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.     

Epithelial Cell Proliferation in Duodenal Ulcer

Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 ± 0.4% (mean ± SEM), at the edge of perforated ulcers 19.1 ± 2.0%, at the edge of elective ulcers 18.6 ± 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 ± 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 ± 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.     

Epithelial cell proliferation in duodenal ulcer

Epithelial cell proliferation in the duodenum was investigated in 50 patients by incubating mucosal biopsy samples with tritiated thymidine, followed by autoradiography. Fifteen patients had a normal duodenum, 15 duodenal ulcer undergoing elective surgery, 10 perforated duodenal ulcer, and 5 severe non-ulcer-associated duodenitis. The mean crypt cell labelling index in the duodenal bulb of controls was 8.8 +/- 0.4% (mean +/- SEM), at the edge of perforated ulcers 19.1 +/- 2.0%, at the edge of elective ulcers 18.6 +/- 1.4%, and in biopsy specimens from non-ulcer-associated duodenitis 14.0 +/- 1.2%. The mean labelling index in the distal first part of duodenum of control patients was 9.1 +/- 0.8 similar to the values found in histologically normal specimens distal to ulcer or duodenitis. The results indicate active epithelial cell proliferation in both duodenal ulcer and duodenitis. There was no evidence of impairment of epithelial cell proliferation in duodenal ulcer patients.     

Pain provocation test in peptic duodenitis

Controversy exists as to whether or not duodenitis alone can cause peptic ulcer symptoms. A modified provocation perfusion test has been performed in 10 symptomatic patients with duodenitis confirmed by endoscopy and histology. The test was conducted without the patient being aware of whether 0.1 N hydrocholoric acid, normal saline, or 8.5% sodium bicarbonate was being perfused directly on the area of duodenitis through the endoscopic irrigation cannula at a fixed rate of 10 ml/min for 10 min. The test was also performed in eight patients with dyspepsia alone and in five patients with chronic duodenal ulceration. Intraduodenal infusion of acid reproduced the epigastric pain in all patients with peptic duodenitis and duodenal ulcer patients, including the feeling of nausea in several which was partially relieved by bicarbonate infusion. In patients with dyspepsia but no peptic duodenitis, the symptoms were not reproduced. It would appear that "peptic duodenitis" can cause symptoms and that this "pain provocation test" may prove useful in its diagnosis.     

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.     

Quantitative noninvasive testing for Helicobacter pylori does not predict gastroduodenal ulcer disease

Background: Helicobacter pylori is strongly associated with gastric and duodenal ulcer disease. However, the diagnosis of gastroduodenal ulcers requires an endoscopic or radiographic examination. In this study, we attempted to establish a relationship between the magnitude of [¹³C]urea breath test results or serum H. pylori IgG levels and endoscopic findings in H. pylori-infected individuals. Methods: Patients who had undergone endoscopy and had a positive [¹³C]urea breath test and/or positive H. pylori IgG serology were identified. Endoscopic diagnoses included duodenal ulcer, gastric ulcer, nonulcer dyspepsia, and others. Results of 6% or greater on the [¹³C]urea breath test was defined as positive for H. pylori infection. H. pylori IgG serology was determined by an enzyme linked immunosorbent assay with values of greater than or equal to 1.0 being seropositive. Results: One hundred seventy-five patients were seropositive (mean = 3.01 ± 1.58). One hundred sixty-eight patients had a positive [¹³C]urea breath test (mean = 25.43 ± 16.90). One hundred fifty-five patients were common to both the groups. Statistical analysis did not reveal any relationship between quantitative [¹³C]urea breath test results or H. pylori IgG values and endoscopic diagnoses. Conclusion: The magnitude of [¹³C]urea breath test or H. pylori IgG serology cannot be used to predict the presence or absence of gastroduodenal ulcer disease. (Gastrointest Endosc 1996;44:679-82.)     

Conceivable mechanisms by which Helicobacter pylori provokes duodenal ulcer disease

A conceivable concept for the development of duodenal ulcers in Helicobacter pylori(H. pylori) infected subjects is presented in this chapter. The concept includes an explanation of the fact that only a minority of all H. pylori -infected subjects will develop a duodenal ulcer. Helicobacter pylori infection of the antrum induces a hypersecretion of gastric acid secretion, giving rise to gastric metaplasia in the duodenal bulb. This gastric metaplasia is a prerequisite for H. pylori colonization of the bulb. These events are common to all H. pylori -infected subjects. However, a much higher density of H. pylori bacteria and colonization with virulent organisms has been found in the bulb of duodenal ulcer patients, resulting in a much stronger inflammatory reaction with active duodenitis and an impaired bicarbonate secretion. These characteristics, together with acid hypersecretion, seem to be the important factors in evoking a duodenal ulcer.     

Increased dopamine receptor binding in duodenal mucosa of duodenal ulcer patients

High-affinity and saturable membrane-bound dopamine binding sites have been characterized in rat and human gastrointestinal tissues. Although their role in experimental ulcerogenesis has been suggested, dopamine receptor activity in peptic ulcer disease has not been investigated. Radioligand binding studies were performed with mucosal tissue homogenates obtained from the antrum and duodenum of six male healthy volunteers and six male duodenal ulcer patients. The binding assay was performed in triplicate with a crude membrane fraction using [³H] dopamine as a ligand at a final concentration of 1 nM at 22 °C in the dark. Nonspecific binding (which usually comprised about 30% of total binding) was determined in the presence of a 100-fold excess of unlabeled dopamine. A significant (P<0.05) increase of [³H]dopamine binding was found in duodenal mucosa of duodenal ulcer patients. [³H]Dopamine binding in stomach (antrum) of normal and duodenal ulcer patients did not differ significantly. These findings provide preliminary evidence for a role of dopamine receptors in duodenal ulcer and suggest that biochemical abnormalities of gut dopamine function may be operative in the pathogenesis of peptic ulcer disease.     

Prevalence of Helicobacter pylori infection and related gastroduodenal lesions in spouses of Helicobacter pylori positive patients with duodenal ulcer.

BACKGROUND: To date, very few studies have evaluated the risk of infection among spouses of Helicobacter pylori positive patients and their results are conflicting. AIM: To assess the seroprevalence of H pylori infection in spouse of H pylori positive patients with duodenal ulcer as compared with age and sex matched volunteer blood donors, as well as the frequency of endoscopic gastroduodenal lesions in these spouses, according to the presence or absence of gastrointestinal complaints. METHODS: Some 124 spouses (48% males) of patients with duodenal ulcer consecutively seen over a 10 month period were studied. They were all screened for serum IgG anti-H pylori antibodies and asked to complete a questionnaire with particular reference to the presence of chronic or recurrent dyspepsia. Upper gastrointestinal tract endoscopy with antral and corpus biopsy specimens taken for histological examination and urease rapid test was offered to all seropositive spouses. Volunteer blood donors (248), living in Milan and matched for age, sex, north-south origins, and socioeconomic status to the cases, were used as controls. RESULTS: Spouses of patients with duodenal ulcer had a significantly higher seroprevalence of H pylori infection than controls (71% v 58%, p < 0.05); 30 of 88 (34%) H pylori positive spouses complained of dyspeptic symptoms compared with only four of 34 (12%) seronegative spouses (p < 0.02). At endoscopy, H pylori infection was confirmed in 48 of 49 (98%) seropositive spouses. The endoscopic findings in those spouses showed active duodenal ulcer in eight (17%), duodenal scar and cap deformity in two (4%), active gastric ulcer in two (4%), erosive duodenitis in three (6%), antral erosions in two (4%), antral erosions plus duodenitis in one, and peptic oesophagitis in another patient. The prevalence of major endoscopic lesions was significantly higher in symptomatic spouses than in those who had never been symptomatic. CONCLUSIONS: These findings show that being the spouse of an H pylori positive patient with duodenal ulcer may increase the risk of H pylori colonisation and perhaps of peptic ulcer disease, and raises questions as to whether serological screening of cohabiting partners of H pylori positive patients with duodenal ulcer may be indicated.     

Basal gastric acid secretion in nonulcer dyspepsia with or without duodenitis

Nonulcer dyspepsia with or without duodenitis and duodenal ulcer disease are often considered to be a spectrum of the same acid-peptic process. Some reports evaluating basal gastric acid secretion in nonulcer dyspepsia and duodenal ulcer disease have supported that impression; however, results from different studies have been mixed. In order to compare basal gastric secretory profiles in nonulcer dyspepsia and duodenal ulcer disease, we determined basal acid outputs in 66 consecutive patients with the diagnosis of nonulcer dyspepsia. All patients with nonulcer dyspepsia had at least a three-month history of epigastric abdominal pain, and all had negative upper gastrointestinal endoscopies except for 14 with duodenitis. The 66 patients with nonulcer dyspepsia were compared to 40 asymptomatic normal subjects and 114 patients with endoscopically documented duodenal ulcer disease. There was no significant difference in mean basal acid output among all 66 patients with nonulcer dyspepsia (2.9±2.7 meq/hr),the group of normal subjects (3.2±2.7 meq/hr),the 14 patients with nonulcer dyspepsia with duodenitis (3.0±2.1 meq/hr),and the 52 patients with nonulcer dyspepsia without duodenitis (2.9±2.9 meq/hr).However, mean basal acid output of the patients with duodenal ulcer disease (9.1±7.6 meq/hr)was significantly higher than all the other groups (P <0.001).The gastric acid secretory profiles determined in this study do not appear to support the view that nonulcer dyspepsia with or without duodenitis and duodenal ulcer disease are a spectrum of the same acidpeptide process.     

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.     

Gastric emptying andHelicobacter pylori infection in duodenal ulcer disease

The pathogenetic link betweenHelicobacter pylori gastritis and duodenal ulcer is still unknown. Fast gastric emptying of liquids might be important in the pathogenesis of gastric metaplasia of the duodenum and duodenal ulcer through an increased exposure of the duodenum to gastric acid. InH. pylori-infected subjects, an abnormal gastric emptying could affect urea breath test results and correlate with the histological gastritis. This study was performed to evaluate the gastric emptying of liquids in duodenal ulcer patients withH. pylori infection and the possible relation between the bacterial load, gastric emptying, and urea breath test results. Seventeen duodenal ulcer patients withH. pylori gastritis and 15 healthy volunteers were studied by a combined [¹⁴C]octanoic acid and [¹³C]urea breath test to evaluate gastric emptying rate andH. pylori status simultaneously. Endoscopy with antral biopsies was performed in all duodenal ulcer patients. Duodenal ulcer patients withH. pylori infection have a normal liquid gastric emptying that is unrelated with the histological severity of gastritis. The urea breath test results and the gastric emptying parameters do not correlate with histology. A significant correlation between the gastric emptying and the urea hydrolysis rate is found. It is concluded thatH. pylori infection in duodenal ulcer patients is not associated with abnormally fast liquid gastric emptying, and this finding should be taken into account when a causal link betweenH. pylori infection and duodenal ulcer disease is searched for. The correlation between gastric emptying and urea hydrolysis rate explains why no conclusions on intragastric bacterial load can be drawn from the urea breath test results.This study was presented in part as an oral communication at the Annual Meeting of the American Gastroenterological Association, May 1994, New Orleans, and published in abstract form inGastroenterology 106:A160, 1994.     

14C]-urea breath test to confirm eradication of Helicobacter pylori

BACKGROUND: Treatment for Helicobacter pylori reduces ulcer recurrence. Eradication rates of the organism vary with different drug regimens from 30% to 90%. There is a need to identify patients who have failed treatment. [14C]-Urea breath test (UBT) is non-invasive, sensitive, safe and highly reliable test for diagnosis of H. pylori infection. As there is a paucity of reports on the utility of [14C]-UBT in confirming H. pylori eradication, this study was undertaken. METHODS: Thirty-eight patients (age 34 +/- 17 years, range 16-84 years, 27 men) with upper gastrointestinal symptoms underwent upper gastrointestinal endoscopy. Baseline H. pylori infection was diagnosed by identification of the organism on antral biopsies and positive rapid urease test (RUT). After 1 month of completion of treatment, repeat RUT and histological examination of antral endoscopic biopsies were performed. Eradication of H. pylori was defined as absence of the organism on histology, and negative RUT. The [14C]-UBT was performed using 185 kBq [14C]-urea dissolved in 300 mL water. Breath samples were collected once before ingestion of [14C]-urea, and subsequently at 5 and 15 min. Results were expressed as 14CO2/mmol CO2 exhaled as per cent of administered urea. RESULTS: Endoscopy revealed antral gastritis (n = 14), duodenal ulcer (n = 8), duodenitis (n = 2), oesophagitis (n = 1), antral gastritis and duodenal ulcer (n = 3), antral gastritis and duodenitis (n = 7) and normal upper gastrointestinal endoscopy (n = 3). All the 20 patients who were negative for H. pylori on RUT and histology, tested negative for H. pylori on [14C]-UBT. However, of 18 patients shown to have H. pylori infection on RUT and histology, 16 were positive for H. pylori on [14C]-UBT. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of [14C]-UBT were 100, 89, 91, 100 and 95% respectively. CONCLUSIONS: The [14C]-UBT is a reliable indicator of H. pylori eradication after treatment. It can obviate the need for antral biopsies to confirm eradication of H. pylori after completion of treatment.     

Helicobacter pylori infection, gastric metaplasia in the duodenum and the relationship with ulcer recurrence

OBJECTIVE: To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. METHODS: Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). RESULTS: GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and > or = 3rd episode, 90% and 79% (P < 0.001 when comparing 1st vs 2nd or > or = 3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). CONCLUSIONS: Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.     

Clinical relevance of Helicobacter pylori CagA-positive strains: gastroduodenal peptic lesions marker.

OBJECTIVES: peptic ulcer is characterized by its recurrent nature, which necessitates maintenance treatment in most patients. But this natural history can be changed in patients with peptic ulcer associated to Helicobacter pylori, as shown by the low rates of recurrence and decreased hemorrhagic recidivism associated with this infection. Whether CagA or VacA strains are associated with a greater risk of peptic ulcer is controversial. This study was designed to examine endoscopic findings and their relation with H. pylori phenotype (CagA or VacA). METHODS: 106 selected dyspeptic patients underwent upper gastrointestinal tract endoscopic examination between September 1996 and May 1997 [69 with H. pylori (Hp) and 37 without this infection]. Endoscopic findings were classified as gastric ulcer (GU), duodenal ulcer (DU), gastric erosions (GE), duodenitis (Du), chronic gastritis (CG) and normal mucosa (NM). Hp phenotype was analyzed with a western blot test. RESULTS: 75% of H. pylori strains were CagA-positive and 54.2% were VacA-positive. 82.4% of the cases of DU were associated with a CagA+ phenotype, but the association was not statistically significant. Otherwise 100% of gastric ulcers were associated with CagA+ strains (p < 0.005). VacA phenotype was not associated with any particular endoscopic finding. Peptic ulcer (DU or GU) was also associated with the CagA+ phenotype (p < 0.05). CONCLUSIONS: the CagA+ H. pylori phenotype seems to be a peptic lesion marker, but was more frequently related with GU than with DU in our sample of Spanish patients.     

The endoscopic diagnosis of duodenal ulcer disease. A randomized clinical trial of bias and of interobserver variation

In a randomized design we examined whether endoscopists are biased by knowledge of the radiologic diagnosis of duodenal ulcer and deformity of the duodenal bulb when recording the corresponding endoscopic diagnoses. A total of 156 patients had a barium meal and were subsequently randomized into 2 groups. In 74 of the cases the 2 endoscopists knew the result of the X-ray examination when doing the endoscopy; in 82 of the cases they did not. One endoscopist was significantly biased by his knowledge of the radiologic diagnosis of deformity of the duodenal bulb. Neither of the endoscopists was biased by his knowledge of the radiologic diagnosis of duodenal ulcer. In addition, the interobserver variation between the two endoscopists with regard to the endoscopic diagnoses of duodenal ulcer, deformity of the duodenal bulb, and duodenitis was examined. The interobserver variation was expressed by the overall agreement and by the kappa statistics, which adjusts the overall agreement for expected chance agreement. For duodenal ulcer, deformity of the duodenal bulb, and duodenitis, the overall agreements and kappa values were 0.91, 0.78, and 0.75, and 0.54, 0.42, and 0.33, respectively.     

Antibody-dependent cell-mediated growth inhibition of rat thyroid cells, FRTL-5, in patients with autoimmune thyroid diseases

We studied antibody-dependent mononuclear cell-mediated growth inhibition of thyroid cells in 18 untreated patients with Graves' disease, 18 patients with chronic thyroiditis, and 15 normal subjects by measuring the ability of their sera to inhibit [3H]thymidine incorporation into DNA in a rat thyroid cell line, FRTL-5, in the presence of normal mononuclear cells. [3H]thymidine incorporation was significantly inhibited in the presence of sera from patients with Graves' disease and chronic thyroiditis (P less than 0.001), whereas it was not affected in normal subjects. A significant correlation was observed between the inhibition of [3H]thymidine incorporation and the titre of anti-microsomal antibodies (P less than 0.05). The inhibitory effect on [3H]thymidine incorporation was significantly abolished when serum pre-absorbed with human thyroid membranes was used (P less than 0.005). These inhibitory effects on [3H]thymidine incorporation significantly correlated with those obtained by using IgG fractions (P less than 0.01). These data indicate that antibody-dependent mononuclear cell-mediated growth inhibition may play a role in thyroid cell growth regulation in patients with autoimmune thyroid disease.     

Autoradiographic study on healing process of cysteamine-induced duodenal ulcer in rat

The healing process of cysteamine-induced duodenal ulcer was studied by [³H]thymidine autoradiography. After the development of ulcer in the duodenum, cell proliferation was markedly activated not only in the crypts but also in the Brunner's glands near the ulcer. In the initial stages of ulcer healing, they both contributed to form the surface covering regenerating epithelium. Granulation tissue also proliferated at the base of the ulcer. In later stages of ulcer healing, new crypts were formed in the floor of the ulcer. New villi regenerated from these crypts and Brunner's glands regenerated by proliferationin situ. The ulcer base then was completely covered with new villi and granulation tissue was replaced by dense fibrous connective tissue. The present study suggested that the Brunner's glands, together with the crypts of Lieberkühn, play an important role in the healing process of cysteamine-induced duodenal ulcer.     

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.