examined in 781 patients by the measurement of serum immunoglobulin (Ig)G antibody, bacteriological culture and histological examination of biopsy specimens. The prevalence of HH, endoscopically identified gastric mucosal atrophy (closed- or open-type) and reflux esophagitis were investigated by reviewing endoscopic films. Investigated patients were divided into three age groups, under 49, 50-69, and over 70 years. The prevalence of esophagitis, H. pylori infection, gastric mucosal atrophy, and HH were compared to identify the possible predictive factors for reflux esophagitis by using logistic regression analysis. RESULTS: Sixty-nine patients with reflux esophagitis were found among the 781 investigated cases. The odds ratios of negative H. pylori infection, endoscopically identified closed-type gastric mucosal atrophy, and HH for the prevalence of reflux esophagitis were 1.342, 1.751 and 5.527, respectively. These results indicated that the presence of H. pylori infection was only a weak negative risk factor, and that HH was the most reliable endoscopic predictive factor for reflux esophagitis. CONCLUSION: Helicobacter pylori infection is a weak negative risk factor for the prevalence of reflux esophagitis, while HH is the most reliable predictive factor.     

Does Fasting Serum Gastrin Predict Gastric Acid Suppression in Patients on Proton-Pump Inhibitors?

Proton pump inhibitors (PPIs) block gastric acid secretion and may increase serum gastrin concentration. The aim of this study was to determine whether fasting serum gastrin concentration predicts gastric acid suppression in patients on PPI therapy. Ambulatory pH monitoring with one pH probe in the distal esophagus and a second probe in the stomach was performed in patients with persistent symptoms of GERD despite PPI treatment. Upon completion of pH monitoring, blood was drawn for measurement of fasting serum gastrin concentration. In all, 51 patients were studied: 26 on PPIs, 1 on H₂-receptor antagonists, and 24 off acid suppression. Fasting serum gastrin correlated inversely with percent time of gastric pH < 4 for all patients (r = –0.553; P < 0.001) and for the subgroup of 26 patients on PPIs (r = –0.435; P = 0.027). In patients on PPIs, an elevated gastrin (100 pg/ml) was associated with gastric pH < 4 for 25 ± 7% of the time compared to 54 ± 5% when the gastrin was normal (P = 0.004). Therapeutic gastric acid suppression (gastric pH < 4 for <50% of time) was present in 6 of 7 (86%) patients with an elevated fasting serum gastrin, compared with only 8 of 19 (42%) patients with a normal serum gastrin (P < 0.05). In conclusion, there is a significant inverse correlation between the fasting serum gastrin concentration and gastric acid profile in patients with GERD. An elevated fasting serum gastrin concentration while on PPI therapy suggests that gastric acid secretion is adequately suppressed.     

The pH Measurement of Fasting Gastric Juice in Acute Gastric Mucosal Lesions

Abstract: Fasting gastric juice acidity was assessed to elucidate its role in the cause of acute gastric mucosal lesions (AGML). Gastric juice was aspirated through an auxiliary endoscopic channel during routine endoscopic examinations, and its pH was measured with a glass electrode PH meter. The pH of 100 cases with AGML (acute hemorrhagic erosions (AHE), acute gastric ulcer and acute hemorrhagic gastritis), and 586 cases with other ulcerative or inflammatory lesions were compared with the gastric juice pH in 1775 endoscopically normal subjects. The pH value was classgied into four acid groups: Hyperacidity (pH < 1.4), Normoacidity (1).5 < pH < 2.0), Hypoacidity (2).1 < pH <4.0) and Anacidity (4). 1 < pH). In cases with AHE, a signifcant hyperacidity was recognized both in the periods preceding and just after the onset. This hyperacidity was followed by signgicant anacidity, and thereafter a return to normoacidity. These pH changes coincided well with endoscopic appearances; preceding stage-hypernormacidity, black-slough stage—hyperacidity, white-slough stage-anacidity and scarring stage-;normoacidity. These results suggest that an elevation of gastric acidity etiologically relates with the formation of AGML, especially Shin.     

MODIFIED ENDOSCOPIC CONGO RED TEST: A RAPID METHOD TO VISUALIZE GASTRIC ACID SECRETION

Background: The conventional endoscopic Congo red test (CRT) permits visualization of acid‐producing mucosa. However, the CRT has not been disseminated into clinical endoscopy, which is partly due to the substantial prolongation of the gastroscopic examination. Methods: Five healthy volunteers and 551 patients were included in a study designed to develop a more rapid approach based on the CRT. In this modified endoscopic Congo red test (MCRT), 0.2 µg/kg of pentagastrin was given intravenously to stimulate gastric acid production. The technical feasibility, tolerability, reproducibility, and inter‐ and intra‐observer reliability of the MCRT were evaluated. Results: The MCRT was as effective as the CRT (i.e. 6 µg/kg of pentagastrin was administered intramuscularly) in visualizing the extent of acid‐producing gastric mucosa. Moreover, the MCRT significantly reduced the duration of examination by 63% (almost 8 min), compared to the CRT. Conclusions: This MCRT is a simple, inexpensive, well‐tolerated and reproducible method with low inter‐ and intra‐observer variability and is well suited for endoscopy units with high workloads.     

Time pattern of gastric acidity in Barrett's esophagus

Increased gastroesophageal acid reflux is frequently found in patients with Barrett's esophagus, and it has been hypothesized that gastric acid hypersecretion could be an important factor aggravating the exposure of esophageal mucosa to acid and then contributing to the development of this disorder. The aim of the present study was to assess whether the circadian pattern of gastric acidity differs between refluxer patients with and without Barrett's esophagus and normal subjects. Continuous 24-hr gastric pH monitoring was performed in 119 healthy volunteers, 20 patients with Barrett's esophagus, 37 patients with moderate and 10 patients with severe reflux esophagitis without Barrett's esophagus. In all these diseases the final diagnosis was ascertained by means of endoscopy plus biopsy. There was no difference in the 24-hr and daytime patterns of gastric pH between healthy subjects and patients with Barrett's esophagus, while nocturnal acidity was significantly lower (P<0.05) in the latter population. Gastric acidity, in contrast, was higher (P<0.05) in controls than in patients with both moderate and severe reflux esophagitis without Barrett's esophagus during the whole 24-hr period. There was no difference between refluxer patients with and without Barrett's esophagus in any of the three time intervals we analyzed. Because normal subjects had lower gastric pH than patients with Barrett's esophagus during the night and than patients with reflux esophagitis during the whole 24-hr period, gastric hyperacidity is not a relevant factor in the development of both metaplastic columnar epithelium and inflammatory changes in the distal esophagus, and other pathophysiological mechanisms are involved in these histological alterations.     

Low-grade dysplasia in an adenomatous polyp of the esophagus developing on pyloric-type heterotopic gastric mucosa treated with endoscopic mucosal resection: a case report

A 72-year-old woman with an unremarkable medical history underwent an upper gastrointestinal endoscopy in May 2002 because of dyspepsia. An examination showed a pedunculated polyp lesion in an inlet patch on the posterior wall of the esophagus, 20 cm distant from the incisors and measuring 1.5 cm. Forceps biopsies were obtained, and the pathological analysis showed a gastric-like mucosa with well-differentiated pyloric glands below an atrophic squamous epithelium; most of the glands were lined with atypical cells, compatible with low-grade dysplasia. Histological examination after endoscopic removal showed a low-grade dysplasia in an adenomatous polyp of the esophagus developing on pyloric-type heterotopic gastric mucosa (HGM). Three years later, the patient remains well with no evidence of esophageal disease. We review 25 reported cases of adenocarcinoma and 3 cases of high-grade dysplasia arising in HGM.     

Recovery from gastric mucus depletion in the intact guinea pig mucosa

Background: In developed countries one‐third of the population is infected with the gastric pathogen Helicobacter pylori. In the early stages of H. pylori‐induced gastritis, typical symptoms include gastric erosions and mucus depletions. Artificial mucus depletion was generated, demonstrating both consequent irritation and recovery processes in the mucosa. Methods: The mucus depletion was examined by removing a small cylinder of mucus from the surface of the explanted guinea pig corpus mucosa, leaving the epithelial surface intact. pH microelectrodes were inserted into the mucosa in vitro, measuring the epicellular mucus pH, the pH _i of the underlying epithelial cells and the pH inside the gastric glands during mucus regeneration. Using infrared microscopy, the same process of mucus layer renewal was followed in anaesthetized animals. Results: The depletion exposed the tissue surface to low luminal pH levels. At a luminal pH of 2.5, a decrease was observed in the crypt outlet pH and surface cell pH _i , while deeper cells were less affected. However, a subsequent neutralization in the deep gland lumen was found. During the repair process, a quarter of the mucus layer was regenerated within the first 5?min. This newly secreted mucus formed a structure similar to that before depletion. Within 45 min, pH _i and tissue‐near pH values had fully recovered. Conclusion: Following mucus depletion, there is a decrease in surface cell pH _i and crypt outlet pH values. The repair process is then characterized by extensive mucus secretion and local cessation of acid secretion.     

Acid and duodenogastroesophageal reflux after esophagectomy with gastric tube reconstruction

OBJECTIVE: Patients who undergo esophagectomy with gastric tube reconstruction incur increased risk for acid reflux and duodenogastroesophageal reflux. Few postesophagectomy studies of gastroesophageal reflux disease have included simultaneous 24-h pH and bilirubin monitoring. The aim of this study is to evaluate acid reflux and duodenogastroesophageal reflux after esophagectomy with gastric tube reconstruction. METHODS: Reflux symptom evaluation, endoscopy, and simultaneous 24-h pH and bilirubin monitoring in the cervical esophagus were performed in 25 patients who underwent Ivor Lewis esophagectomy, intrathoracic esophagogastrostomy, and digital dilation of the pyloric ring as treatment for esophageal cancer. RESULTS: Reflux symptoms were severe, mild, and absent in 2, 7, and 16 patients, respectively. Reflux esophagitis and Barrett's esophagus was observed in 11 and 1 patients, respectively. Elevated acid reflux occurred in 7 patients (28%). Elevated duodenogastroesophageal reflux was recorded in 11 patients (44%). Reflux profile analysis identified three patterns: 4 subjects (16%) with both elevated acid reflux and duodenogastroesophageal reflux; 3 (12%) with only elevated acid reflux; and 7 (28%) with only elevated duodenogastroesophageal reflux. Of 7 patients with only elevated duodenogastroesophageal reflux, 4 developed reflux esophagitis. Although reflux symptoms did not correlate with endoscopic esophagitis, a significant correlation was observed between endoscopic esophagitis and acid reflux and/or duodenogastroesophageal reflux. CONCLUSIONS: Reflux symptoms represented a poor indication of esophagitis in patients with esophagectomy and gastric tube reconstruction. Simultaneous 24-h pH and bilirubin monitoring can help in identifying patients at high risk for reflux esophagitis, as well as indicating the cause of esophagitis.     

Primary localized gastric amyloidosis: A scoping review of the literature from clinical presentations to prognosis

Localized gastric amyloidosis (LGA) is a rare disease characterized by abnormal extracellular deposition of amyloid protein restricted to the stomach and it is confirmed by positive results of Congo red staining. Over decades, only a few cases have been reported and studies or research focusing on it are few. Although LGA has a low incidence, patients may suffer a lot from it and require proper diagnosis and management. However, the pathology of LGA remains unknown and no overall review of LGA from its presentations to its prognosis has been published. Patients with LGA are often asymptomatic or manifest atypical symptoms, making it difficult to differentiate from other gastrointestinal diseases. Here, we report the case of a 70-year-old woman with LGA and provide an overview of case reports of LGA available to us. Based on that, we conclude current concepts of clinical manifestations, diagnosis, treatment, and prognosis of LGA, aiming at providing a detailed diagnostic procedure for clinicians and promoting the guidelines of LGA. In addition, a few advanced technologies applied in amyloidosis are also discussed in this review, aiming at providing clinicians with a reference of diagnostic process. With this review, we hope to raise awareness of LGA among the public and clinicians.     

Excluded gastric mucosa presenting as a polypoid tumor in the duodenal stump after B II resection

We present endoscopic findings of a polypoid tumor in the duodenal stump after Billroth II partial gastric resection in a 61-year-old male. Histologic examination of the tumor revealed gastric mucosa of antral type. Accordingly, Congo red dyeing test failed to show acid secretion. The excluded antral mucosa did not gain any clinical significance in this patient since there was no history of peptic ulcer relapse within the 25 years after gastric operation.     

Acute esophageal and gastric injury: Complication of Lugol's solution

Several new technologies have been developed to improve the diagnostic capability of conventional endoscopic techniques. One of these most frequently used methods is chromoendoscopy with Lugol's solution in the esophagus to detect malignant lesions. This method has been used for several decades and is generally considered as a safe method, only a few cases of side effects having been reported. We describe a case of acute esophageal and gastric mucosal damage after application of Lugol's solution during endoscopy in an 84-year-old woman. Endoscopists should be aware of the potential for adverse reactions to iodine staining.     

Acid transport through channels in the mucous layer of rat stomach

BACKGROUND & AIMS: We have reported previously that secreted acid moves through the mucous layer in restricted areas above the gastric crypts. The aim of this study was to visualize and study the dynamics of this event. METHODS: Anesthetized rats prepared for intravital microscopy of the gastric mucosa were divided in the following groups with respect to acid secretion: spontaneous; stimulated (pentagastrin, 40 microg. kg(-1). h(-1)); transiently inhibited (omeprazole, 400 micromol. kg(-1) for 7 days); and totally inhibited (omeprazole, 3 x 200 micromol. kg(-1) for 7 days). The mucus was stained with Congo red (blue, pH < 3; red, pH > 5.2), and photographs were taken through a stereomicroscope. RESULTS: During acid secretion, blue-colored crypt openings with attached thread-like (5-7 microm wide) structures (designated channels) were seen passing from the crypt openings through the mucus to the lumen. Red-colored channels and crypt openings were observed when acid secretion was transiently inhibited. Red-colored crypt openings but no channels were found after total inhibition of acid secretion for a week. CONCLUSIONS: The results suggest that secreted acid is transported through channels within the mucus. These channels are probably created by the high intraglandular pressure pushing acid and glandular mucus into the gel.