Asunto(s)

Asunto(s)

RESUMEN

The previously accepted role of gastric acid hypersecretion in peptic ulcer disease has been modified by studies showing no correlation between acid output and clinical outcome of ulcer disease, or between ulcer recurrence rate after vagotomy and preoperative acid secretion. At the same time, studies have been unable to demonstrate increased acidity in the duodenal bulb in patients with duodenal ulcer, and consequently more emphasis has been given to the mucosal protecting mechanisms. The existence of an active gastric and duodenal mucosal bicarbonate secretion creates a pH gradient from the luminal acid to near neutrality at the surface of the epithelial cells, thereby acting as an important mucosal defence mechanism. The regulation of bicarbonate secretion is a complex process related to motility and neural activity. Stimulation is by acid, PGE2, NO, VIP, cAMP, and mucosal protective agents. Bicarbonate secretion is inhibited by atropine, muscarinic antagonists, alpha-adrenoceptor agonists, indomethacin, bile acids, tobacco smoking, and probably also by infection by Helicobacter pylori. Apart from mucus and bicarbonate, the mucosal defence is supported by a hydrophobic epithelial lining, rapid cell removal and repair regulated by epidermal growth factor. Sufficient mucosal blood flow, including a normal acid/base balance, is important for subepithelial protection. In today's model of ulcer pathogenesis, gastric acid and H. pylori work in concert as aggressive factors, with the open question being: why does only a fraction of the infected population develop an ulcer?

Asunto(s)

RESUMEN

Tests for the detection of Helicobacter pylori differ in many respects. The choice of test depends on the clinical situation. In symptomatic patients, endoscopy is an important tool for diagnosing peptic ulcer disease or other gastroesophageal lesions. A biopsy-based detection system for H. pylori, such as the rapid urease test, microscopy or culture of the organisms, is therefore appropriate. The diagnostic sensitivity will increase if more than one of these is performed. In asymptomatic patients, a non-invasive test should be used, and serology with a titre is suitable in this situation. If the results prove positive, confirmation of H. pylori infection is recommended using a urea breath test. Patients who have previously received H. pylori eradication therapy and present with a recurrence of symptoms should receive further eradication therapy if they are still H. pylori-positive, even if no endoscopic abnormality is found. A non-invasive test should be used and the urea breath test is the best option in these individuals, as serology is not suitable within 6-12 months of eradication therapy. If the breath test is unavailable, a biopsy-based test should be used. The outcome of H. pylori eradication therapy should be assessed using a non-invasive test. The urea breath test is appropriate, as serology is not suitable post-treatment. The breath test should be performed 4-8 weeks after the end of treatment to avoid false-negative results caused by temporary suppression of the infection. If the breath test is unavailable, a serology with a titre or a biopsy-based test must be used, at least 6-12 months after the end of treatment.

Asunto(s)

RESUMEN

Helicobacter pylori infection is now recognized as the cause of most cases of chronic gastritis, and a major causal factor in peptic ulcer disease. However, though the presence of intragastric bacteria has been recognized for many years, the connection between H. pylori and peptic ulcers has only been established during the last decade. Pathological studies have suggested that intragastric bacteria damage the gastric mucosa, reducing its resistance to acid, while epidemiological studies have suggested that a non-physiological factor, such as bacterial infection, is involved in the development of peptic ulcer. Subsequently, H. pylori, associated with chronic gastritis, was identified in gastric biopsies from patients with peptic ulcer. Eradication of H. pylori has been shown to reduce the recurrence of peptic ulcer after ulcer healing, and such treatment is now widely accepted.

Asunto(s)

RESUMEN

BACKGROUND: The activity of duodenal ulcer disease varies not only between patients but also from time to time within patients, and earlier studies have concluded that the disease 'burns out' in many cases. It was the aim of this study to examine duodenal ulcer disease activity over a long period, to determine whether the degree of activity is stable within the individual patient. METHODS: A cohort of 145 patients with a first-time duodenal ulcer diagnosed in our department between 1980 and 1985 were followed up for 7 years. The patients' self-reported use of acid-inhibitory drugs was taken as a measure of disease activity. RESULTS: Twenty-eight per cent of the patients had no or minimal ulcer symptoms during the 7 years after healing of the index ulcer, whereas 13% had maximal activity with frequent or continuous use of acid-inhibitory drugs every year or ulcer surgery. A total of 11 patients were operated on because of severe ulcer symptoms or complications to the ulcer disease. The disease activity during the first 2 years after diagnosis did not change much during the following 5 years in most of the patients. CONCLUSIONS: The course of duodenal ulcer disease during the first 2 years after diagnosis was a predictor of the long-term prognosis with a predictive value of approximately 70%, which may be considered satisfactory for decision-making in some clinical situations.

Asunto(s)

RESUMEN

The aim of this study was to test the hypothesis that infection with Helicobacter pylori is essential for recurrence of duodenal ulcer. We performed a randomized controlled trial of the relapse rate of duodenal ulcer during 12 weeks treatment with penicillin V or placebo in 170 out-patients from five centres. The relapse rate was 9% during treatment with penicillin and 50% with placebo, P < 0.0001. It is concluded that infection with penicillin-sensitive bacteria, i.e. H. pylori, plays an important role for recurrence of duodenal ulcer disease. Penicillin V suppresses this infection but does not eradicate it.

Asunto(s)

RESUMEN

The introduction of anti-Helicobacter pylori therapy has increased the number of options available for the management of patients with duodenal ulcer disease. The aim of this paper is to summarize current knowledge and use it to form a strategy relevant to the management of patients with duodenal ulcer disease. Four key aspects are addressed. (i) Selection of duodenal ulcer patients for anti-H. pylori treatment. As the subgroup of patients who will develop minor disease activity in the future cannot be identified with sufficient precision, and the therapeutic gain achieved by curing H. pylori infection is significant, all patients with duodonal ulcer and H. pylori infection should receive eradication therapy. (ii) Confirmation of H. pylori infection before eradication. A diagnostic test confirm H. pylori infection is useful in identifying the small group of H. pylori-negative duodenal ulcer patients with nonsteroidal anti-inflammatory drug (NSAID)-induced ulcer or Zollinger-Ellison syndrome. (iii) Choice of treatment. This should be based on efficacy of eradication, rate of ulcer healing and symptom resolution, adverse effects profile, simplicity and cost. At present, there are four effective eradication therapies documented: omeprazole plus amoxycillin or clarithromycin; omeprazole, amoxycillin and metronidazole; 'classic' triple therapy (bismuth, amoxycillin (or tetracycline) and metronidazole); and ranitidine, amoxycillin and metronidazole. (iv) Confirmation of eradication after treatment. This is needed in cases in which the chosen therapy has an efficacy below 80-90%. The test is important to identify those patients who require repeated treatment, before they present with an ulcer relapse.

Asunto(s)

RESUMEN

Eradication of Helicobacter pylori is associated with a reduced recurrence of duodenal ulcer (DU). The relationship between H. pylori and DU has been interpreted as causal, but the evidence has been criticized for methodologic reasons. To ascertain whether an antibiotic with no effect on epithelial-cell integrity prevents DU recurrence, we conducted a randomized double-blind trial of phenoxymethylpenicillin (PEN), 2.4 twice daily, and placebo (PLA). Patients with an active DU and positive H. pylori culture from antral biopsy specimens were treated with 40 mg omeprazole daily for 4 weeks, but at week 2 they were allocated at random to PEN (85 patients) or PLA (85 patients) for up to 14 weeks. Those without recurrence during this treatment were followed up for another 6 months. Endoscopy and H. pylori culture were performed at the end of the treatment period and at the end of follow-up, and in between if ulcer symptoms recurred. During the treatment period the ulcer relapse rate was 5 of 58 (9%) in the PEN group and 34 of 68 (50%) in the PLA group (P < 0.0001, log-rank test), with 53% and 14%, respectively, of the patients in the two groups being H. pylori-negative. The relapse rate in the PEN group did not differ between H. pylori-negative and H. pylori-positive patients. The recurrence rate in the PEN group remained low for another 5 months but then approached the rate in the PLA group. The prevalence of H. pylori-negative patients at the end of follow-up was 20% in the PEN group and 10% in the PLA group. These data provide strong evidence that DU has a bacterial cause, with H. pylori as the likely agent.

Asunto(s)

RESUMEN

In contrast to the steady low intragastric pH, the pH in the proximal duodenum shows wide, rapid, and frequent fluctuations. This change in pH pattern may be used to localize the pylorus and thereby ensure reproducible measurements of duodenal pH at a known and reproducible distance from the pylorus. To validate this method of localizing the pylorus, simultaneous measurements were performed of the transpyloric pH and potential difference (PD) profile and of the pH and pressure profile in 10 normal subjects. pH-metry and PD-metry localized the pylorus within the same 1.5 cm in 82% of 104 5-min periods, and pH-metry and manometry localized the pylorus within the same 5 cm in 72% of 77 10-min periods. This agreement and accuracy seem satisfactory for most studies of intraluminal pH in the duodenum and make reliable long-term ambulatory recording of duodenal pH possible without serial roentgenogram controls.

Asunto(s)

RESUMEN

To investigate the course of postprandial lipid solubilization in nine patients with chronic, alcoholic pancreatitis, luminal contents were aspirated from the proximal part of the jejunum for 180 min after a meal containing 1.5% fat. Six of the patients had pancreatic insufficiency, whereas three patients were without insufficiency. pH was measured continuously at two sites: at the level of the papilla of Vater and the aspiration site. The fraction of bile acids in the micellar phase of the jejunal aspirates correlated positively to both pH in the aspirates (p less than 0.05) and the fraction of fat solubilized (p less than 0.02). pH was below 4.0 for a longer period of time in the patients with insufficiency, compared to the patients without. However, pH fluctuated rapidly, and there was no correlation between the continuously measured values at the aspiration site and values in the aspirates. Lipid solubilization was not correlated to the lipase activity in the aspirates. We conclude that acidic bile acid precipitation most likely plays a dominant role in the pathophysiology of pancreatic steatorrhea although the methods available are too crude to disclose the precise course of events.

Asunto(s)

RESUMEN

This study tests the hypothesis that reactivation of a latent herpes simplex virus infection may be a cause of recurrent duodenal ulceration. Patients with recently healed duodenal ulcer were entered into a double blind, randomised study of maintenance treatment with the antiviral drug acyclovir (400 mg bid) versus placebo, to determine if suppression of herpes virus infection would influence the natural history of the ulcer disease. One hundred and fifteen patients entered the trial and 76 patients completed it according to the protocol. Endoscopy was performed when ulcer symptoms recurred and at the end of the 25 week trial period. In the acyclovir group the cumulated relapse rate was 63% compared with 56% in the placebo group (NS). This result suggests that reactivation of herpes simplex virus is not a cause of recurrent duodenal ulcer.

Asunto(s)

RESUMEN

Intraluminal pH was measured simultaneously in the stomach and duodenal bulb with six small, glass electrodes tied together at 1.5-cm intervals. Ten patients with duodenal ulcer disease were studied under fasting conditions and for 3 h after a standard liquid meal on three occasions: day 1, before treatment; day 8, when the proton pump blocker omeprazole had been taken in a daily dose of 30 mg for 7 days consecutively, including the day of the pH study; day 9, 24 h after the last dose of omeprazole. Mean hydrogen ion activity and the percentage of time with pH below 3 was calculated from the digital pH data sampled at a frequency of 1 per second from each electrode. On day 8, five of the patients were permanently anacidic (pH greater than 4) in the stomach and duodenum, while the food-stimulation broke off anacidity for shorter periods in the other five patients. The pH pattern in the duodenal bulb was markedly altered in all patients with disappearance of the typical pH fluctuations, and a decrease in the time that the pH was below 3 from a median value of 30% before treatment to 0% in seven patients and close to 0% in three patients. On day 9, a large patient-to-patient variation was observed in gastric pH: three patients were still anacidic, four were markedly suppressed, but three patients reached near pre-treatment acidity. Duodenal bulb acidity was still decreased significantly on day 9 in all patients, with post-prandial pH below 3 for less than 5% of the time, compared with 30% before treatment.

Asunto(s)

RESUMEN

Gastric and duodenal bulb pH was measured simultaneously with a multiple pH electrode system in 15 duodenal ulcer patients. A single dose of 10 ml antacid was given 120 min after a liquid standard meal, and the pH was measured for another 90 min. The effect of antacid on duodenal pH, expressed as the time pH is kept above 3.0, was on an average 60 min--shorter in patients with a high gastric acid secretion and longer in normosecretors (p less than 0.01). Regression analysis of simultaneously measured gastric and duodenal bulb pH after antacid showed a highly significant linear correlation with a slope of 1.43, which is significantly greater than 1.0 (p less than 0.01), indicating that antacid has a more pronounced effect on duodenal pH than on gastric pH.

Asunto(s)

RESUMEN

We conducted a six week double blind randomised study of 176 patients with prepyloric gastric ulcer to determine whether the proton pump inhibitor, omeprazole 30 mg daily would accelerate healing and pain relief, as compared with cimetidine 1 g daily. At two, four, and six weeks after entry ulcers healed in a larger percentage of patients treated with omeprazole (54, 81, and 86%) than of those treated with cimetidine (39, 73, and 78%) ('intention to treat' cohort; p less than 0.05 at two weeks). A higher proportion of patients on omeprazole became free of pain during the first week of treatment (p less than 0.05). No major clinical or biochemical side effects were noted. Omeprazole is an efficient treatment for patients with prepyloric gastric ulcers.

Asunto(s)

RESUMEN

Using data from published clinical trials of acid inhibitory drugs it can be shown that a linear relationship exists between the rate of ulcer healing and the degree of acid inhibition. Since the data used to demonstrate this relationship are group averages of acid reduction and of healing rate, and since there are known to be great individual variations in sensitivity to acid inhibitory drugs as well as in healing rate, it seems likely that the individual relationship between pharmacologic acid inhibition and increase in rate of ulcer healing is different from that which comes out of meta-analysis. Future identification of individual healing curves may form basis for individualized medical treatment in duodenal ulcer diseases.

Asunto(s)

Asunto(s)

RESUMEN

The diagnostic value of gastric secretion tests has been found to be lower than what was previously believed. Thus basal and stimulated acid output is normal in most ulcer patients, and this is also so for gastric and duodenal pH. Gastric acid secretion does not separate patients with rapid recurrence after medical treatment from those with a long period of remission, and acid secretion is usually not higher in patients with recurrence after vagotomy than in patients without relapse. Today a gastric acid secretion test is used in patients suspected of the Zollinger-Ellison syndrome and it seems also to be valuable in ulcer patients who do not respond clinically satisfactory to medical treatment.

Asunto(s)

RESUMEN

Intraluminal pH was measured simultaneously in the human stomach and proximal duodenum with six small glass electrodes tied together at 1.5-cm intervals. Twenty-four healthy control subjects and 44 patients with duodenal ulcer disease were studied under fasting conditions and for 3 h after a standard liquid meal. Mean and median hydrogen ion activity, percentage of time with pH below 2 and 3, and the frequency of pH fluctuations were calculated from digital pH data sampled at a frequency of once per second from each electrode. None of these measurements of acidity differed significantly between the two groups or between subgroups of normosecretor controls and hypersecretor ulcer patients. At the time of pH study 15 of the patients had endoscopically verified active ulcer disease and 13 patients were without disease activity. Gastric as well as duodenal bulb acidity was the same in these two subgroups. We conclude that even though duodenal ulcer patients deliver more acid into the duodenum, this does not cause increased luminal acid aggression.

Asunto(s)

RESUMEN

In situ pH was measured simultaneously with microelectrodes in the stomach, duodenal bulb, midduodenum, duodenojejunal junction, and proximal jejunum. Fourteen healthy subjects and 8 patients with exocrine pancreatic insufficiency were studied under fasting conditions and for 3 h after a standard liquid meal. The luminal pH gradient was steepest in the proximal 10 cm of the duodenum, where acidity was reduced from pH 2 to pH 5 in the fasting state and from pH 1.7 to pH 4.3 in the second and third postprandial hour. Acidity was further reduced in the distal duodenum to a pH between 5 and 6 at the duodenojejunal junction. The frequent wide and rapid pH fluctuations seen in the duodenal bulb were gradually reduced along the duodenum and became rare in the jejunum. In patients with pancreatic insufficiency, duodenal or jejunal acidity did not differ significantly from the controls, with the exception of the single 10-min period occurring 70-80 min after the meal when duodenal bulb pH was 2.1 as compared with 3.1 in the normal subjects (p less than 0.05). All patients, including 2 patients with a very high duodenal acidity, demonstrated a duodenal pH gradient as steep as that found in the normal subjects, indicating sources of bicarbonate other than the pancreas.

Asunto(s)