Fiberoptic Endoscopy of the Gastrointestinal Tract in Infants and Children

Fiberoptic endoscopy of the upper gastrointestinal tract was performed on 53 patients without incident, ranging in age between two months and 18 years, of whom 35 were out patients at the time of examination. Of 27 patients with recurrent abdominal pain and normal upper gastrointestinal series, eight had abnormal findings at endoscopy: a duodenal ulcer in four, a gastric ulcer in two and duodenitis in two. Of 18 patients with hematemesis and/or melena, esophageal varices were demonstrated both by endoscopy and x-ray in two, gastric ulcer by endoscopy in three and x-ray in one, duodenal ulcer by endoscopy in three and by x-ray in two, esophagitis by endoscopy only in one patient, erosive gastritis by endoscopy in five and by x-ray in two and duodenitis by endoscopy in three and by x-ray in two. Of the remaining eight patients with abnormal x-rays findings and other symptomatology, endoscopy demonstrated foreign bodies in two (coins, esophagus and stomach), duodenitis in two, a gastric ulcer in one, a duodenal ulcer in one and normal examination in two. The data indicate that fiberoptic endoscopy significantly improves diagnostic accuracy in the evaluation of disorders of the upper gastrointestinal tract in children and is a safe and effective procedure in ambulatory pediatric patients.     

Upper endoscopy for occult bleeding in renal failure

We studied 41 patients with renal failure prospectively to assess the value of upper gastrointestinal endoscopy in detecting occult bleeding after an abrupt fall in hemoglobin (Hb) level. Thirty-four patients were on maintenance dialysis, six on plasma exchange, and one on dialysis and plasma exchange. At gastroscopy two patients (4.9%) had bleeding lesions, five patients (12%) peptic ulcers without bleeding, and 18 patients (44%) mild esophagitis, gastritis, or duodenitis. Although mucosal abnormalities in the upper gastrointestinal tract were common, clinically inapparent gastrointestinal bleeding was only rarely responsible for sudden changes of Hb in these patients.     

Patterns of inflammation linked to ulcer disease.

Peptic ulcers are accompanied by different patterns of chronic gastritis and duodenitis that generally run parallel to the topography of colonization by Helicobacter pylori (H. pylori). Duodenal ulcers arise on a background of a gastroduodenitis; the gastritis is antrum-predominant while the duodenitis requires acid-induced gastric metaplasia in the duodenal mucosa before bacterial colonization can occur. The colonized and inflamed metaplastic areas in the duodenum (and inflamed pre-pyloric antrum) are the initial sites of ulceration. Proximal gastric ulcers arise in a diffuse (pan-) gastritis or a corpus-predominant H. pylori gastritis when the weakened gastric mucosa (especially in the antrum-body transitional zone) is susceptible to ulceration even in the presence of subnormal acid production. These distinctive patterns of gastritis are sufficiently consistent for them to be used to predict ulcer risk.     

Duodenal histology, ulceration, and Helicobacter pylori in the presence or absence of non-steroidal anti-inflammatory drugs.

Duodenitis and gastric metaplasia, which is often colonised by Helicobacter pylori (H pylori), are increasingly recognised for their importance in the pathogenesis of duodenal ulcers. The situation is not clear in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs), who have a higher risk of peptic ulceration. The aim of this study was to identify the duodenal histological abnormalities in the presence or absence of NSAIDs, H pylori, and duodenal ulceration. Endoscopic duodenal biopsy specimens were taken from healthy looking mucosa of 172 patients (74 took NSAIDs, and 98 did not). Duodenitis was graded according to the degree of neutrophilic and plasma cell infiltration, villus height, Brunner's gland prolapse, and gastric metaplasia. The activity of duodenitis was dependent on the neutrophilic infiltration. A global score covering all the above factors was constructed, and H pylori in both the stomach and duodenum, was also assessed. The results showed that duodenitis with varying degrees of neutrophilic infiltration and gastric metaplasia was found in 20 patients (27%) taking NSAIDs, compared with 56 patients (57%) not taking NSAIDs (chi 2 = 16.24, p < 0.001). This degree of duodenitis was also found in 20 of 25 patients (80%) with duodenal ulcers, regardless of NSAID intake (chi 2 = 15.38, p < 0.001). Gastric metaplasia was identified in 20 patients (27%) receiving NSAIDs and 38 (39%) not receiving NSAIDs. Duodenal H pylori was only seen in patients with gastric metaplasia 10 (50%) receiving NSAIDs, and 34 (89%) not receiving NSAIDs. H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration. It is concluded that active duodenitis is less common in patients taking NSAIDs but is strongly associated with gastric metaplasia, H pylori positive gastritis, and duodenal ulceration. These findings are relevant to the pathogenesis and treatment of duodenal ulcers in patients taking NSAIDs.     

Upper gastrointestinal mucosal lesions in chronic renal failure.

The upper gastrointestinal mucosa was studied endoscopically in 182 patients (140 males, 42 females) with chronic renal failure prior to hemodialysis. Endoscopy revealed normal mucosa in 77 patients (42.3%), inflammatory mucosal lesions in 88 (48.4%), peptic ulcer in 16 (8.8%; duodenal 15, gastric 1) and Barrett's ulcer in one patient. Upper gastrointestinal bleeding was noted at presentation in 16 (8.8%) cases and was associated with erosive gastritis, duodenitis and duodenal ulcer in 11, 3 and 2 patients respectively. Thus patients with chronic renal failure had a high prevalence of inflammatory mucosal changes.     

Endoscopic ethanol sclerotherapy in non-variceal gastrointestinal bleeding

Upper gastrointestinal bleeding still causes significant morbidity and mortality in spite of an aggressive medical and surgical approach. Endoscopic methods of treatment promise early and effective non-surgical control of bleeding. Endoscopic injection of ethanol has been used to control gastrointestinal bleeding in a prospective study of 28 high risk patients. Twenty-two had chronic ulcers (12 duodenal, 10 gastric) and six had angiodysplastic lesions (three gastric, three caecal). The 22 patients with chronic peptic ulcers were either elderly (median age 69 years) or had serious associated medical disorders (73%); 64% presented with shock. Primary haemostasis was achieved in all, but two re-bled from their ulcer. Surgery was required in one patient who re-bled 48 h after treatment and in one patient with an ulcer which perforated 45 days after injection; three patients with chronic ulcers refractory to medical therapy also underwent surgery. One patient developed a closed perforation of an antral ulcer after treatment which settled with conservative management; two patients died from causes unrelated to their ulcer. It is concluded that ethanol sclerosis is a safe, effective method for controlling bleeding from chronic peptic ulcers and angiomatous malformations.     

Acute upper gastrointestinal hemorrhage in patients with chronic renal disease

In order to reassess the role of duodenal ulcers as a cause of acute upper gastrointestinal hemorrhage in patients with chronic renal failure, 20 consecutive patients with moderate to severe chronic renal failure and a comparison group of patients without renal disease who were seen for acute upper gastrointestinal hemorrhage were reviewed. Gastric bleeding sites (gastric ulcer in 35 percent and gastritis in 20 percent) rather than duodenal ulcers were the most common sources of bleeding and were significantly associated with the use of ulcerogenic drugs. Patients with renal disease in whom acute upper gastrointestinal hemorrhage developed had significantly more morbidity and a trend toward higher mortality than the comparison group of patients without renal disease. It is concluded that gastric mucosal lesions, at least in part due to the use of ulcerogenic drugs, are the most common cause of significant acute upper gastrointestinal hemorrhage in patients with chronic renal failure.     

The pathogenesis of stomach and duodenal involvement in chronic opisthorchiasis. 1. The urease test]

The study using the urease test on mucous biopsies from the antral gastric part and from the duodenum of patients with chronic opisthorchiasis with endoscopic evidence of antral gastritis and gastroduodenitis, and from noninvaded patients with gastritis and duodenitis, some of them with the gastric or duodenal ulcers showed that the test was positive. The test was negative in both groups of patients when the mucosa of the gastric body was examined as well as in those without gastroduodenal pathology. It is supposed that in the both groups of patients gastroduodenal pathology was provoked by the colonization of the gastric and duodenal mucosa by gastric campylobacteria.     

The prevalence of Campylobacter pylori gastritis: a study of symptomatic nonulcer dyspepsia and bile gastritis

We assessed the prevalence of Campylobacter pylori in various forms of endoscopic gastritis, including ulcer and nonulcer dyspepsia and bile gastritis and correlated it with histological evidence of inflammation. Multiple biopsy specimens were taken from 120 patients, including four normal controls, who underwent upper gastrointestinal endoscopy for evaluation of upper abdominal pain and discomfort, nausea, bilious vomiting, weight loss, and anemia. The patients included 58 men and 62 women, with a mean age of 53 years. Of these, 16 patients had gastric ulcers, 19 had duodenal ulcers, 26 had reflux gastritis (after either gastric surgery or cholecystectomy), one had a gastric polyp, one had Barrett's esophagus, and the remaining 53 had gastritis due to unspecified causes. Campylobacter-like organisms were demonstrated by light and electron microscopy in 50 of 69 patients of the nonbile gastritis group (72%) and in seven of 15 patients of the bile gastritis group (47%) (p0.05). The presence of bacteria in both groups correlated with histologically significant inflammation (particularly chronic active gastritis); similar histologic changes were noted in both major groups of nonbile gastritis and bile gastritis. Campylobacter pylori is common in all forms of gastritis in association with histologic inflammation.     

Helicobacter pylori infection in patients with haemophilia in Poland: prevalence and risk of upper gastrointestinal bleeding

Infection with Helicobacter pylori is the main aetiological factor for erosive gastritis and duodenal or gastric peptic ulcers often complicated with life-threatening bleeding in patients with coagulation disorders. The aim of this prospective study was to evaluate the prevalence of Helicobacter pylori infection in haemophilia patients, and to assess the risk of gastrointestinal bleeding associated with this infection. From 2000 to 2002, 146 patients with haemophilia (129, haemophilia A; 13, haemophilia B), mean age, 39.9 years (+/-7.3), were investigated for H. pylori infection using IgG and IgA latex serological test. The control group included 100 men with no coagulation disorders, mean age, 40.9 years (+/-9.2). For 72 (49.3%) patients with haemophilia and 39 controls (39.0%) serological tests were positive indicating the presence of H. pylori infection (P =0.1112). A history of gastrointestinal bleeding was reported in 46 patients (31.5%) with haemophilia and in two control group patients (2.0%) (P < 0.0001). Gastrointestinal bleeding was significantly more frequent in patients with haemophilia infected with H. pylori (33/46; 71.7%) than in patients with no H. pylori infection (13/46; 28.3%; P = 0.0002). In conclusion, the prevalence of H. pylori infection in haemophilic patients in Poland is comparable with that in patients with no coagulation disorders. Helicobacter pylori infection is a risk factor for duodenal and gastric ulcer bleeding in haemophilia patients. In view of the high frequency of upper gastrointestinal bleeding associated with H. pylori infection, we believe that screening and eradication therapy are appropriate in haemophilia patients.     

Factors influencing mortality from bleeding peptic ulcers

The mortality, causes of death, and the factors that are influencing deaths from bleeding acute and chronic peptic ulcers were evaluated retrospectively. During a 2-year period (1986-87) 272 patients were endoscoped for acute gastrointestinal hemorrhage and were found to have bled from a peptic ulcer (chronic gastric ulcers, 90; chronic duodenal ulcers, 114; acute gastroduodenal ulcers, 66; stomal ulcers, 2). The overall mortality was 9.6% (n = 26) (gastric ulcers, 6.7%; duodenal ulcers, 11.4%; acute ulcers, 10.6%). Statistically significant factors adversely affecting prognosis for gastric ulcer were re-bleeding, need for operation and serious intercurrent illness; for duodenal ulcer were units of transfused blood, re-bleeding, signs of recent hemorrhage at endoscopy, need for operation, and serious intercurrent illness; and for acute ulcer were increasing age, shock, units of transfused blood, re-bleeding, and serious intercurrent illness. Multivariate analysis was only attempted for duodenal ulcers because of sample sizes; it suggested that active bleeding or visible vessel at endoscopy, re-bleeding, and serious intercurrent illness were independent factors for mortality. From this study it is apparent that the major determinants of a fatal outcome in bleeding peptic ulcer diseases were serious intercurrent illness and rebleeding. As it must be anticipated that patients with these particular problems are at high risk of a poor outcome, it follows that it is important they have access to skilled treatment as provided by a specialist team in an intensive care ward. It also follows that every effort should be made to keep ulcers in remission to free the ulcer patient of potentially lethal complications.     

Comparison of Diagnostic Methods for Helicobacter pylori Infection in Patients with Upper Gastrointestinal Bleeding

Background: Accuracy of the most frequently used tests for diagnosing Helicobacter pylori infection in patients with upper gastrointestinal bleeding of peptic origin is determined. Methods: Seventy-eight patients with endoscopically-proven upper gastrointestinal bleeding of peptic origin were included. The presence of H. pylori was considered when observed from the histology or, if negative, when serology and breath test were both positive. Accuracy of the rapid urease test was estimated in accordance with results obtained with other diagnostic methods. Results: Lesions causing gastrointestinal bleeding were 56 duodenal ulcers, 13 gastric ulcers, 7 pyloric channel ulcers, 13 acute lesions of the gastric mucosa and 16 erosive duodenitis. H. pylori infection was present in 68 patients (87.2%). Forty-four patients had received non-steroidal anti-inflammatory drugs. The sensitivity/specificity (%) of the diagnostic methods was 48.5/100 for the rapid urease test, 91/77.8 for the breath test, 89.5/80 for serology and 86.3/100 for histology. The prior consumption of proton-pump inhibitors and antibiotics induced false-negative results in the rapid urease test and breath test, with no effect on serology and histology. Conclusions: The prevalence of H. pylori infection in patients with upper gastrointestinal bleeding from peptic lesions is high. Sensitivity of the rapid urease test for diagnosing H. pylori is low in this setting. Cases with negative rapid urease test need the combination of two or more additional tests if diagnosis is to be achieved. Cases with positive rapid urease test do not need further investigation for diagnosis.     

Comparison of diagnostic methods for Helicobacter pylori infection in patients with upper gastrointestinal bleeding.

BACKGROUND: Accuracy of the most frequently used tests for diagnosing Helicobacter pylori infection in patients with upper gastrointestinal bleeding of peptic origin is determined. METHODS: Seventy-eight patients with endoscopically-proven upper gastrointestinal bleeding of peptic origin were included. The presence of H. pylori was considered when observed from the histology or, if negative, when serology and breath test were both positive. Accuracy of the rapid urease test was estimated in accordance with results obtained with other diagnostic methods. RESULTS: Lesions causing gastrointestinal bleeding were 56 duodenal ulcers, 13 gastric ulcers, 7 pyloric channel ulcers, 13 acute lesions of the gastric mucosa and 16 erosive duodenitis. H. pylori infection was present in 68 patients (87.2%). Forty-four patients had received non-steroidal anti-inflammatory drugs. The sensitivity/specificity (%) of the diagnostic methods was 48.5/100 for the rapid urease test, 91/77.8 for the breath test, 89.5/80 for serology and 86.3/100 for histology. The prior consumption of proton-pump inhibitors and antibiotics induced false-negative results in the rapid urease test and breath test, with no effect on serology and histology. CONCLUSIONS: The prevalence of H. pylori infection in patients with upper gastrointestinal bleeding from peptic lesions is high. Sensitivity of the rapid urease test for diagnosing H. pylori is low in this setting. Cases with negative rapid urease test need the combination of two or more additional tests if diagnosis is to be achieved. Cases with positive rapid urease test do not need further investigation for diagnosis.     

Prevalence of Campylobacter pylori in esophagitis, gastritis, and duodenal disease

The relationship between the presence of Campylobacter pylori and esophagitis was studied in patients undergoing paired biopsies of distal esophagus and gastric antrum during esophagogastroduodenoscopy. Biopsy specimens were examined for urease activity and for the presence of C pylori by culture and by histologic examination of hematoxylin-eosin- and Warthin-Starry-stained sections. Sixty-two patients were entered into the study. All esophageal biopsy specimens, regardless of histologic findings, were negative for the presence of C pylori by urease test, culture, and histologic examination. Of 35 patients with normal esophageal biopsy specimens, 11 (31%) had antral specimens that were positive for C pylori, while 11 (41%) of the 27 patients with esophagitis had antral specimens that were positive for the organism. Campylobacter pylori was detected in 14 (70%) of 20 patients with chronic gastritis, in 8 (67%) of 12 patients with endoscopically documented duodenal ulcers and erosions, but in only 3 (33%) of 9 patients with endoscopically defined duodenitis. We conclude that histologic esophagitis is not associated with increased prevalence of either gastric or esophageal C pylori. The well-described association of chronic gastritis and duodenal ulcers with C pylori was present in our study population.     

Bleeding duodenal ulcer

Basal gastric acid output was analyzed prospectively in 110 patients with endoscopically documented duodenal ulcer disease to determine the frequency of gastric acid hypersecretion in patients with bleeding versus nonbleeding ulcers. Thirty-eight patients with stigmata of an actively or recently bleeding duodenal ulcer had a mean basal output of 12.6±8.9 meq/hr. In comparison, 72 patients with nonbleeding duodenal ulcers (and no history of prior bleeding) had a significantly lower mean basal acid output of 8.7±7.5 meq/hr (P<0.05). Twenty-four of the 38 patients (63%) with bleeding and 28 of the 72 (39%) with nonbleeding duodenal ulcers had gastric acid hypersecretion, defined as a basal acid output of greater than 10.0 meq/hr. There was a statistically significant association between bleeding duodenal ulcer and acid hypersecretion (P=0.01). All 110 patients were treated with standard doses of H₂-receptor antagonists for eight weeks. In that time, 87 patients healed and 23 patients (14 with prior bleeding and nine with nonbleeding duodenal ulcers) remained unhealed. Significantly more patients who had bled had nonhealing duodenal ulcers (P=0.004). Irrespective of bleeding history, all 23 patients with nonhealing duodenal ulcers at eight weeks had basal acid outputs of greater than 10.0 meq/hr (range 10.1–49.1 meq/hr). These 23 patients with nonhealing duodenal ulcers were treated with increased doses of ranitidine (mean 690 mg/day, range 600–1200 mg/day) for up to eight additional weeks. All were observed to have complete endoscopic healing documented within that period. These results suggest that bleeding duodenal ulcers are often associated with gastric acid hypersecretion and that these ulcers are less likely to heal after eight weeks of standard dose H₂-receptor antagonist therapy. Similarly, nonbleeding duodenal ulcers associated with gastric acid hypersecretion are also less likely to heal after standard doses of antisecretory therapy.     

老年人上消化道出血134例临床分析

目的探讨老年人上消化道出血及导致死亡的病因。方法回顾性总结分析上消化道出血老年患者１３４例，并与同期非老年患者１２０例比较。结果老年人上消化道出血病因中主要为酸相关疾病（十二指肠溃疡、胃溃疡、胃炎、十二指肠炎、食管炎）７１例，占７３．９％；胃癌１４例，占１４．５％。发生低血压或休克，老年组１８例，非老年组８例（Ｐ＜０．０５）。使用阿司匹林或非甾体类抗炎药物，老年组２８例，显著高于非老年组（７例，Ｐ＜０．０１）。老年组死亡１８例，病死率为１３．４％，其中１５例因全身慢性疾病恶化和出血后并发症死亡；非老年组死亡６例，病死率为５．０％（Ｐ＜０．０１）。结论酸相关疾病是老年人上消化道出血的主要病因，其次为胃癌。全身慢性疾病恶化和出血后并发症是影响老年人上消化道出血预后的重要因素，特别是肺部感染、心脑血管疾病是主要的死亡原因。     

Upper Gastrointestinal Bleeding in dengue Fever

Twenty-six virologically and serologically confirmed Dengue patients with signs of upper gastrointestinal tract bleeding (13.1%) were studied during the 1987 outbreak in southern Taiwan. Within a 1-yr period from 1987 to 1988 in Kaohsiung Chang Gung Memorial Hospital, there were 198 patients with Dengue fever confirmed. Viral isolation and serological studies indicated that type I Dengue was the cause. There was no evidence of sequential secondary infection among them. The 26 patients were evaluated gastroduodenoscopically. Most of the Dengue patients who developed upper gastrointestinal bleeding had gastric ulcers or duodenal ulcers; superficial and hemorrhagic gastritis are the other relevant endoscopic findings. Thirteen patients (50%) had a past history of peptic ulcer symptoms, whereas the other 13 did not. Dengue infection is a precipitating factor in inducing peptic ulcer bleeding because of hemostatic derangements. Supportive therapy and blood transfusions alone were adequate treatment, except for one patient who required surgery due to massive bleeding of a duodenal ulcer. No mortality was observed in this study.     

泮托拉唑钠粉针剂治疗上消化道出血疗效观察

目的　评价泮托拉唑钠 (诺森 )粉针剂对消化性溃疡所致的上消化道出血的疗效和安全性 ,并与奥美拉唑 (洛赛克 )粉针剂作对照。方法　选择消化性溃疡出血患者 90例 ,泮托拉唑治疗组 60例 ,其中胃溃疡 (GU) 2 4例 ,十二指肠球部溃疡 (DU) 33例 ,糜烂性胃炎 3例。奥美拉唑对照组 30例 ,其中GU 9例 ,DU 1 6例 ,糜烂性胃炎 5例。治疗方法 :分别用泮托拉唑或奥美拉唑 80mg加入 5 %葡萄糖液 2 50ml内 ,静脉滴注 (30～ 60min) ,1次 /d ,共 5d。观察生命体征与出血情况的改变。结果　两组出血情况差异无显著性 (P >0 .0 5)。治疗后 3d内泮托拉唑组有 51例止血 (85 % ) ,奥美拉唑组有 2 4例止血 (80 % ) ;4～ 5d内止血分别为 7例 (1 1 .7% )和 5例 (1 6 .7% )。止血显效率 ,泮托拉唑组为 85 % ,奥美拉唑组为 80 % ,治疗总有效率两组均为 96 .7%。两组各有 1例出现恶心症状 ,不良反应发生率分别为1 .7%和 3 .4%。结论　泮托拉唑钠粉针剂是治疗消化性溃疡出血安全、有效的药物     

Combined Endoscopy in Upper Gastrointestinal Haemorrhage

Summary: Combined endoscopic examination was performed in 206 patients presenting with upper gastrointestinal haemorrhage. This represents 92% of all patients admitted with this emergency to one hospital over a 12 month period.
Endoscopy achieved a diagnosis of the cause of bleeding in 92% of patients. The causes were: Pyloroduodenal ulcer 32%, haemorrhagic gastritis and gastric erosions 23%, gastric ulcer 20%, oesophageal varices 6%, Mallory Weiss lesion 5%, haemorrhagic duodenitis 5%, gastric carcinoma 4%, miscellaneous causes 5%. Combined lesions were found in 12% of patients.
Follow up assessment revealed endoscopy to be an accurate investigation.
The mortality for the series was 4.8%. Half the deaths resulted from bleeding oesophageal varices with advanced liver disease.
It is suggested that because of its accuracy and high diagnostic yield, early endoscopy may replace contrast radiography as the first investigation in upper gastrointestinal haemorrhage.     

Assessment of the Upper Gastrointestinal Tract in Hemodialysis Patients Awaiting Renal Transplantation

Seventy-five dialysis patients awaiting renal transplantation were studied. Investigations included single contrast barium meal, serum gastrin assay, gastric acid studies, and fiberoptic gastroduodenoscopy with multiple biopsies. Radiological studies revealed five duodenal ulcers and one gastric ulcer. Endoscopy showed gastroduodenal lesions in 57 patients (49%). Superficial gastritis was present in 50 patients (66.7%), atrophic gastritis in 11 (14.6%), and duodenitis in 30 (40%). Hypergastrinemia was observed in 48 patients (64%). Maximum acid output was markedly elevated in 33 patients. Acid hypersecretion was found to be correlated with the presence of endoscopic lesions and histological evidence of gastritis. Nine of the 11 patients with atrophic gastritis were acid hyposecretors and had low gastrin levels. Pretransplant gastric assessment identified a relevant number of gastroduodenal lesions in these patients. The increased risk of severe posttransplant ulceration justifies thorough gastric assessment and prophylactic antiulcer therapy in all renal transplant candidates.