Maximal Acid Output Research Articles

Relationship among acid secretion, antral distension, and liquid gastric emptying in active and healed duodenal ulcer.

The aim of this study was to assess the relationship between fasting antral distension and basal and maximal acid output and to examine the link between the gastric emptying rate of liquids and the amount of acid secretion. Twenty consecutive male patients with H. pylori-positive noncomplicated duodenal ulcer disease received a measurement of basal and maximal gastric acid secretion and underwent ultrasonographic (US) evaluation of fasting antral distension and gastric emptying of liquids on two separate days. Ten of these patients were studied again three months after ulcer healing. The width of the fasting antral area was not correlated with basal acid output, but a significant relationship was found between maximal acid output and fasting antral distension (r = 0.55; P = 0.012). No significant correlations were found between gastric emptying and gastric acid output. The gastric emptying rate, expressed as half-time gastric emptying and remaining liquid component at 60 min, was not influenced by basal or maximal acid output. After ulcer healing, no correlations were found between acid secretion, fasting antral distension, and gastric emptying rate. Our results suggest that in duodenal ulcer patients, fasting antral distension is not influenced by basal gastric secretion and that, on the contrary, a correlation exists between fasting antral distension and maximal acid output, but only in active duodenal ulcer. No relationship exists in both active and healed duodenal ulcer between gastric emptying and gastric acid secretion.

Cure of Helicobacter pylori Infection Improves Gastric Acid Secretion in Patients with Corpus Gastritis

Background: For more than 30 years it has been known that gastric acid secretion is inversely related to the extent and severity of corpal gastritis. We therefore evaluated the effect of cure of Helicobacter pylori infection on basal and pentagastrin-stimulated acid secretion. Methods: Basal acid output (BAO) and maximal acid output (MAO) were assessed in 11 H. pylori-infected dyspeptic patients (8 women and 3 men; mean age, 28 years) before and after successful anti-H. pylori therapy. Results: The gastritis index was significantly lower after therapy and was associated with an increase in both BAO and MAO after cure of the H. pylori infection (BAO from 0.3 mmol/h to 3.1 mmol/h and MAO from 4.8 mmol/h to 19 mmol/ h). Basal and stimulated acid concentrations also increased (29.1 ± 36.6 to 54 ± 31 mmol/1 and 72.5 ± 46 to 120.1 ± 30 mmol/1, respectively, for basal and stimulated acid concentrations; P < 0.05 for peak and MAO, P = 0.07 for BAO). Conclusion: Gastric acid secretion increased into the normal range after successful treatment of, pylori infection, suggesting that gastric function can recover to normal or almost normal after cure of H. pylori infection.

Association between serum gastrin levels, gastric acid secretion and age in early gastric cancer.

This study evaluated the effect of gastric acid secretion and serum gastrin response on tumor differentiation for early gastric cancer according to patients' age. We investigated the association between serum gastrin levels, gastric acid secretion and the histologic types of 335 early gastric carcinomas limited to the mucosal and submucosal layers in comparison with 450 gastric and 197 duodenal ulcers. The preoperatively examined basal acid output, maximal acid output and peak acid output after administration of tetragastrin and serum gastrin levels before and after ingestion of a test meal were determined. Patients with differentiated cancer and duodenal ulcer showed a significant negative correlation between gastric acid secretion and age, while the former group also had a significant positive correlation between serum gastrin levels and age. On the other hand, patients with undifferentiated cancer did not show any such correlation between gastric acid and age, but showed a significant positive correlation between serum gastrin, integrated gastrin response and age. Patients with gastric ulcer did not show any such correlations. These data suggest that both low acid secretion and endogenous hypergastrinemia, especially in the elderly, may play an important role in differentiated and undifferentiated gastric carcinomas.

Changes in parietal cell structure and function in HIV disease

The mechanisms underlying acid secretory failure in patients with HIV disease are unknown. We evaluated, in a series of preliminary studies, changes associated with parietal cell structure and function in early and late HIV disease, in an attempt to elucidate possible underlying mechanisms. Gastric acid and intrinsic factor secretion, vitamin B12 absorption, and light and electron microscopic evaluation of gastric mucosa were evaluated in patients with early and late HIV infection (AIDS) and compared to non-HIV-infected controls. Immunolocalization of HIV-related antigens in gastric mucosa was also examined. Fasting gastric juice pH and intrinsic factor (IF) concentration in AIDS and HIV infected subjects were significantly different from controls (P = 0.012 and P = 0.025, respectively for pH, and 0.029 and 0.035 for IF; ANOVA LSD test). By contrast, maximal acid output (MAO) was significantly lower in AIDS, but not HIV-infected subjects (P = 0.043 and P = 0.322, respectively). Similarly, Schilling test phases 1 and 2 results were significantly lower in AIDS, but not HIV-infected subjects. Varying degrees of vacuolar degeneration of parietal cells were seen on light microscopy. On electron microscopy (EM), tubulovesicles were reduced and intracellular canaliculi dilated with striking loss of microvilli. Immunofluorescent staining with antibodies to gp120, gp41, p24, and p17 demonstrated positive punctate signals in the cytoplasm of gastric glands, which includes parietal cells. Immunogold EM with anti-gp120, localized predominantly to the microvilli of intracellular canaliculi in parietal cells. Abnormal secretory function of parietal cells occurs early in HIV disease, affects acid as well as intrinsic factor secretion, and is associated with morphological changes in the acid secretory apparatus.

Proximal Gastric Vagotomy

The authors compared open and laparoscopic proximal gastric vagotomies for efficacy of acid reduction and preservation of gastric emptying. Laparoscopic methods have been used to perform vagotomy in patients with duodenal ulcer; however, no direct comparisons are available of laparoscopic and open surgical procedures regarding acid reduction and gastric emptying. Thirty-one consecutive dogs were randomized to open proximal gastric vagotomy (OPGV; n = 11), laparoscopic anterior seromyotomy and posterior truncal vagotomy (ASPTV; n = 10), or laparoscopic proximal gastric vagotomy (LPGV; n = 10). Intraoperative endoscopic Congo red testing assured complete vagotomy. Basal acid output (BAO) and maximal acid output (MAO) during pentagastrin and insulin-induced hypoglycemia were measured with marker dilution techniques, and gastric emptying was assessed with radionuclide-labelled solid and liquid markers before and 5 weeks after operation. Operative time (mean +/- standard error of the mean) for OPGV was shorter compared with ASPTV and LPGV (86 +/- 7 minutes vs. 124 +/- 7 minutes and 115 +/- 7 minutes; p < 0.002). Postoperative BAO did not decrease in any group. Open proximal gastric vagotomy and LPGV, but not ASPTV, decreased MAO (p < 0.05); (after pentagastrin, OPGV from 26.4 +/- 1.7 mEq/hour to 11.3 +/- 0.1 mEq/hour, LPGV from 21.4 +/- 1.0 mEq/hour to 6.4 +/- 0.5 mEq/hour; after insulin-induced hypoglycemia, OPGV from 9.9 +/- 0.5 mEq/hour to 2.2 +/- 0.3 mEq/hour, LPGV from 7.9 +/- 0.5 mEq/hour to 1.9 +/- 0.4 mEq/hour). Gastric emptying of liquids and solids, as quantitated by the time for one half of the marker to empty (T 1/2) and the shape of the emptying curve, were similar before and after all three surgical procedures. Laparoscopic proximal gastric vagotomy was comparable to OPGV in decreasing stimulated gastric acid production without significantly altering gastric emptying. Anterior seromyotomy and posterior truncal vagotomy was less effective in decreasing MAO and required more operative time. Laparoscopic proximal gastric vagotomy has the potential to become accepted therapy for patients with duodenal ulcer managed presently with OPGV.

Gastric Acid Secretion and Gastroduodenal pH after Pancreaticogastrostomy in Dogs

Pancreaticogastrostomy has been reintroduced as a useful alternative procedure to pancreaticojejunostomy after Whipple resection or pylorus-preserving pancreaticoduodenectomy because of the very low incidence of leakage and disruption. In this study, gastric acid secretion, serum gastrin level, and 24-hr dual gastroduodenal pH after pancreaticogastrostomy were examined on the assumption that a canine model was a pylorus-preserving pancreaticoduodenectomy. Basal acid output (BAO), maximal acid output (MAO), and dual gastroduodenal pH were measured in eight dogs with gastric fistula. After pancreaticogastrostomy, BAO levels showed a slight increase significantly, but MAO levels showed no change. Serum gastrin levels in the fasting and postprandial states showed the similar patterns between before and after surgery. In the 24-hr dual gastroduodenal pH monitoring, gastric pH and duodenal pH also did not change in the fasting and postprandial states. These results suggested that the maintenance of the normal gastric pH after pancreaticogastrostomy was caused by a little increase of BAO, and the neurohumoral relationship between the stomach, duodenum, and pancreas was preserved even after pancreaticogastrostomy. Therefore, the pancreaticogastrostomy is a recommendable reconstructive procedure physiologically after pylorus-preserving pancreaticoduodenectomy.

Inhibitory effect of PYY on vagally stimulated acid secretion is mediated predominantly by Y1 receptors

Two molecular forms of peptide YY (PYY), PYY-(1--36) and PYY-(3--36), are abundant in rabbit intestine and blood. We have previously shown that PYY-(1--36) (PYYI) activates equipotently Y1 and Y2 receptors and PYY-(3--36) (PYY II) is a highly selective agonist for Y2 receptors. In the present study, we examined the effect of exogenous infusion of PYY on vagally stimulated gastric acid secretion in awake rabbits with chronic gastric fistula. To determine the specific PYY receptor(s) that mediates this effect, we used a highly selective Y1 agonist, Pro34-PYY, a synthetic PYY, and a Y2-selective agonist, PYY II. Vagal stimulation of acid secretion was elicited by an intravenous bolus injection of insulin (0.125 U/kg) 30 min after beginning a 180-min intravenous infusion of either PYY I, PYY II, or [Pro34]-PYY after a 50 micrograms/kg i.v. bolus of atropine followed immediately by a 500 micrograms/kg sc injection. During infusion of 200 pmol.kg 1.h-1 PYY I, acid output was significantly inhibited to 45 +/- 13% of maximum acid output 60 min after injection of insulin. Similarly, acid output during infusion of 200 pmol.kg-1.h-1 [Pro34]-PYY was significantly inhibited to 52 +/- 12% of maximum. In contrast, acid output during infusion of 200 pmol.kg-1.h-1 of PYY II was not significantly inhibited (101 +/- 18% of maximum). Infusion of double the dose (400 pmol.kg-1.h-1) of PYY II resulted in acid inhibition (51 = 15% of maximum), whereas infusion of the same dose did not significantly enhance acid inhibition by infusion of either PYY I or [Pro34]-PYY (28 +/- 11 and 42 +/- 15% of maximum). These results indicate that PYY, acting predominantly at Y1 receptors, is a potent inhibitor of vagally stimulated acid secretion in adult rabbits.

Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease

Background & Aims : The mechanism by which Helicobacter pylori predisposes to duodenal ulcers (DUs) remains unclear. The aim of this study was to investigate the effect of the infection on acid secretion. Methods : Acid output was examined basally and in response to gastrin-releasing peptide (GRP) and gastrin in healthy volunteers with and without H. pylori infection and in patients with DUs before and after eradication of the infection. Results : Compared with H. pylori-negative healthy volunteers, patients with DUs with H. pylori had the following abnormalities of acid secretion: (1) threefold increase in basal acid output, (2) sixfold increase in acid response to GRP, (3) increased maximal acid response to exogenous gastrin, (4) increased ratio of basal acid output to maximal gastrin-stimulated output, and (5) increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output. All of these abnormalities resolved fully after H. pylori eradication except for increased maximal acid output to gastrin, which was unchanged. Infected healthy volunteers showed a threefold increase in acid response to GRP that resolved after eradication of H. pylori infection. Conclusions : These disturbances in acid secretion caused by H. pylori infection are consistent with impaired inhibitory control and are likely to be relevant to the mechanism by which the infection predisposes to DU.

Regulation of murine acid secretion by CO2

To determine whether endogenous metabolic sources alone provide sufficient CO2 for acid secretion in mammals, basal and stimulated acid secretion and metabolic CO2 production were measured concurrently in mouse stomachs, in vitro, without exogenous CO2, and after addition of 5% CO2 serosally. Basal acid secretion was varied by changing luminal pH from 3.2 to 4.0. In the absence of an exogenous supply of CO2 acid secretion was stable under basal conditions and increased during cholinergic stimulation with carbachol. Serosal CO2 supply increased basal and stimulated acid secretion. The increase in basal acid secretion depended on the initial level of acid secretion. At pH 4.0, exogenous CO2 increased acid output (mean +/- SD) by 13% from 112 +/- 11 nmol/min to 126 +/- 8 nmol/min (P < 0.03), whereas at pH 3.6 the increase was 40% (63 +/- 14 to 88 +/- 20 nmol/min, P < 0.04) and 157% at pH 3.2 (21 +/- 13 to 54 +/- 14 nmol/min, P < 0.002). Following cholinergic stimulation a maximal acid output of 321 +/- 38 nmol/min was attained without serosal CO2, whilst addition of 5% CO2 to the serosal solution increased maximal acid secretion by 49% to 479 +/- 96 nmol/min (P < 0.005). Metabolic activity, measured as total gastric CO2 production, was greater as acid secretion rates increased [239 +/- 20 nmol/min at 21 +/- 13 nmol/min (luminal pH 3.2) versus 406 +/- 28 nmol/min at 321 +/- 17 nmol/min (after cholinergic stimulation)]. The data support the concept that basal and sub-maximal acid secretion can be maintained by CO2 available from metabolic sources, but full expression of the acid secretory apparatus requires exogenous CO2.

Incidence and risk factors of duodenal ulcer. A retrospective cohort study.

We evaluated the incidence and risk factors of duodenal ulcer (DU) in a cohort of patients who had undergone esophagogastroduodenoscopy in our institution from 1978 to 1982, without then finding a gastric or duodenal ulcer. Six hundred and twenty-one subjects entered the study, and 526 (84.7%) were traced in 1992. Forty-one cases of DU were found, an incidence rate of 6.7 per 1,000 person-years; the male/female ratio was 2:1. The diagnoses of peptic ulcer (PU) were validated by means of medical documentation. The odds ratio of DU was 2.3 (95% confidence interval 0.8-6.3) and 3.5 (1.4-9.0) in the II and III tertile of basal acid output (BAO) compared with the I tertile, and 2.6 (0.8-8.3) and 7.0 (2.3-20.7) in the II and III tertile of maximal acid output (MAO) compared with the I tertile. Cigarette smoking and the presence of PU among siblings of DU patients were risk factors for DU. Multiple logistic regression confirmed only the association of DU with MAO, cigarette smoking, and family history. By means of a nested case-control study, the risk of developing DU was assessed in subjects with Helicobacter pylori (HP) at the biopsy of gastric mucosa performed before the ulcer diagnosis. The odds ratio of DU in HP-positive subjects was 5.0 (95% confidence interval 0.6-45). The results of this study confirm the influence of gastric acid secretion, cigarette smoking, and family history in the pathogenesis of DU and suggest that HP infection not only favors relapse but could have an important role in the onset of the disease.

Helicobacter pylori infection, serum gastrin, and gastric acid secretion in teen-age subjects with duodenal ulcer, gastritis, or normal mucosa.

Many studies have confirmed the close association of Helicobacter pylori with duodenal ulcer (DU) in adults. However, in the subtype of DU known as 'childhood' or 'early onset DU' genetic factors seem to play a prominent role in the pathogenesis. The aim of this study was to investigate the prevalence of H. pylori in teen-age subjects with DU, gastritis, and normal mucosa and to examine the relationship of H. pylori to serum gastrin levels and gastric acid secretion. Sixty-one teen-age subjects (24 with DU, 14 with gastritis, and 23 normal subjects) were investigated for the presence of H. pylori, antral histology, gastrin levels, basal acid output (BAO), and maximal acid output (MAO). All 24 patients with DU and 8 of 14 with gastritis were infected with H. pylori; none of the normal subjects were infected. Mean gastritis scores and fasting serum gastrin levels were significantly higher in patients with DU or H. pylori-positive gastritis than in subjects with H. pylori-negative gastritis or normal mucosa (p < 0.05). The difference in serum gastrin levels was also significant when patients with DU were compared with those with H. pylori-positive gastritis (p < 0.05). BAO and MAO were significantly higher in patients with DU than in subjects with H. pylori-positive gastritis or normal mucosa (p < 0.05), but there was no difference between subjects with H. pylori-positive gastritis and those with normal mucosa. H. pylori infection is associated closely with teen-age DU and gastritis and with hypergastrinemia but does not affect BAO and MAO in most infected teen-age subjects.

Esophageal Function and Occurrence of Barrett’s Esophagus in Zollinger-Ellison Syndrome

Manifestations of esophageal disease are present in up to 60% of patients with Zollinger-Ellison syndrome (ZES), although esophageal function has been studied in only a few patients and the prevalence of Barrett's mucosa is unknown in these patients. It is unclear whether the high prevalence of esophageal disease is related to gastric acid hypersecretion alone or to abnormalities of esophageal motility or lower esophageal sphincter (LES) function in addition. To address these issues in the present study esophageal function was evaluated prospectively in 92 consecutive patients with ZES (66 with active disease, 26 disease-free after curative resection) seen during a 1-year period after controlling acid hypersecretion. In the patients with active disease the mean basal acid output (BAO) was 33 +/- 3.0 mEq/h, the maximal acid output (MAO) was 56 +/- 4.0 mEg/h, fasting serum gastrin was 8,736 +/- 4,813 pg/ml and duration of disease prior to study was 12.5 +/- 2.0 years. At the time of manometry, gastric acid secretion was controlled in all patients and no patient had evidence of gastroesophageal reflux disease at upper gastrointestinal endoscopy. Esophageal manometry revealed normal motility in 85% of patients. Eleven percent had low LES pressures, and only 1% of patients had an elevated LES pressure. The frequency of Barrett's mucosa (3%) was similar to that found in the general population but much less than that reported in patients with idiopathic GERD. No correlation was noted between LES pressures or manometric abnormalities and the fasting serum gastrin, BAO, MAO or the presence or absence of multiple endocrine neoplasia type I or previous vagotomy. Esophageal manometric results and LES pressure were similar in disease-free patients and those with active ZES. In conclusion, these results suggest that hypergastrinemia or other disease-specific abnormalities are not contributing to the high incidence of esophageal disease in patients with ZES because esophageal function in patients with ZES is similar to normals. Specifically, motility disorders in patients with ZES occur in similar frequency to normals, and LES pressure is normal in most patients. Despite the high levels of acid secretion and prominence of symptoms, the occurrence of Barrett's mucosa was uncommon (3%) raising the possibility of additional protective mechanisms in patients with ZES.

Activation of somatostatin receptor subtype 2 inhibits acid secretion in rats.

Somatostatin is a potent inhibitor of gastric acid secretion. Recently, at least five distinct somatostatin receptor subtypes (SSTR) have been characterized and evaluated using relatively selective peptide analogues of somatostatin. We sought to determine which somatostatin receptor subtypes are involved in peripheral regulation of gastric acid secretion. Fasted, male Sprague-Dawley rats were anesthetized and were implanted with a double-lumen cannula in the stomach. Acid secretion was measured in gastric samples collected every 10 min by backtitration to pH 7. After a 30-min basal period, a 2-h intravenous infusion of pentagastrin (24 micrograms.kg-1.h-1 i.v.) was started. During the second pentagastrin hour, a 1-h intravenous infusion of either vehicle (0.1% canine serum albumin in 0.9% saline) or somatostatin receptor agonists was begun. The somatostatin receptor agonists included peptides with relative specificity for SSTR1-5 (somatostatin-14; 10 nmol.kg-1.h-1); SSTR2, SSTR3, and SSTR5 [SMS-(201-995); 10 nmol.kg-1.h-1]; SSTR2 (1-1,000 nmol.kg-1.h-1); SSTR3 (10-1,000 nmol.kg-1.h-1); and SSTR5 (10-1,000 nmol.kg-1.h-1). The SSTR2 agonist decreased pentagastrin-stimulated acid secretion dose dependently, from 82 +/- 7% of maximum acid output at 1 nmol.kg-1.h-1 to 4 +/- 7% of maximum at 100 nmol.kg-1.h-1. At 10 nmol.kg-1.h-1, the SSTR2 agonist inhibited acid secretion (40 +/- 7% of maximum) similarly to somatostatin (37 +/- 4% of maximum) and SMS-(201-995) (31 +/- 4% of maximum). The SSTR2 agonist inhibited acid secretion approximately 10- to 100-fold more potently than either the SSTR3 or the SSTR5 agonist. These results indicate that somatostatin regulates gastric acid secretion by activation of SSTR2 receptors.

Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis.

This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

Duodenal ulcer, Helicobacter pylori, and gastric secretion.

Patients with chronic dyspepsia were categorised by macroscopic appearance at oesophagogastroduodenoscopy as having duodenal ulceration (DU), other diagnosed lesions such as reflux oesophagitis, carcinoma of stomach, etc, or no organic lesion (non-ulcer dyspepsia, NUD). Material was collected to identify gastric infection with Helicobacter pylori (H pylori) by CP urease test, culture, and histological examination and to make the microscopic diagnosis of active chronic gastritis. Each patient in the DU and NUD categories was then invited to volunteer for a gastric secretion study in which maximal gastric secretion in response to histamine was measured. Sixty two gastric secretion tests were performed (31 DU, 31 NUD). The presence of H pylori was associated with active chronic gastritis (100%). DU patients secreted more acid than the NUD patients. H pylori positivity was associated with decreased maximal gastric secretion in both groups. There was a positive correlation between smoking and maximal acid output shown only in H pylori negative but not in H pylori positive patients. These findings were clear cut when all corrections of maximal gastric secretion were made for pyloric loss, duodenogastric reflux, and stature. This study failed to show any aetiological link between H pylori and DU by increased maximal gastric secretion.

Relationship Between Helicobacter pylori Infection and Gastric Acid Secretion in Young Healthy Subjects

We studied the relationship between Helicobacter pylori (H. pylori) infection and gastric acid secretion, along with fasting serum gastrin levels, in 55 asymptomatic healthy volunteers under 30 years old (29 H. pylori-positive, 26 H. pylori-negative). Mean scores of antral gastritis were significantly higher in H. pylori-positive subjects than in H. pylori-negative subjects. There was no significant difference in both basal and maximal acid output between H. pylori-positive and H. pylori-negative subjects. Fasting serum gastrin levels were significantly higher in H. pylori-positive subjects than in H. pylori-negative subjects. Sex did not significantly affect gastritis scores, gastric acid secretion, or fasting serum gastrin levels, although maximal acid output was slightly higher in H. pylori-negative men than in H. pylori-positive men. Our results suggest that H. pylori infection has no direct effect on gastric acid secretion in young healthy subjects, although it induces hypergastrinemia.

Comparison of roxatidine and ranitidine in the treatment of refractory duodenal ulcer

Fourteen patients with duodenal ulcer not healed after treatment with ranitidine at the standard dosage of 300 mg/day for 12 weeks were enrolled in the study. Eight patients were treated with roxatidine acetate, 150 mg/day, for 8 weeks (group A); six patients received treatment with ranitidine, 600 mg/day, for 8 weeks (group B). Efficacy of treatment was evaluated on the basis of reduction of ulcer pain, lowering of maximal acid output (MAO) levels, and cicatrization of ulcer lesion. The patients treated with roxatidine showed a significant reduction in MAO levels after 4 weeks, whereas the patients treated with ranitidine showed a significant reduction in MAO levels after 8 weeks. The differences in reduction of ulcer pain or cicatrization percentage were not significant between groups.

Helicobacter pylori Infection in Children with Antral Gastrin Cell Hyperfunction

SummaryAntral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a gastrin‐producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp) infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations were investigated in six children presenting with gastrointestinal bleeding of unknown origin, sideropenic anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid output (BAO), maximal acid output (MAO), and pentagastrin‐stimulated acid output (PAO). Circulating pepsinogen I was also significantly increased. Three children had Hp infection, as assessed by enzyme‐linked immunosorbent assay, urease test, and histology. Endoscopy showed duodenal erosions in three children, with ulcer in two Hp‐positive cases. At histology, moderate gastritis was observed only in the three Hp‐positive cases. In all patients, quantitative assessment of antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP infection as an overlapping factor complicating the clinical picture in some cases.

Hemorrhagic duodenal ulcer disease: Clinical and biochemical findings in a case-control pilot study

A retrospective study of 31 consecutive bleeding duodenal ulcer (DU) patients and, as controls, 62 active DU subjects without bleeding episodes was conducted in order to ascertain whether bleeding DU patients have particular clinical or functional characteristics. The patients were followed for 15.6 and 17.4 months, respectively, after diagnosis. The following parameters were taken into account: sex, age, family history of ulcer, blood group (ABO system), ulcer pain, nonsteroidal anti-inflammatory drug (NSAID) consumption, cigarette smoking, alcohol and coffee consumption, ulcer site, fasting serum gastrin and pepsinogen group A, basal acid output (BAO), and maximal acid output (MAO). Statistics were gathered using the Student's t test and Fisher's exact test. Bleeding DU patients had less ulcer pain ( P < 0.005) and used more NSAIDs ( P < 0.05) than controls. All other clinical and functional data considered in both groups were comparable. Results showed that NSAID consumption was very dangerous in our DU patients even though bleeding episodes were observed. Usually no pain is felt immediately before hemorrhage, and cigarette smoking does not appear to affect this complication of DU.

Thrice-yearly rhythm of duodenal ulcer disease

Various studies have emphasized a periodic trend in ulcer disease, with a higher incidence of relapse, complications, and painful symptoms in spring and autumn for duodenal ulcer (DU) and in winter for gastric ulcer (GU). It has been suggested that this seasonal trend may be linked with experimentally demonstrated year-round rhythmic changes in gastric acid output. This study retrospectively evaluated the seasonal nature of ulcer activity, symptoms, and complications in 293 endoscopically diagnosed patients (52 GU: 20 women, 32 men, mean age 56 years, range 22 to 82 years; 241 DU: 56 women, 185 men, mean age 51 years, range 21 to 87 years) with a mean follow-up of 20.3 months. Relapses occurred in 27% of the GU and 22% of the DU cases, and complications occurred in 6% of the GU and 12% of the DU cases. Clinical endoscopic check-ups were repeated every 6 to 12 months. A record was kept of alcohol and coffee intake, smoking habits, symptoms at time of diagnosis and check-up, endoscopic results, relapses, remission, and complications. Statistical analysis was made by Student's t test and the chi-square test. On diagnosis, 63% of patients reported a seasonal trend in symptoms (68% in the DU group and 44% in the GU group). During follow-up, painful symptoms occurred mainly in February, June–July, and October in DU cases whereas in GU cases the picture was more varied. Endoscopy revealed that in DU cases symptoms were closely related to activity, found mainly in February, May, and October. As for complications, no significant difference was found at different times of the year for either DU or GU cases. This study confirmed a thrice-yearly trend in DU (probably linked with the year-round rhythm demonstrated for basal acid outputs and maximal acid outputs), but no such seasonal trend for GU (although the low number of GU cases studied may influence this finding). These data may have useful therapeutic implications for a tailored seasonal maintenance therapy, thus ensuring better relapse prevention and avoiding unnecessary expense.