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Objective: To verify whether a prolonged (therapeutic) treatment with ranitidine or famotidine may affect blood alcohol concentrations (BAC) in patients with duodenal ulcer (DU)., Methods: Sixteen male patients with DU were studied. Subjects with Helicobacter pylori-associated DU did not enter the study. Patients randomly received either 300 mg ranitidine (n = 8) or 40 mg famotidine (n = 8) at bedtime for 2 months. They had a standard lunch (1:00 PM), and 0.3 g/kg of alcohol was given 15 min after the meal. BAC were measured by head-space gas chromatography up to 150 min., Results: The rate of GFPM was checked in all patients before they entered the study; we found it to be 53%, by comparing the area under the curve (AUC) of BAC after either intravenous or oral (po) administration of 0.3 g/kg ethanol. Ranitidine did not significantly modify either the mean AUCpo (5.8 +/- 1.8 vs. 6.2 +/- 1.4 mM/h, before vs. after treatment) or the peak BAC (4.6 +/- 1.1 vs. 5.3 +/- 1.7 mM) after 2 months of treatment. Famotidine failed to affect BAC in the second group of patients (AUCpo 5.0 +/- 1.4 vs. 5.6 +/- 1.7 mM/h, peak BAC 4.0 +/- 1.7 vs. 4.3 +/- 1.8 mM; before vs. after treatment)., Conclusions: These findings suggest that, in males with DU, prolonged treatment with ranitidine or famotidine had no effect on BAC after administration of a small dose of postprandial alcohol.

Platelet serotonin uptake was measured in 10 duodenal ulcer patients and 10 controls by determining the concentration of radioactivity in platelets after incubation with tritium-labelled serotonin binoxalate. Platelet 5-HT uptake in ulcer patients (312.0 +/- 125.0 CPM/10(7) platelets) was significantly higher than that in the control group (186.0 +/- 53.0 CPM/10(7) platelets; p < 0.01). Since the kinetics of 5-HT uptake by platelets may be a reflector of enhanced serotonergic activity, this finding may have implications in future therapeutic strategies for this disease.

The kinetics of aluminium absorption were determined in patients with duodenal ulcer and in 2 normal males after taking the antacid Tisacid (Biogal, Hungary). A peak serum aluminium of 54.5 micrograms/l was reached at 30 min, returning to the initial value of 6.8 micrograms/l at 3 h after the oral intake. Urinary but not serum aluminium increased in parallel to the amount of drug taken. The serum Al values are considerably influenced by the time of sampling. Owing to the rapid absorption and excretion of aluminium, there appears to be no danger of aluminium deposits in the tissues or of neurological alterations, provided renal function is normal.

In 20 patients (8 women and 12 men) aged of 20-56 years (38 years on the average) with the yet untreated duodenal bulb ulcer selected indices of nonspecific immunity in peripheral blood (total leukocytes number and absolute neutrophils (N) number, N adherence to fibre, spontaneous leukocytes migration in a 3 hour test, N phagocytic activity and bactericidal activity of plasma and leukocytes) were estimated. Those indices were again estimated after two week of treatment with ranitidine, 150 mg every 12 hours. After ranitidine treatment reduction of the total leukocytes number and absolute N number was found, as compared with the pretreatment results. In addition to that treatment an increase of N adherence and their phagocytic activity was observed with unchanged leukocyte capacity for spontaneous migration. No statistically significant difference was observed in bactericidal activity of plasma and leukocytes. The following conclusions were reached. 1. Two-week treatment of duodenal ulcer patients with 150 mg ranitidine every 12 hours was followed by reduction of the total leukocytes and N numbers in peripheral blood, and by augmentation of their adherence and phagocytic activity. 2. Bactericidal activity of plasma and leukocytes and leukocytes capacity for spontaneous migration did not show any changes after two-week ranitidine treatment of duodenal patients.

GR122311X (ranitidine bismuth citrate, Glaxo Group Research Ltd.) is a salt of ranitidine with a complex of bismuth and citric acid which is being developed for the treatment of peptic ulceration. In this study, 4 groups of 12 healthy male subjects were dosed for 10 days with either GR122311X 500 mg bid (301 mg bismuth per day), GR122311X 1.0 g bid (602 mg bismuth per day), tripotassium dicitrato bismuthate (TDB, DeNoltab, Gist Brocades Ltd., Weybridge, England) 240 mg bid (431 mg bismuth per day) or placebo. After the last dose the geometric mean for Cmax for 500 mg bid of GR122311X was 5 ng.g-1, for 1.0 g bid GR122311X it was 12 ng.g-1 and it was 21 ng.g-1 for 240 mg TDB bid. The corresponding trough plasma levels were 2 ng.g-1, 4 ng.g-1 and 4 ng.g-1, respectively. The AUC over a dosing interval after the last dose (AUC tau) were 34 ng.h.g-1, 71 ng.h.g-1 and 79 ng.h.g-1, respectively. The bismuth urinary recoveries over the last dosing interval (Ae tau) were 97 micrograms, 227 micrograms and 309 micrograms, respectively, which is less than 1% of the administered doses. The renal clearance of bismuth was less than the glomerular filtration rate. After adjustment for bismuth dose, the Cmax for GR122311X 500 mg was 35% that of TDB, while for GR122311X 1.0 g the Cmax was 42% that of TDB. Similar differences were observed for Ae tau. In conclusion bismuth pharmacokinetics after oral administration of GR1223311X exhibited lower Ae tau and Cmax, with a much narrower Cmax range than those observed for TDB.

In this prospective study, we investigated gallbladder (GB) contraction and plasma cholecystokinin (CCK) levels in response to food intake before and 1 month after vagotomy in 27 patients with complicated duodenal ulcer. Highly selective vagotomy (HSV) was carried out in 6 patients, truncal vagotomy and pyloroplasty (TVP) in 4, truncal vagotomy and antrectomy (TVA) in 7, selective vagotomy and pyloroplasty (SVP) in 5 and selective vagotomy and antrectomy (SVA) in another 5 patients with pyloric stenosis. The results of our studies indicated that (1) basal plasma CCK levels increased significantly after vagotomy, (2) none of the vagotomy operations altered the integrated CCK response, (3) unlike HSV, SVA and TVA, SVP and TVP decreased GB emptying and (4) antrectomy significantly enhanced CCK release after food intake. We concluded from these findings that the operative procedure of HSV, SVA or TVA to circumvent bile stasis-related postvagotomy cholelithiasis is superior to SVP or TVP in the surgical treatment of complicated duodenal ulcer.

The prevalence of high total IgE serum levels was evaluated in 232 consecutive patients suffering from peptic ulcer. Twenty-one percent of the patients presented total IgE serum levels above 200 KU/L compared with the 5% found in a healthy control population (p < 0.004). Similar prevalence was found in gastric and/or duodenal ulcers. No significant differences in the duration of the disease, smoking habits, familiarity for peptic ulcer, symptomatology and frequency of complications were observed between patients with high and with normal total IgE serum levels. Gastric function studies (gastric acid secretion, serum pepsinogen and gastrin levels) did not show any significant differences between the two groups. The incidence of Helicobacter pylori infection was 65% in patients with normal IgE levels and 75% in those with high IgE levels (p: n.s.). The response to treatment with full dose of H2-receptor antagonists was comparable in both groups (91.25% and 90.7% of ulcer healing after 6-8 weeks of treatment). A relapse of the ulcer after 6 months of maintenance therapy (half dose of H2-receptor antagonists) was observed in 39.5% of the patients with ulcer and high total IgE serum as against the 11.9% observed in patients with normal IgE (p < 0.001). These data lend further support to the hypothesis of an underlying immuno-allergic reaction in some forms of gastric or duodenal ulcer.

Enprostil, a synthetic E2-prostaglandin efficacious for duodenal ulcer healing, presents both antisecretory and antigastrinic effects. This is at variance with the elevation of plasma gastrin observed with ranitidine. OBJECTIVE--This leads us to compare enprostil and ranitidine on the following points: a) variations of plasma gastrin (basal and postprandial) parameters over a 6-week conventional treatment; b) correlation studies between ulcer relapses (frequency and temporal evolution) after treatment discontinuation and various gastrinic criteria. METHODS--Among a group of 642 patients followed for ulcer relapse, 165 were considered for gastrin (78 of the "Enprostil" group and 87 of the "Ranitidine" group). RESULTS--Initially, both populations were comparable for clinical and plasma gastrin parameters. After 6 weeks of treatment, the increases in the various gastrin parameters (basal, postprandial, peak, integraded) were significantly greater and the absolute values higher (Wilcoxon, P < 0.001) with ranitidine than with enprostil. No correlation was found between relapse occurrence after drug discontinuation and these gastrin parameters. CONCLUSIONS--Ranitidine hypergastrinemia seems directly related to gastric hyposecretion whereas its absence with enprostil is likely more dependent upon a specific antigastrinic activity than on a reduced antisecretory activity. Those differences in mechanism of action have no consequence on the stability of ulcer obtained by either drug.

Radioimmunoassay and immunomorphological methods were used in the study of pepsinogen 1, basal and food-stimulated gastrin and somatostatin blood levels, the number of gastroduodenal G- and D-cells as well as gastric secretion during routine-dose treatment with gastrozepin and ranisan of 45 gastroduodenal ulcer patients versus 15 controls. The patients were divided into 2 types according to blood gastrin levels and the number of pyloric G-cells: with hypergastrinemia and/or hyperplasia of the G-cells, with normogastrinemia and normal number of G-cells. A course treatment with gastrozepin of type 1 patients brought about normalization of serum gastrin and the number of the G-cells with elevation of blood somatostatin levels. In patients of type 2 the above parameters did not change. The same picture in them remained after ranisan treatment, though they developed hypergastrinemia. In patients of type 1 after ranisan treatment the above parameters did not change. The data obtained demonstrate once more heterogeneity of duodenal ulcer.

Objectives: To compare gastric secretory function in patients with duodenal ulcer and in healthy volunteers with and without Helicobacter pylori infection., Methods: Basal acid output, peak acid output, meal-stimulated acid output, fasting and meal-stimulated serum gastrin concentrations were measured in 136 healthy volunteers (63 H. pylori positive, 73 H. pylori negative) and 52 duodenal ulcer patients, all but one of whom were H. pylori positive., Results: By multivariate linear regression analysis, H. pylori infection was a significant negative predictor of basal acid output and a positive predictor of fasting and meal-stimulated gastrin concentrations. When compared to truly normal (i.e., H. pylori-negative) control subjects, duodenal ulcer patients had elevated basal acid output, peak acid output, fasting and meal-stimulated gastrin concentrations., Conclusions: Our results show that in patients with duodenal ulcer disease, hypergastrinemia is largely related to gastric H. pylori infection, whereas acid hypersecretion is due to factors other than H. pylori.

Evaluation of serum alpha 1-antitrypsin levels in the South Asian population and its possible involvement in disease conditions such as duodenal ulcer has not been given due consideration. This is mainly because reports from European and North American countries indicate that the genetic deficiency of this protease inhibitor is rare among Asians of the subcontinent. Using isoelectric focusing (IEF) and radial immunodiffusion (RID) techniques, we analysed serum samples from 100 normal, healthy adults and 50 patients with endoscopically proven duodenal ulcers to determine if there is a possible relationship between alpha 1-antitrypsin phenotype and this disease. Five duodenal ulcer patients had low alpha 1-antitrypsin levels as well as SZ and S phenotype. None of the controls showed presence of S or SZ phenotypes. The normal or most common genetic form, MM, is the predominant phenotype in both controls and patients.

Duodenal ulcer is a multifactorial entity where a genetic predisposition and extrinsic elements seem to concur in its origin. A series of genetic and extrinsic markers were determined in 50 patients with duodenal ulcer and 50 controls matched by age, sex and socioeconomical status. HLA antigens dit not have significant differences. Blood group O Rh+ was predominant (p < 0.01). Secretor status of antigen HBO in saliva was positive in 70% of patients (p < 0.001). Serum Pepsinogen I was increased in 85% of cases (p < 0.001). Immunoglobulin G anti H. pylori was positive in 62% of ulcerous (p < 0.001). The highest sensibility and negative predictive value was represented by increased serum pepsinogen levels (85%); the highest specificity and positive predictive value was to Ig G anti H. pylori (90 and 86%). These results affirm the polygenic character of the duodenal ulcer disease.

Levels of gexosamines, free oxiprolin, gexuronic acids, malonic dialdehyd, reduced glutathione and total content of gexosamines in blood as well as spontaneous chemiluminescence of blood serum were studied in 89 patients with duodenal ulcer during rehabilitative treatment and in 35 healthy subjects. Rehabilitative stage-by-stage treatment was demonstrated to ensure normalization of anti-radical protective systems of the body, beneficially influence connective tissue structures of gastric and duodenal mucosa, prevent exacerbation of the disease.

Plasma concentrations of oxyntomodulin-like immunoreactivity, a group of intestinal peptides capable of mediating an enterogastrone signal, were measured during a 24-h period in 6 duodenal ulcer patients and compared with those of 16 age-matched controls. Each subject was submitted to 18 oxyntomodulin-like immunoreactivity determinations. Four standardized meals were given during the test. Furthermore, each patient was evaluated for peak acid output after pentagastrin stimulation. The values of the duodenal ulcer subjects were predominantly within normal acid secretion limits. Fasting levels, meal-induced variations, and nocturnal production of oxyntomodulin-like immunoreactivity were similar in the two groups. A negative correlation was observed between peak acid output and oxyntomodulin-like immunoreactivity evaluated either as nocturnal production or as maximum nyctohemeral concentration. We conclude that, taken as a whole, duodenal ulcer disease is not caused by a defect in oxyntomodulin-like immunoreactivity secretion. However, this study does not rule out the possibility of a selective deficiency of these peptides in some duodenal ulcer subgroups such as hypersecretory patients.

Of 112 patients with peptic ulcer disease examined for oral carriage of Candida, 66 (59%) were carriers. Candida carriage was associated with blood group O (P < 0.05) and, independently, with nonsecretion of blood group antigens (P < 0.01). For each subject, the presence or absence of yeasts was found to be a constant characteristic, and only among patients positive for Candida was blood group O or nonsecretion more frequent than expected in the general population. The quantity of yeasts isolated was significantly greater in patients than in normal subjects (P < 0.002), as was the frequency of carriage in the patient population (59% vs 32%). This increase was not associated with treatment with H2-receptor antagonists. The results of paired oral and gastroduodenal aspirate cultures suggested that identifying Candida in the oral cavity was a good indicator of the presence of yeasts elsewhere in the gastrointestinal tract. Mechanisms whereby overgrowth of Candida in the upper gastrointestinal tract might contribute to the inflammatory background of peptic ulcer disease are discussed.

The parameters of proteinogram were studied in 182 patients. It was shown that autotransfusions of UV-irradiated blood was an effective measure for the correction of the disturbed protein metabolism.

Omeprazole may exert an effect on gastric mucosal proliferation by inhibiting gastric acid secretion and increasing serum gastrin levels. It may also influence the kinetics of endocrine cells and the oxyntic mucosa. The aim of the present study was to evaluate the cell cycle in different gastric compartments following short- (1 month) and long-term (6 months) administration of two different dosages of omeprazole by means of a flow cytometric method. We also determined serum gastrin levels at the same time. No differences in cell cycle distribution of the antrum, body, and fundus were found in the two different dosage groups after 1 month of therapy, considering the synthetic phase (S-phase) of the cell cycle. A statistically significant increase in S-phase was reported after long-term therapy in the mucosa of the fundus and body of the stomach in both groups. Gastrin levels showed no clear correlation with cell cycle distribution variables. We postulate a proliferative adaptation of the oxyntic mucosa to long-term drug administration not mediated by gastrin influence.

To investigate whether antral colonization by Helicobacter pylori (Hp) modifies gastrin-cell population, the number of G-cells was evaluated in antral biopsy specimens from 22 apparently healthy subjects and from 48 duodenal ulcer patients using a morphometric method. The level of serum immunoreactive gastrin in a sample of fasting serum obtained at the time of biopsy was also measured. In healthy subjects the G-cell count (evaluated according to G/I index) and the serum gastrin levels were not significantly different than those found in duodenal ulcer patients. When the antral colonization by Hp was assessed, we found that, both controls and duodenal ulcer Hp-positive patients had a mean G-cell count and fasting serum gastrin levels not significantly higher than in patients without Hp.

In 12 duodenal ulcer patients, gastric emptying (GE) of a radiolabelled solid meal, gastric acid secretion, and gastrin release were examined before and during the early postoperative period (median 13.5 days) after a highly selective vagotomy (HSV). HSV significantly delayed GE; the median slope of GE curves (K) decreased from 11.86 to 6.52 min-1 x 10(-3) (p < 0.01). A significant inhibition of the late phase of GE was reflected by a diminution of the curve shape parameter (S) from a median of 1.41 to 0.98 (p < 0.02). A profound impairment of GE after HSV was found in 4 of 12 patients (33%). HSV resulted in a 49% decrease in the basal acid output (6.9 +/- 1.0 before to 3.5 +/- 1.0 mmol.h-1 after HSV, and a 56% reduction in the pentagastrin-stimulated gastric acid secretion (31.1 +/- 5.1 before vs 13.8 +/- 2.4 mmol.h-1 after HSV (p < 0.01). A significant increase in both the fasted serum gastrin (38.9 +/- 3.7 to 66.9 +/- 8.4 ng.l-1, p < 0.05) and the meal-stimulated gastrin release (AUC0-120: 7179 +/- 440 to 11158 +/- 1062 ng.l-1 min, p < 0.05) was observed after HSV.

The relation between Helicobacter pylori (H pylori) infection and fasting gastrin and pepsinogen-I and -II concentrations was evaluated in 278 volunteers without symptoms and the results were compared with the values obtained in 35 patients with duodenal ulcers. H pylori infection was determined with the 13C-urea breath test in subjects without symptoms and with endoscopy, biopsy (histology and culture), and quick urease test (CLO-test) in patients with duodenal ulcers. Gastrin and pepsinogen-I and -II concentrations were assayed with specific radioimmunoassay systems. The results clearly indicate that fasting gastrin and pepsinogen-I and -II concentrations were significantly higher in H pylori positive compared with H pylori negative subjects. Neither age nor sex affected basal gastrin and pepsinogen concentrations in H pylori negative subjects. Fasting gastrin, pepsinogen-I and -II concentrations in serum samples were similar in H pylori positive persons with no symptoms and those with duodenal ulcers suggesting that similar mechanisms are involved in increasing plasma concentrations of these variables in both populations. Hypergastrinaemia and hyperpepsinogenaemia are therefore probably secondary to active H pylori infection.

In the past five years 12 patients have been identified presenting with chronic duodenal ulcer (DU) disease and with no evidence of current or recent Helicobacter pylori (H pylori) infection. Four of them were taking regular non-steroidal anti inflammatory agents, one was subsequently found to have Crohn's disease of the duodenum, and one to have the Zollinger-Ellison syndrome. The remaining six patients with idiopathic DU disease were remarkable for their absence of the A1 blood antigen gene. Detailed studies of gastric function were performed in these six patients and compared with H pylori positive patients with DU and with healthy volunteers. The median integrated gastrin response in the patients with idiopathic DU (2810 (range 750-8750) ng/l min) was similar to that of the H pylori positive patients with DU (3355 (550-8725)) and higher than that of the H pylori negative healthy volunteers (560 (225-1125)). The median peak acid output in the patients with idiopathic DU (37 mmol/h, range 17-52) was similar to that of the H pylori positive patients with DU (40 (15-57)) and higher than that of the non-ulcer controls (22 (16-29)). The median percentage of a liquid meal retained in the stomach at 60 minutes was less in the patients with idiopathic DU (23 (15-33)) than in H pylori negative healthy volunteers (34 (30-53) p < 0.01). The median percentage of a solid meal retained at 60 minutes was less in the patients with idiopathic DU (54 (9-83)) than in either H pylori negative healthy volunteers (87 (49-95) p<0.01) or H pylori positive patients with DU (79 (51-100) p<0.01). In conclusion, three abnormalities of gastric function are prevalent in patients with H pylori negative idiopathic DU disease - hypergastrinaemia, increased acid secretion, and the one feature distinguishing them from H pylori positive patients with DU - rapid gastric emptying of both liquids and solids. Each of these abnormalities will increase the exposure of the duodenal mucosa to acid and thus explain its ulceration. The absence of the blood group A1 antigen gene is consistent with a genetic basis for the disturbed gastric function linked to the ABO blood group antigen genes.

Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.

Contents of cAMP and cGMP in blood plasma as well as ratio cAMP/cGMP were studied by radioimmunoassay in 56 patients with duodenal ulcer of various severity. The examination was performed twice: before the treatment and 4 weeks after the treatment in a hospital. The analysis carried out with regard to the treatment efficacy in every variant of the clinical course of the disease showed that poor treatment results are associated with the dynamics of cyclic nucleotide (CN) plasma levels, especially with the increased ratio cAMP/cGMP, regardless of the disease severity which is characteristic of blood plasma CN taking part in compensatory-adaptive mechanisms in duodenal ulcer and evidences the necessity of differentiated approach to the treatment in accordance with developed adaptive reactions.

Serum pepsinogen I (PGI) levels were measured in 231 duodenal ulcer (DU) patients and 100 sex- and age-comparable healthy controls. Significantly higher mean serum PGI levels were found in DU patients than in controls (124.7 +/- 3.4 ng/ml v. 92.9 +/- 2.3 ng/ml; P < 0.001) (mean +/- SE). These levels were higher in male DU patients than in female DU patients (128.5 +/- 3.9 ng/ml v. 107.4 +/- 6.4 ng/ml; P < 0.05). Smoking was associated with elevated serum PGI levels in DU patients (145.3 +/- 5.1 ng/ml v. 109.0 +/- 4.2 ng/ml; P < 0.001). Healed DUs were associated with lower mean serum PGI levels than active ulcers (110.9 +/- 7.6 ng/ml v. 129.4 +/- 3.8 ng/ml, P < 0.05). Whether patients were positive or negative for Helicobacter pylori, infection did not affect mean serum PGI levels. All the risk factors for DU may not affect serum PGI levels and DU may therefore be considered a multifactorial disease.

The objective of this study was to evaluate the accuracy of an indirect immunofluorescence (IIF) test for serodiagnosis of Helicobacter pylori infection in children and to determine how the test is affected by the presence of antibodies against Campylobacter jejuni. We studied 65 consecutive children (two with endoscopically confirmed duodenal ulcer) and a series of 18 children with duodenal ulcer. Thirty children were H. pylori negative, as determined by culture, by the preformed urease test, and by carbolfuchsin-stained smears. The microorganism was identified by microbiological methods in 35 of the 65 (53.85%) consecutive patients studied and in all children with duodenal ulcer. The titer of the IIF test was > or = 1:20 in the sera of all children with duodenal ulcer and in the sera of 30 of 33 H. pylori-positive children without duodenal ulcer. No H. pylori-negative children had titers > 1:10. A serum dilution of 1:20 discriminated between H. pylori-infected and noninfected children. Absorption with C. jejuni did not change the levels of IgG against H. pylori. When five patients who had been successfully treated with metronidazole, amoxycillin, and furazolidone for 7 days were retested, a slight decrease in anti-H. pylori IgG levels was noted from the third month on. The decrease was more significant 9 months after the eradication of the microorganism.

Ranitidine bismuth citrate was compared with an equipotent dose of ranitidine, to determine whether the former, by an anti-Helicobacter pylori activity, would counteract the rise of gastrin resulting from ranitidine's gastric acid antisecretory activity. Twenty four men with duodenal ulcers were studied before and on the 8th day of dosing with either ranitidine bismuth citrate 800 mg twice daily or ranitidine 300 mg twice daily (double blind, randomised, parallel groups). Fasting and postprandial plasma gastrin and plasma pepsinogen I and II concentrations were measured, and a 13C-urea breath test was performed before and on the 8th day of dosing. The 13C-urea breath tests were positive in 21 patients before dosing and remained positive in nine of nine of the ranitidine dosed patients, whereas only two of 12 patients treated with ranitidine bismuth citrate remained positive. The expected rise in meal stimulated plasma gastrin with ranitidine was seen in the 12 patients who received ranitidine but, despite suppression of H pylori urease activity in 10 of 12 patients taking ranitidine bismuth citrate, there was no attenuation of the meal stimulated gastrin rise. There was no significant difference in the mean derived (4 hour) plasma pepsinogen I and II concentrations after dosing with ranitidine or ranitidine bismuth citrate.

Objective: To find out whether patients with acute bleeding peptic ulcers have hypercoagulable blood., Design: Prospective open study., Setting: District hospital in Sweden., Subjects: 54 consecutive patients with duodenal ulcer (n = 25) and gastric ulcer (n = 29) admitted with haematemesis or melaena, or both., Interventions: Diagnosis verified on admission by endoscopy, and healing was examined at follow up. Consumption of non-steroidal anti-inflammatory drugs, and smoking habits, were recorded., Main Outcome Measures: Coagulation of the blood monitored by concentrations of plasma thrombin-antithrombin III (TAT) complex in samples obtained on admission for the acute bleeding episode and at follow up 1-2 months later., Results: The plasma TAT complex concentrations were raised during the acute bleeding episode (p < 0.001) compared with an age matched reference group. The TAT complex concentrations measured at follow up had returned to the reference range in all patients, whether or not their ulcers had healed., Conclusion: The results indicate that patients with acute haemorrhage from peptic ulcers have hypercoagulable blood during the acute episode.

80 liquidators of Chernobyl disaster with aggravation of duodenal ulcer were examined, as well as a control group of 70 patients. In the group of liquidators some characteristic features were disclosed, namely peculiarities in the state of abdominal mucosa and clinical course of the disease. These data were obtained in the results of hematological, immunological and biochemical researches.

The author summarizes the experience of UDT in 140 patients with chronic gastritis (53) and gastroduodenitis (87) and 46 with duodenal ulcer. It was found that chronic diseases of the gastroduodenal zone were characterized by changes in the hematological and biochemical indices of the blood against the background of altered immune reactivity and that UDT favoured their normalization.

Forty-two patients with peptic ulceration of the duodenum, stomach or oesophagus, who had not responded to 3 or more months of high-dose treatment with ranitidine (450 or 600 mg/day), were treated with oral lansoprazole at 30-60 mg daily. In 40 patients (95.2%) the ulcers healed within 2-12 weeks. In the remaining 2 patients healing took several months but eventually all ulcers healed. After healing, 40 patients underwent long-term maintenance treatment with 30-60 mg lansoprazole daily for 1-3 years (continuing). During maintenance therapy with lansoprazole, no endoscopically verified relapses occurred when the drug was taken regularly. In 1 patient treatment had to be discontinued because of a drug-related colitis that disappeared soon after treatment had been stopped. There were no significant changes in routine laboratory tests in any patient. Basal serum gastrin concentrations, which were already elevated by the previous high-dose ranitidine treatment (125 +/- 25 pg/ml), rose to four times the normal values after 4 weeks of treatment with lansoprazole (255 +/- 65 pg/ml). Thereafter no further increases in basal serum gastrin concentrations were observed, even after 3 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased slightly during lansoprazole treatment; until now no dysplasia of the enterochromaffin-like cells has been observed. In conclusion, 30-60 mg lansoprazole daily healed ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with 30-60 mg lansoprazole daily was found to be highly effective and safe over the time observed.

Absolute and corrected by creatinine excretion urinary Epidermal Growth Factor (EGF) values were determined in 23 duodenal ulcer patients and compared to a control group. Basal serum pepsinogen I levels were measured in the patient group. Absolute urinary EGF values in patients were lower than in control group, such difference however, as such of EGF corrected by urinary creatinine excretion were not statistically significant (p > 0.05). Absolute urinary EGF excretion in male patients was higher than in female patients (p < 0.05), but after establishing the ratio EGF/Creatinine, the difference disappeared. There was no correlation between EGF and Pepsinogen I, it was inverse with age and positive with creatinine excretion. Some mechanisms are considered to explain the urinary EGF normality in these patients. The increasing importance given to EGF in ulcerous diseases and further trends in research are analyzed.

A passive microhemagglutination test was applied for the detection of H. pylori antibodies. The presence of elevated antibody titers was most frequently encountered in the sera of patients from whom H. pylori was isolated. No relationship between the level of antibodies and the clinical picture of peptic ulcer disease was noted. In addition, negative results from bacteriologic and serologic studies in patients with confirmed histopathologic changes and typical clinical symptoms may suggest that peptic ulcer disease and chronic inflammation of gastric mucosa is not always accompanied by the presence of H. pylori. It is concluded that the passive microhemagglutination test is a convenient and easily performed screening method.

Chief cell mass and serum Pepsinogen I were calculated in 25 duodenal ulcer patients and in 40 healthy controls. Comparisons were also made with parietal cell mass and the stimulated acid secretion. Chief cell mass was expressed bay a Zymogenous Index (ZI) obtained by multiplying the number of chief cells per mm2 for the thickness of the glandular layer. The analysis of the data shows a significant decrease of ZI in duodenal ulcer patients in comparison with controls. The grouping of the subjects according to the age (over and under fifty years), confirms that ZI decreases significantly in duodenal ulcer groups in relation with the respective groups of control. In case of duodenal ulcer with fundic superficial gastritis no behavioural changes of ZI are observed in comparison to those affected by duodenal ulcer with normal fundic mucosa. The serum Pepsinogen I significantly increases in duodenal ulcer patients in comparison to the controls, either in the subjects over and under fifty. In the group of duodenal ulcer patients with superficial fundic gastritis a significant increase of serum Pepsinogen I can be pointed out in comparison to the ulcer patients with normal fundic mucosa. The grouping of the patients on the basis of hyperparietalism and normoparietalism has shown in the former group hypozymogenism and in the latter normozymogenism. Finally, no correlation has emerged between Zymogenous Index and serum Pepsinogen I.

Estimation of protein-bound hexoses, fucose and sialic acids in the blood and urine of 64 patients with gastroduodenal ulcers within later periods after various types of gastric vagotomy showed that the denervation inhibited the protective barrier of gastric and duodenal mucosal membrane. Protective functions of gastroduodenal mucosal membrane were most distinctly inhibited after selective proximal vagotomy which may be responsible for higher amounts of recurrences of ulcerous disease after this type of vagotomy than other types of denervation.

The efficacy of lansoprazole (30 mg/d) and omeprazole (20 mg/d) has been assessed in active duodenal ulcer disease in 144 patients included in a multicentric, randomized, double-blind trial. After two weeks, the healing rates were 74% and 58% in the lansoprazole and omeprazole groups, respectively (P = 0.049). After 4 weeks, the healing rates were 94% in each group (NS). The delay to pain relief was 2 days for lansoprazole and 3 days for omeprazole (NS). Minor side effects occurred in 12% of the lansoprazole treated patients and in 13% of the omeprazole treated patients. No severe adverse events were reported. A slight increase in serum gastrin level was observed, similar in both groups (+35 UI/L and +19 UI/L for lansoprazole and omeprazole respectively). This study confirms previous results concerning the efficacy of both treatments in duodenal ulcer disease. The statistical difference observed for healing rates after 2 weeks could correspond to a faster efficacy for lansoprazole (30 mg) than for omeprazole (20 mg).

In 25 patients with duodenal ulcer, before treatment and after three weeks, and another 30 days of treatment with ranitidine, plasma concentrations were determined of IgA, IgG, IgM immunoglobulins, and of 10 other proteins. In comparison to the control group of 20 persons, a statistically significant decrease was found in the concentration of alpha 2-M, prealbumins, and IgG, as well as a significant increase of alpha 1-AT, C4 complement component, and a non-significant increase of coeruloplasmin, haptoglobin and IgM. During the treatment a tendency was observed for an increase of IgG and IgM level, as well as a statistically significant decrease of alpha 1-AT, C4, and coeruloplasmin concentration. The treatment exerted no effect on the decreased level of alpha 2-M. It was accepted that the tendency for an increase of IgG and IgM level was due, most probably, to the immunostimulating action of ranitidine, and the changes of concentrations of other parameters induced by the treatment were related to the presence and healing of the ulceration. The observed decrease of alpha 2-M level was probably due to binding of alpha 2-M to pepsinogen whose blood level was increased during gastric ulcer.

Aims: Representation of common characteristics and peculiarities of the treatment with H2-receptor antagonists of duodenal and gastric ulcer and gastro-esophageal reflux in childhood in comparison with adults, taking ranitidine as an example., Major Points: In the treatment of primary and chronic duodenal and gastric ulcers, ranitidine at doses of up to 10 mg/kg/day, given in two fractions (up to 300 mg daily) is a proven form of therapy. The endoscopically confirmed healing rates after 6 to 8 weeks of acute treatment vary between 80 and 100%. The recurrence rate in children with duodenal ulcer is high, so that long-term treatment with 4 to 5 mg/kg/day (evening dose) is added. Following a recurrent ulcer, treatment should be continued for one to two years. Ranitidine has been used with success for the treatment of gastroesophageal reflux. Shorter intervals between administrations (3 times a day) with a total dose of up to 10 mg/kg/day are to be recommended. More experience is required in this area. At therapeutic doses, ranitidine shows hardly any side effects in children, even with long-term treatment, and can be considered to be very well tolerated by this age group, including babies.

Adequately good consumption of beta-carotene was observed in patients with duodenal ulcer and erosive gastritis after daily treatment with 18 mg of the carotinoid used as 0.1% oil solution: concentration of beta-carotene was increased approximately 3-fold in blood serum of these patients. Concentration of retinol was not increased in blood serum after treatment with beta-carotene, thus indicating that the drug treatment was not dangerous. Treatment with beta-carotene led to improvement in the state of the antioxidative system of these patients as resistance of erythrocytes to peroxide hydrolysis was increased while content of malonic dialdehyde was decreased in blood serum. The carotene treatment contributed to arresting pain syndrome in patients with ulcers, to cicatrization of ulcers and to disappearance of gastric mucosal membrane erosion.

Serum gastrin levels were measured under basal conditions and after hyperproteic meal stimulation in 24 patients with non-stenotic duodenal ulcer, 78% of them were males with a mean age of 36.4 years. Results were compared with those obtained in 20 volunteers. Basal gastrin levels in patients with duodenal ulcer 46.2 +/- 17.5 pg/ml did not show any significant statistical differences when compared with those in the control group (51.01 +/- 28.1 pg/ml). After meal stimulation gastrin levels at different time intervals, were similar in patients with duodenal ulcer and in the control group. We conclude that serum gastrin does not seem to play a relevant pathogenic role in the development of duodenal ulcer; its measurement is of no value as a biological marker of duodenal ulcer disease.

We have investigated the possibility that hypergastrinaemia in chronic Helicobacter pylori infection is a compensatory response to reduced parietal cell sensitivity to gastrin. The acid response to 45-min infusions of pentagastrin at sequential doses (micrograms/kg/h) of 0, 0.031, 0.062, 0.124, and 0.6 was compared before and 1 month after eradication of H. pylori in eight duodenal ulcer patients. The median acid outputs (mmol/h) with the respective infusions were 5.0, 7.5, 26.5, 30.8, and 37.0 when H. pylori-positive and similar at 4.5, 7.1, 22.7, 28, and 31.5 when H. pylori-negative. The median estimated dose of pentagastrin required to produce 50% maximal response (D50) was similar before (0.060 micrograms/kg/h) and after (0.057 micrograms/kg/h) eradication of H. pylori. The median estimated maximal response to pentagastrin (mmol/h) was also similar before (39.2) and after (32.3) treatment. The median basal gastrin concentration was 48 ng/l (range, 22-77) before treatment and fell to 33 ng/l (range, 8-37) after eradication of H. pylori (p = 0.03). These findings show that the parietal cell sensitivity to pentagastrin is unaffected by chronic H. pylori infection in duodenal ulcer subjects and that the hypergastrinaemia cannot be attributed to the bacterium inhibiting parietal cell function.

Prostaglandins (PG) and cyclic nucleotides (CN) were assessed radioimmunologically in the blood plasma under basal conditions and after a standard breakfast in 20 patients with duodenal ulcer, 16--with gastric body ulcer and 18 patients with atrophic gastritis. It was established that the patients showed an increased PG level, cAMP-dependent processes. Neurohumoral mechanisms of regulation of gastric secretion were abnormal.

Thirty patients with active duodenal ulcer who were Helicobacter pylori positive (HP+) by HLO test and by histology (Giemsa stain) were given omeprazole (OME) 20 mg/d for a two-week period. Estimation of fasting serum gastrin concentration (RIA) was performed before treatment and 24 hours after the last dosage of OME, and HP was searched for an antral biopsies at the end of the treatment as well. Mean fasting serum gastrin concentration increased significantly after treatment in all patients studied (p less than 0.05). However, the increase remained significant only in those patients who continued to be HP+ while no significant increase was observed in those who became HP-. The results could be considered as further evidence of the 'clearing' effect of Omeprazole on HP.