Frequency, diagnosis and dependance of duodenitis upon the morphological status of the gastric mucosa (author's transl)

In a attempt to prove the dependence of duodenitis upon the morphological status of the gastric mucosa, a biopsy of the corpus, antrum, and duodenal canal had been made of 354 patients. In 56 cases, a superficial duodenitis was histologically verified; however, this infection had not contaminated the Brunner' glands. A duodenitis was found to be more often associated with surface gastritis of the corpus and antrum than it was with atropic gastritis. A duodenitis was discovered by a biopsy in 16 patients possessing a normal antrum mucosa and in 25 patients having a normal corpus mucosa, thus proving the possibility of isolated duodenitis.     

Low activities of disaccharidases associated with inflamed duodenal bulb mucosa

In order to establish whether an enzymatic method (a "functional" test) could be used instead of the histological picture as an indicator of damage to enterocytes of duodenal mucosa, biopsies were taken from 39 patients with upper gastrointestinal symptoms suggestive of peptic ulcer disease, but without active ulcers at endoscopy. Eleven patients with a normal appearance of the duodenal bulb mucosa and twenty-eight patients with various degrees of endoscopic inflammation ("bulbitis") were evaluated. The histological degree of duodenitis was assessed, and the activities of maltase, invertase, trehalase and lactase in the biopsy specimens were measured. Disaccharidase activities were inversely proportional to severity in both endoscopic and histological scoring of degree of inflammation. Low disaccharidase activities were also present in patients with endoscopic inflammation of the duodenal bulb, but without histological duodenitis. Focal and especially widespread gastric metaplasia was, in itself, significantly associated with low disaccharidase activities. The correlation between endoscopic and histologic scoring of inflammation of duodenal mucosa was not significant as assessed by kappa statistics. A previous history of peptic ulcer disease was significantly more common in patients with, than in those without, endoscopic inflammation of the duodenal bulb.     

Mucosal cell proliferation in duodenal ulcer and duodenitis.

Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 0.4% (SEM). Increased labelling indices of 15.6 +/- 1.7% were found near the edge of duodenal ulcers and 17.8 1.8% in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer of duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in out study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.     

Does malabsorption occur in chronic atrophic duodenitis?

Absorption behavior was studied in 6 patients with chronic atrophic duodenitis and compared with that observed in 6 cases of untreated celiac disease. The histobioptic study of the duodenal and jejunal mucosa showed that in atrophic duodenitis the lesions involve just one or two duodenal portions with normal jejunal mucosa: in contrast it was confirmed that in celiac disease atrophic lesions extended from the duodenal to the jejunal mucosa. From the clinical point of view, patients with chronic atrophic duodenitis do not show evidence of malabsorption while such phenomena occur consistently, even though in varied form, in celiac disease. The possible reason for this clinical behavior seems to be linked to the different extention of the histological damage in the two diseases. In conclusion, chronic atrophic atrophic duodenitis is a clinically autonomous entity as compared with gluten enteropathy.     

Duodenal bulb plasma cells in duodenitis and duodenal ulceration

Using an immunoperoxidase technique IgA, IgM, IgE and IgG plasma cells were studied in endoscopic duodenal bulb biopsies taken from 14 controls, 25 patients with grade 1 duodenitis (Whitehead classification), 12 patients with grade 2 duodenitis and three with grade 3 duodenitis. The control counts were compared with those in the jejunum and rectum. In addition cell counts were compared in 16 pairs of patients, with and without duodenal ulcer, exactly matched for grade of duodenitis. The control counts were not significantly different from counts in jejunum or rectum except for IgG which were higher in the jejunum (p = 0.03). IgA plasma cell counts were significantly increased in both grade 1 and grade 2 duodenitis compared with controls (p less than 0.05 and p less than 0.01). There was no significant difference for the other plasma cells. All plasma cell counts were decreased in the small group of grade 3 duodenitis compared with the other groups. There was no significant difference between counts in duodenitis whether or not there was associated duodenal ulceration. The isolated IgA plasma cell response of the duodenal bulb mucosa in duodenitis is very different from that of the jejunal mucosa in coeliac disease, and the rectal mucosa in inflammatory bowel disease and bacterial colitis and probably represents the basic response to any mucosal damage.     

Is Duodenitis Always a Peptic Disease?

Acid secretory behavior as well as gastrin levels were evaluated in 38 cases of chronic duodenitis. Basal HCl secretion was normal in 39% of cases, hypochlorhydria was observed in 29%, and hyperchlorhydria in 32%. Maximal acid output was normal in 71% of patients with duodenitis, decreased in 19%, and increased in 10%. Fasting serum gastrin was always within normal limits. The secretory behavior correlated with age but not with the histological pattern of duodenal mucosa. In chronic duodenitis, normal secretion or hypochlorhydria is the prevailing finding. This does not exclude the possibility of a peptic pathogenetic mechanism which could be involved in the rare cases of chronic duodenitis with hyperchlorhydria. Acid-peptic disease is not etiopathogenetic in the causation of most cases of chronic duodenitis.     

Quantitative histological study of mucosal inflammatory cell densities in endoscopic duodenal biopsy specimens from dyspeptic patients using computer linked image analysis.

Inflammatory cell counting in endoscopic biopsy sections was carried out on duodenal mucosal samples from defined sites in patients with duodenal ulcer, duodenitis but no ulcer, non-ulcer dyspepsia, and asymptomatic controls using computer linked image analysis. The variables measured included polymorphonuclear and mononuclear cells per mm of superficial epithelium and per mm2 lamina propria. Duodenal ulcer crater margin and mucosal biopsy specimens from endoscopically inflamed mucosa in the group with duodenitis but no ulcer showed significantly higher inflammatory cell counts than endoscopically normal non-ulcer dyspepsia and control mucosa. Biopsy specimens from non-ulcer dyspepsia patients showed significantly higher lamina propria polymorphs than control group mucosa. Endoscopically normal duodenal ulcer and duodenitis but no ulcer mucosa also showed significantly higher acute and chronic inflammatory cell counts than controls. The prevalence of Helicobacter pylori in duodenal biopsy specimens was low (0-22%) and unrelated to local inflammatory response. Despite histological appearances, duodenal biopsy specimens from non-ulcer dyspepsia patients showed significantly higher inflammatory cell infiltration than control specimens, suggesting that at least some represent part of a spectrum of subclinical peptic disease.     

Ultrastructural changes in non-specific duodenitis

AIM: To investigate the ultrastructural and morphological changes of non-specific duodenitis (NSD) in an attempt to grade them according to the extent of the lesions. METHODS: Biopsies were taken from the mucosa of duodenal bulb of 44 patients selected from the patients undergoing upper gastrointestinal endoscopy for epigastric discomforts. From each patient, two pinch biopsies on the same area were obtained from duodenal bulb. One was for scanning electron microscopy and the other was stained with hematoxylin-eosin, Warthin-Starry silver and both were then examined under light microscope. A total of 12 specimens (three from each degree of the normal and I-III of NSD diagnosed and graded by histology) selected from the 44 patients were dehydrated, critical point dried, coated with gold palladium and examined under a JEOL JSM-30 scanning electron microscope (SEM) at 20 kV. RESULTS: According to the ultrastructural morphologic changes, non-specific duodenitis was divided into normal (as control group), mild, moderate and severe degrees according to results of SEM. The normal villi of duodenal bulb were less than 0.2 mm. There were inflammation cells, occasionally red blood cells and macrophages on the mucosal epithelial surface. Erosion and desquamation of epithelium could be seen. Three cases (25%, 3/12) had gastric metaplasia and Helicobacter pylori(H pylori) infection could be found in 5 cases (41.67%, 5/12) in duodenal bulb mucosa. The most distinctive feature was the ulcer-like defect on the surface of epithelial cells. CONCLUSION: Non-specific duodenitis is a separate entity disease caused by different factors. SEM is of value as an aid in the diagnosis of mucosal diseases of duodenum.     

十二指肠炎的内镜和组织学研究

目的 探讨十二指肠炎内镜和组织学诊断。 方法 内镜下正常(n=26)与炎症(n=44)患者进行组织学形态定量研究。 结果 内镜下轻度充血、红斑不足以诊断十二肠炎,需病理组织学证实。固有层炎性细胞密度,特别是园细胞密度是诊断的依据。胃上皮化生有助诊断,绒毛高度、宽度和肠腺深度对诊断无价值。 结论 固有层炎性细胞密度是诊断十二指肠炎的依据。     

Functional characterization of luminal enterocyte membranes of the small intestine mucosa using isolated brush border membranes

Atrophy of the small intestinal mucosa is functionally characterized by a reduction in non-electrolyte transport in vivo. In order to elucidate the cellular defect being responsible for this malabsorption, we have studied the Na+-dependent D-glucose accumulation as well as the activities of aminopeptidase M and maltase in brush border membrane vesicles prepared from jejunal self-emptying blind loops and corresponding intestinal segments of sham-operated control rats. Membrane vesicles from atrophic mucosa did not show any differences in D-glucose uptake or in enzyme activities when compared with those derived from normal intestine. Thus it is unlikely that the impaired non-electrolyte absorption in the atrophic mucosa in vivo is due to a defect in cellular transport processes. It is more probable that the functional impairment is the result of the diminished absorptive surface in this pathophysiological condition.     

Duodenitis.

Many questions regarding duodenitis remain unanswered. However, the evidence suggests that duodenitis is a clinical entity which can give rise to dyspepsia and, on rare occasions, gastrointestinal haemorrhage. Conventional and double contrast radiology has only a small part to play in the diagnosis of duodenitis but is important in helping to exclude other lesions such as duodenal ulcer. Provided care is taken during the fibre-optic visualization of the duodenal bulb, the endoscopic appearances of moderately severe duodenitis correlate well with the histological changes seen. A diagnosis of apparent duodenitis should be confirmed by the histological criteria described. Treatment at present is similar to that of peptic ulcer, with the withdrawal of any predisposing and precipitating factors such as aspirin, alcohol and smoking. Antacids may relieve the symptoms. It is not yet known what effect these measures may have on the duodenitis as opposed to the symptoms of dyspepsia. The H2-receptor antagonist, cimetidine, should be effective in treating duodenitis but double blind clinical and endoscopic studies are required to confirm this. The place of surgery is as yet undefined. With the data at present available, it appears that duodenitis is part of the pathophysiological spectrum of the duodenal ulcer diathesis rather than a separate disease. It may represent both the production and healing phases of duodenal ulceration. In some patients the duodenal mucosa may proceed from normal to duodenitis and then to normal again without the development of frank duodenal ulceration (Figure 4). Prospective studies are required which should include a long-term clinical follow-up of a large number of patients with duodenitis accurately and specifically diagnosed by endoscopy and histopathology.     

Coincidence of chronic pancreatitis and duodenitis

Biopsies taken from various regions of the duodenal mucosa were investigated with a quantitative histological method with a view to frequency, quantity, and localisation of the duodenitis in clinically proven chronic pancreatitis. The histologic classification of duodenitis was made according to Whitehead et al. Out of 46 patients suffering from a chronic pancreatitis, 19 had a duodenitis grade 1 in the pars superior and pars descendens. A more frequent occurrence of duodenitis with concomitant chronic gastritis or a pathologic condition of the bile duct or a chronic alcohol abuse could not be proved statistically.     

Histological appearances of oesophagus, antrum and duodenum and their correlation with symptoms in patients with a duodenal ulcer.

Clinical data and histology from the oesophagus, gastric antrum, and duodenum were collected from 36 patients undergoing surgery for duodenal ulcer. Gastritis was present in 94% of the patients (25% of atrophic type), oesophagitis in 72% and duodenitis in 39%. Abnormal biopsies were present from all three sites in 33% of the patients. Only one patient showed three normal biopsies. The low incidence of duodenitis does not support the theory that duodenitis is part of the same spectrum as duodenal ulcer. Heartburn was related to the presence of gastritis (100%) and oesophagitis (76%) but not to duodenitis (52%). No relationship was found between the length of history, severity of pain, and histological abnormalities.     

Progression of antral and body gastritis in patients with active and healed duodenal ulcer and duodenitis

The dynamics of the antral and body mucosa has been studied in biopsy specimens obtained during endoscopy of patients with duodenal ulcer (103 cases), patients with duodenal ulcer scars (108 cases), and patients with duodenitis (44 cases). A representative Finnish population sample consisting of 434 subjects was used as reference material. The antral mucosa of all patient series showed an increase in the severity and prevalence of gastritis similar to that of the general population, whereas virtually no progression of gastritis with age was seen in the body mucosa, which remained normal or at the stage of superficial gastritis up to geriatric age. In contrast, in the present controls and in all earlier population samples studied by us so far, there was a significant and steady increase in the severity and prevalence of body gastritis with age. It is concluded that the age behavior of the antral and body mucosa was in duodenal ulcer scars and duodenitis similar to that of patients with active duodenal ulcer. The persistence of normal conditions in the acid-secreting area may serve as one explanation of the strong tendency of the disease to recur. In addition, it is tentatively concluded that in duodenal ulcer disease there are factors that have a 'protecting' influence on the body glands and which are abolished by antrectomy, according to our earlier studies.     

Duodenal epithelial thymidine uptake in patients with duodenal ulcer or endoscopic duodenitis

To evaluate the relationship between duodenal ulcer disease and duodenitis, duodenal epithelial cell renewal was measured in mucosal biopsies by the incorporation of [³H]thymidine. When 14 patients with duodenal ulcer were compared to 13 control subjects or 7 with endoscopic duodenitis alone, the crypt size was the same in all groups. Similar to other inflammatory processes of the gastrointestinal tract, patients with endoscopic duodenitis showed increased proliferative indices including a greater number of cells incorporating [³H]thymidine. In contrast, the proliferative indices from the duodenal mucosa of patients with duodenal ulcers did not differ from a control group. In a group of 6 patients with both endoscopic duodenitis and duodenal ulcer, the [³H]thymidine incorporation was intermediate between control subjects or patients with duodenal ulcer alone and those with endoscopic duodenitis alone. When subjects were divided according to the histologic appearance of the duodenal mucosa, those having chronic duodenitis demonstrated enhanced [³H]thymidine incorporation in comparison to a control group or patients with chronic active duodenitis (polymorphonuclear leukocytes present). Although there are many possible explanations of these findings, one may speculate that duodenal ulceration does not stimulate duodenal epithelial proliferation. This project was supported by the Yale Digestive Cancer Research Fund. Dr. Gorelick was supported by a Research Fellowship Award from the National Foundation for Ileitis and Colitis during a portion of this study and is currently a recipient of a Clinical Investigator Award (KO8-AM-00659) from the National Institute of Arthritis, Metabolism and Digestive Diseases.     

Small-bowel obstruction due to bilharziasis

The dynamics of the antral and body mucosa has been studied in biopsy specimens obtained during endoscopy of patients with duodenal ulcer (103 cases), patients with duodenal ulcer scars (108 cases), and patients with duodenitis (44 cases). A representative Finnish population sample consisting of 434 subjects was used as reference material. The antral mucosa of all patient series showed an increase in the severity and prevalence of gastritis similar to that of the general population, whereas virtually no progression of gastritis with age was seen in the body mucosa, which remained normal or at the stage of superficial gastritis up to geriatric age. In contrast, in the present controls and in all earlier population samples studied by us so far, there was a significant and steady increase in the severity and prevalence of body gastritis with age. It is concluded that the age behaviour of the antral and body mucosa was in duodenal ulcer scars and duodenitis similar to that of patients with active duodenal ulcer. The persistence of normal conditions in the acid-secreting area may serve as one explanation of the strong tendency of the disease to recur. In addition, it is tentatively concluded that in duodenal ulcer disease there are factors that have a ‘protecting’ influence on the body glands and which are abolished by antrectomy, according to our earlier studies.     

十二指肠球部微小黏膜隆起的临床分析

目的探讨十二指肠球部直径≤0.5cm黏膜隆起性病变的内镜特征、病理及其与临床的关系。 方法回顾性分析解放军总医院海南分院消化科2012年8月至2018年3月期间25例十二指肠球部微小黏膜隆起性病变的内镜表现特点及病理。 结果25例患者内镜表现为单个或多个广基息肉状隆起,10例患者于十二指肠球部黏膜隆起行活检病理检查,其中,十二指肠球慢性炎3例,十二指肠球慢性炎伴腺体增生2例,十二指肠球胃黏膜异位5例。 结论十二指肠球部黏膜直径≤0.5 cm的广基息肉状隆起多为慢性炎症所致的良性增生性病变及胃黏膜异位。     

Collagenous gastroduodenitis coexisting repeated Dieulafoy ulcer: A case report and review of collagenous gastritis and gastroduodenitis without colonic involvement

Collagenous gastritis (CG) is a rare disorder characterized by the thick collagenous subepithelial bands associated with mucosal inflammation. There have been approximately fifty reports in the literature since it was first described in 1989. According to previous reports, CG is heterogeneous and classified into two groups—(1) cases limited to the gastric mucosa in children or young adults, and (2) CG associated with collagenous colitis in elderly adults presenting with chronic watery diarrhea. In Japan, only nine previous cases were reported, and all of them were young adults. We report a case of CG with collagenous duodenitis in a 22-year-old female. She had repeated upper gastrointestinal bleeding from a Dieulafoy lesion of the fornix, but had no symptoms of malabsorption or diarrhea. Endoscopic findings revealed striking nodularity with a smooth islet-shaped normal area in the antrum and the body. The pathological findings of nodular mucosa showed the deposition of collagen bands just under the mucoepithelial lesion. In addition, she had collagenous duodenitis in part of the bulbs, and a colonoscopy showed no abnormalities. We provide a literature review of CG and collagenous gastroduodenitis without colonic involvement.     

Nodular duodenitis

This prospective study evaluated the radiographic, endoscopic, histologic, and clinical characteristics of nodular duodenitis found in 17 of 50 (34%) patients with end-stage renal disease. By comparison, nodular duodenitis was noted in only 23 of 557 (4%) consecutive endoscopies in a general medical population. Endoscopic nodular duodenitis consisted of two or more nodules, 2.5-7.0 mm in diameter, with apical erythema, with or without tip erosions. Eight patients had nodules in the bulb only, eight had diffuse duodenal nodules, and a single patient had nodules only in the second portion of the duodenum. Single-contrast barium x-rays were sensitive in detecting the nodules only when they were 5 mm or greater in diameter. Some degree of inflammatory infiltrate was found in 14 of 17 (82%) of the patients with nodular duodenitis; 10 of 17 had a moderate to severe histologic grade compared to 3 of 18 (P = 0.015) patients with a normal endoscopic appearance to the duodenum. Several patients with endoscopic nodular duodenitis, in whom biopsies were taken both of the nodule and surrounding mucosa, were found to have a focal histologic lesion which consisted of villous blunting and thickening due to fibrosis and a chronic inflammatory infiltrate or lymphoid aggregate in the stroma. A higher incidence of peptic ulcers occurred in the nodular duodenitis group (3 of 17) compared to the remainder of the group (0 of 33) during a mean follow-up of 38 months (P = 0.03). Resolution of the nodules occurred in six patients following successful renal transplant (four patients) and following vagotomy and pyloroplasty (two patients).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.