Serological tests to monitor treatment of Helicobacter pylori.
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Biomedical subjects
Publications and source records attributed to F Di Mario.
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Tryptase, a serine endoprotease, was determined in mucosal biopsies from fundus, corpus, antrum and corpus-fundus of the stomach and from the duodenum in 15 controls, 66 patients with duodenal ulcer, 22 with gastric ulcer and 9 with duodenitis. Intra- and inter-assay coefficients of variation ranged from 3.3% to 8.0% and from 3.5% to 8.6%, respectively. In controls, the highest values for tryptase were found in the fundus and progressively decreased in the corpus, antrum and duodenum. Analysis of variance of data from repeated measurements, performed in six subjects having multiple determinations, achieved statistical significance (F = 16.85, P less than 0.001). Data from the corpus-fundus area documented a significant difference among patient groups (F = 2.70, P less than 0.05). Patients with an active gastric ulcer had higher mean values when compared to controls and to patients with healed gastric ulcer. A similar trend was found in patients with active duodenal ulcer. Furthermore, corpus-fundus tryptase evaluated longitudinally in three patients with an active ulcer (point A) and after healing (point B), showed significant decrease from point A to point B. By contrast it remained elevated or showed only minor decrease in two patients with a persistent active ulcer.
This experimental and clinical study examined the relationship between oesophageal damage and optimal pH of refluxate, and whether 24-h pH monitoring at optimal pH could discriminate the severity of oesophagitis. The rabbit oesophagus was perfused in vivo with pepsin and hydrochloric acid solutions of differing pH for 60 min. Maximal oesophageal damage coincided with peptic solutions at pH 1.5-2.5. Fifty-nine patients with proven gastro-oesophageal reflux disorders were tested for manometric features of the lower oesophageal sphincter (pressure, overall length and abdominal length) and oesophageal exposure to different pH levels. They were classified into four groups according to the endoscopically demonstrated severity of oesophagitis. Supine exposure at the optimal pH level for pepsin activity (pH 1.5-2.5) and overall sphincter length were found to discriminate the severity of oesophagitis reliably in 75 per cent of cases.
This study was carried out in order to compare the effects of mealtime and bedtime regimens of ranitidine on gastric acidity. Fifteen duodenal ulcer patients in clinical remission were randomized to receive in single-blind fashion either placebo, ranitidine 300 mg at night (2200 hr) or ranitidine 150 mg three times a day given before each of the three daily meals (1800, 0800 and 1200 hr). Over 24 hr, the two active treatments produced a significantly greater acid inhibition than placebo, while the single daily regimen was superior to the three times a day regimen of ranitidine in terms of both rise in pH values (P less than 0.001) and duration of action expressed as time spent above 3.0 pH units (P less than 0.05). The analysis of these two parameters during fractioned periods of the circadian cycle showed that the three divided doses of ranitidine were more effective during the daytime (P less than 0.01) and the evening (P less than 0.001), whereas the bedtime dose of ranitidine was superior during the night (P less than 0.0001). Thus a short-lasting antisecretory action, which is, however, capable of fully controlling the high acidity of postprandial periods, might be the key to understanding the results of several recent clinical trials in which the suppression of daytime gastric acidity has been shown to promote similar or even faster duodenal ulcer healing rates than the suppression of nocturnal acidity.
Basal serum gastrin levels were measured in 237 patients with endoscopically confirmed duodenal ulcer and were higher than normal in 16 cases. Protein meal gastrin stimulation was performed on this group of 16 patients and on a control group of 48 patients with normal basal gastrin concentrations but high rates of either ulcer recurrence or of complications (e.g., bleeding or perforation); 21 patients from the two groups were also tested for serum gastrin inhibition with secretin. Four cases (25%) of antral G-cell hyperfunction were found in the first group, plus 1 case compatible with Zollinger-Ellison syndrome (6.2%). Only 1 case (2%) of antral G-cell hyperfunction was found among the 48 controls. These results suggest the clinical utility of routine basal gastrin measurement in screening for hypergastrinemic patients with duodenal ulcer disease.
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This prospective study was undertaken to evaluate the correlation between densitometric values of gall stones assessed by computed tomography and the success rate of litholytic therapy in 28 patients eligible for oral treatment. A densitometric study of the stones was performed in all patients before treatment. A cut off point of 60 Hounsfield units (HU) was chosen to divide the subjects into two groups--group 1, 14 patients with low density stones (less than 60 HU) and group 2, 14 patients with high density stones (greater than 60 HU). All patients were treated with ursodeoxycholic acid (8-10 mg/kg/day) for 12 months and followed up by ultrasound. In group 1, dissolution was complete in 50% of the patients and partial in a further 20%. In group 2 patients, complete dissolution was not observed but 33% showed partial dissolution. The number of patients with total dissolution at 12 months was significantly higher in group 1 compared with group 2 (p less than 0.02). These results suggest that computed tomography can be used to select patients with a better likelihood of successful stone dissolution after bile acid therapy.
UNLABELLED: A substantial number of duodenal ulcer (DU) patients relapse despite maintenance treatment with antisecretory drugs. The influence of certain risk factors and the heterogeneity of the disease could explain such behavior. The present prospective, open study compares the one-year clinical outcome (with upper GI endoscopy at the beginning of the study, at 6 and 12 months, and at every symptomatic relapse) of four groups of DU subjects, consecutively recruited from December 1987 to December 1988, separated in accordance with whether or not a bleeding DU episode had previously occurred, and whether or not an evaluation of gastric acid secretion had been made. Thus, Group I (17 patients; 12 males, 5 females) included heavy smokers and/or gastric acid hypersecretors; Group II (13 patients; 12 males, 1 female) non- or light smokers non-hypersecretors; Group III (34 patients; 22 males, 12 females) subjects with unknown gastric acid secretion; Group IV (33 patients; 30 males, 3 females) previously bleeding DU patients. All patients, except those in Group II (who were left untreated), were given ranitidine 150 mg at bedtime. The outcome of Groups I+II was compared with that of Group III (considered as "standard therapy") and Group IV patients, the latter presumably with a low risk of relapse because of the low prevalence of smokers. STATISTICS: Chi-square test, Fisher's exact test, analysis of variance and the logrank test. During the year of follow-up, 27/97 patients withdrew from the study, while 18 had a DU relapse (remission rates 82.1% +/- 7.4% in Groups I+II, 70.5% +/- 8.4% in Group III, 87.5% +/- 5.9% in Group IV).(ABSTRACT TRUNCATED AT 250 WORDS)
An unusual case of a patient with two biliary stones of different densities that responded differently to oral litholytic treatment with ursodeoxycholic acid (UDCA) is reported. The findings confirm, in an unusual experimental model, that CT is useful in the selection of those stones which have a high probability of dissolution under treatment with oral bile acids.
Mucosal blood flow performs an extremely important role in microcirculation wherein alterations necessarily lead to severe gastric and duodenal mucosal lesions. The removal of back-diffused H+ ions through the adaptation of microcirculatory flow represents a valid defence mechanism. The blood flow's inability to contain H+ back-diffusion lies at the bottom of rapid-onset acute mucosal lesions; moreover, it probably contributes to the onset of chronic ulcer in certain areas already precariously supplied, because of the breakdown of the mucosal barrier or a further reduction in blood supply. Portal hypertension leads to altered blood flow in the gastric microcirculation. This haemo-dynamic condition brings about a series of endoscopically evident changes which are probably a consequence of the conspicuous increase in mucosal and submucosal vascular area. This haemodynamic situation may be an aetiopatho-genetic factor in the cirrhotic subject's marked sensitivity to gastric mucosal damage.
With a view to describing the natural history of duodenal ulcer, currently linked with powerful and widely used drugs, we retrospectively reviewed all patients followed-up at our unit between 1978 and 1989. All DU subjects with at least 5 years of clinical-endoscopic follow-up were admitted to the study. Concomitant gastric ulcer, previous gastrointestinal surgery and treatment other than with H2-blockers (where necessary) were considered exclusion criteria. Forty-four patients (35 males, 9 females, mean age 44.5) proved eligible for this study. At monthly intervals in the patients' history of ulcer disease (starting from a baseline month 0 when ulcer symptoms first appeared), we compared all cases in which the duration of disease coincided, i.e. for each month of the clinical course of the ulcer there was a certain number of patients at the same point in time; patients' histories coincided variously over a period ranging from 0 to 15 years. We considered endoscopically-diagnosed relapses (both symptomatic and asymptomatic) and hemorrhages as marker events for the activity of DU disease. A year-by-year duodenal ulcer activity rate was obtained for both treated and untreated subjects, as follows: No. of events/mean No. of patients followed-up per month x 100. Fisher's exact test and multivariate analysis (stepwise logistic regression) were used to investigate risk factors of poor outcome. We found that the years between the 1st and 5th and between the 10th and 15th from the onset of duodenal ulcer disease had higher peaks of activity, mostly in untreated subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum CA 19-9 and alpha-fetoprotein (AFP) levels were determined in 211 patients with liver cirrhosis and 27 with primary hepatocellular carcinoma (HCC) associated with liver cirrhosis. This was done to determine the usefulness of CA 19-9 level with respect to AFP level in distinguishing between these two illnesses, and to assess the influence of some clinical and biochemical variables on these tests in patients with liver cirrhosis with or without primary HCC. Pathologic AFP values were found in 23 of 27 (sensitivity, 85%) patients with HCC; CA 19-9 levels increased in only 12 of 27 (sensitivity, 44%) HCC patients, the values being comparable with those of patients with liver cirrhosis. In liver cirrhosis a substantial number of false-positive values was found for both markers, although they were higher for CA 19-9 (50 of 211 versus 39 of 211). In liver cirrhosis correlations were found between AFP level and alanine amino-transferase level; and between CA 19-9 level and (1) total bilirubin value, (2) alkaline phosphatase level, and (3) pseudocholinesterase level. The authors conclude that CA 19-9 level is a poor biochemical marker, inferior to AFP level, in the detection of a carcinomatous transformation of liver cirrhosis. The finding of false-positive AFP values in liver cirrhosis seems mainly attributable to cellular proliferation and necrosis. Cholestasis seems to greatly affect serum CA 19-9 level variations, probably by reducing its liver metabolism.
CA 50 (a tumor-associated gangliosidic antigen) levels have been determined by an RIA test in serum, gastric juice and urine of patients undergoing upper gastrointestinal tract endoscopy: 22 control subjects (no macroscopic or microscopic lesions), 29 patients with chronic atrophic gastritis, 20 with epithelial dysplasia and 16 with gastric cancer entered the study. Gastric juices were also tested for pH, protein concentration and specific gravity, urines for protein concentration and osmolarity. Serum and gastric juices were also tested for CEA levels and the results obtained with the two markers compared. In patients with gastric cancer, CA 50 gastric juice levels were statistically higher than in controls; a wide overlap was however present among groups, and sensitivity and specificity were respectively 38% and 85% for serum and 69% and 82% for gastric juice. Sensitivity and specificity were respectively 23% and 89% for CA 50 determination in urines. In this case, no statistically significant difference was observed between gastric cancer and control patients. A trend toward higher median values was observed in advanced with respect to early gastric cancer. A correlation was found between gastric juice and serum CA 50 levels, as well as between serum and urine levels of the marker. A correlation was also observed between CA 50 values and protein concentration in gastric juice and with osmolarity in urines. Overall, CA 50 levels were statistically higher in patients with intestinal metaplasia than in those who did not present the lesion. Increased CA 50 gastric juice levels are also observed in patients with chronic atrophic gastritis and epithelial dysplasia. CA 50 gastric juice and urine levels appear to be dependent, at least in part, on the concentration of the fluid.
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To assess the evolution of gastric epithelial dysplasia (GED), a prospective multicenter study was based on a protocol of repeated endoscopies and biopsies. To date, 134 cases (0.4% of all patients endoscopically examined in the same period) have been diagnosed as having GED and 80 of those have had an "adequate" follow-up (at least three endoscopies). Mean follow-up time was 18 months. Gastric epithelial dysplasia was mild in 59% of cases, moderate in 25%, and severe in 10%. Six percent of the patients had lesions that were "indefinite for dysplasia." Chronic atrophic gastritis (40%), gastric ulcer (32%), gastrectomy (10%), and polyps (9%) were the most frequently associated lesions. The term "regression" was adopted for GED no longer detectable during follow-up and the term "progression" was used when more severe changes or cancer was detected. Mild GED regressed in 66% of cases, persisted in 15%, and progressed in 19% (three cases to moderate, one to severe, and five to cancer). Moderate GED regressed in 30% of patients, persisted in 30%, and progressed in 40% (one to severe GED and seven to cancer). Severe GED regressed in 12.5% of patients, persisted in 12.5%, and progressed to cancer in 75%. Of the five patients with lesions indefinite for dysplasia, two had no dysplastic changes at follow-up and three had cancer diagnosed. Ten of 21 cases of cancer (48%) were at the early stage. The diagnosis was reached within the first year of follow-up in 14 cases and after 1 year in seven (13 to 39 months). Fifteen of 21 cases of cancer were diagnosed in gastric ulcer patients. In conclusion, GED is an infrequent finding and its biologically neoplastic significance is confirmed by the results of the follow-up study: (1) in its mild form, it tends to regress but adequate subsequent check-ups are mandatory as it may associate with or evolve as cancer; (2) patients with moderate GED require strict follow-up since the lesion shows a higher cancer risk; (3) surgery is indicated for severe GED because gastric cancer develops in 75% of cases; and (4) patients with lesions indefinite for dysplasia should immediately undergo repeat endoscopy and biopsy. Such an approach allows gastric cancer to be detected at an early stage in a much higher percentage of cases than may be expected.
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Gastric emptying half-time was measured in 10 healthy volunteers on two different occasions over a one-week interval, with an identical test meal. The first was the control evaluation, and at the second assessment, psychological stress was induced by the technique of dichotomous listening. Psychological and physiological parameters were assessed before and during the test period. No significant or consistent modifications of gastric-emptying time were induced by the stress procedure. Looking at individual subjects instead of mean values, gastric emptying was unchanged in 5 subjects, slower in 3, and faster in the remaining 2. These 3 groups had different mean values on two subscales of the Sixteen Personality Factor Questionnaire.