Histological evaluation of chronic pancreatitis by endoscopic ultrasound-guided fine needle biopsy.
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Adult↗
Biomedical subjects
J E Dominguez-Muñoz
Publications and source records attributed to J E Dominguez-Muñoz.
H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer.
BACKGROUND: Peptic ulcer is the main cause for upper gastrointestinal haemorrhage, and Helicobacter pylori infection is the main etiologic factor for peptic ulcer disease. Maintenance antisecretory therapy has been the standard long-term treatment for patients with bleeding ulcers to prevent recurrent bleeding. On the other hand, the precise efficacy of H. pylori eradication for the prevention of rebleeding from peptic ulcer is unknown. OBJECTIVES: To compare the efficacy of H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register (the Cochrane Library issue 4, 2003), MEDLINE (January 1966 to January 2004), EMBASE (January 1988 to January 2004), CINAHL (January 1982 to January 2004), and reference lists of articles. We also conducted a manual search from several congresses. SELECTION CRITERIA: Controlled clinical trials comparing the efficacy of H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. DATA COLLECTION AND ANALYSIS: Extraction and quality assessment of studies were done by two reviewers. Study authors were contacted for additional information. MAIN RESULTS: Seven studies with a total of 578 patients were included in the first meta-analysis: mean percentage of rebleeding in H. pylori eradication therapy group was 2.9%, and in the non-eradication therapy group without subsequent long-term maintenance antisecretory therapy it was 20% (OR 0.17, 95% CI 0.10 to 0.32; there was no statistical evidence of heterogeneity; NNT was 7, 95% CI 5 to 11). Three studies with a total of 470 patients were included in the second meta-analysis: mean percentage of rebleeding in H. pylori eradication therapy group was 1.6%, and in non-eradication therapy group with long-term maintenance antisecretory therapy it was 5.6% (OR 0.25, 95% CI 0.08 to 0.76; heterogeneity was not demonstrated; NNT was 20, 95% CI 12 to 100). SUBANALYSIS: Excluding patients taking non-steroidal anti-inflammatory drugs (NSAIDs) at the time of recurrent bleeding resulted in a rebleeding rate of 2.7% (first meta-analysis) or 0.78% (second meta-analysis) in the group receiving H. pylori eradication therapy. When only patients with H. pylori eradication success were included, rebleeding rate was 1.1% in H. pylori eradication therapy group, and NNT decreased from 7 to 6. In some cases, recurrence of H. pylori infection seemed to be responsible for recurrence of bleeding. REVIEWERS' CONCLUSIONS: Treatment of H. pylori infection is more effective than antisecretory non-eradicating therapy (with or without long-term maintenance antisecretory therapy) in preventing recurrent bleeding from peptic ulcer. Consequently, all patients with peptic ulcer bleeding should be tested for H. pylori infection, and eradication therapy should be prescribed to H. pylori-positive patients.
Anti-Ulcer Agents↗
H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer.
BACKGROUND: Peptic ulcer is the main cause for upper gastrointestinal haemorrhage, and Helicobacter pylori infection is the main etiologic factor for peptic ulcer disease. Maintenance antisecretory therapy has been the standard long-term treatment for patients with bleeding ulcers to prevent recurrent bleeding. On the other hand, the precise efficacy of H. pylori eradication for the prevention of rebleeding from peptic ulcer is unknown. OBJECTIVES: To compare the efficacy of H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register (the Cochrane Library issue 1, 2003), MEDLINE (January 1966 to March 2003), EMBASE (January 1988 to March 2003), CINAHL (January 1982 to March 2003), and reference lists of articles. We also conducted a manual search from several congresses. SELECTION CRITERIA: Controlled clinical trials comparing the efficacy of H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. DATA COLLECTION AND ANALYSIS: Extraction and quality assessment of studies were done by two reviewers. Study authors were contacted for additional information. MAIN RESULTS: Six studies with a total of 355 patients were included in the first meta-analysis: mean percentage of rebleeding in H. pylori eradication therapy group was 4.5%, and in the non-eradication therapy group without subsequent long-term maintenance antisecretory therapy it was 23.7% (OR 0.18, 95% CI 0.09 to 0.37; there was no statistical evidence of heterogeneity; NNT was 5, 95% CI 4 to 8). Three studies with a total of 470 patients were included in the second meta-analysis: mean percentage of rebleeding in H. pylori eradication therapy group was 1.6%, and in non-eradication therapy group with long-term maintenance antisecretory therapy it was 5.6% (OR 0.25, 95% CI 0.08 to 0.76; heterogeneity was not demonstrated; NNT was 20, 95% CI 12 to 100). Subanalysis. Excluding patients taking non-steroidal anti-inflammatory drugs (NSAIDs) at the time of recurrent bleeding resulted in a rebleeding rate of 4% (first meta-analysis) or 0.78% (second meta-analysis) in the group receiving H. pylori eradication therapy. When only patients with H. pylori eradication success were included, rebleeding rate was 1% in H. pylori eradication therapy group, and NNT decreased from 5 to 4. In some cases, recurrence of H. pylori infection seemed to be responsible for recurrence of bleeding. REVIEWER'S CONCLUSIONS: Treatment of H. pylori infection is more effective than antisecretory non-eradicating therapy (with or without long-term maintenance antisecretory therapy) in preventing recurrent bleeding from peptic ulcer. Consequently, all patients with peptic ulcer bleeding should be tested for H. pylori infection, and eradication therapy should be prescribed to H. pylori-positive patients.
Anti-Ulcer Agents↗
Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis.
OBJECTIVE: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori (H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. METHODS: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. RESULTS: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) (p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. CONCLUSION: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.
Adult↗
Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease?
BACKGROUND: Intestinal metaplasia, whether in the cardia or the distal oesophagus, has been uniformly defined as specialised columnar epithelium, suggesting a relation with Barrett's oesophagus. It is, however, not clear whether the risk factors associated with intestinal metaplasia are identical at both sites. AIMS: To investigate biopsy specimens obtained below the squamocolumnar junction (SCJ) in relation to endoscopic aspect, gastric histology, and clinical presentation. PATIENTS AND METHODS: In 423 patients investigated the endoscopic aspect of the SCJ was classified as unremarkable (group I, n = 315) or suggestive of Barrett's oesophagus (group II, n = 108). Standardised biopsy specimens from the antrum, corpus, and directly below the SCJ were investigated. RESULTS: Intestinal metaplasia was detected at the SCJ in 13.4% of group I patients, where it was significantly associated with gastric intestinal metaplasia (odds ratio (OR) 6.96; confidence interval (CI) 2.48 to 19.54) and H pylori (OR 7.85; CI 2.82 to 21.85), and in 34.3% of group II patients where it was significantly associated with reflux symptoms (OR 19.98; CI 6.12 to 65.19), erosive oesophagitis (OR 12.16; CI 3.86 to 38.24), and male sex (OR 6.25, CI 2.16 to 18.14), but not with H pylori or gastric intestinal metaplasia. CONCLUSION: This study suggests that the pathogenesis of intestinal metaplasia at the SCJ is not uniform: at an endoscopically unremarkable SCJ it is a sequela of H pylori gastritis, but coexisting with endoscopic features of Barrett's oesophagus it is associated with male sex and gastro-oesophageal reflux disease.
Barrett Esophagus↗
Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently.
BACKGROUND: Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. AIMS: To investigate whether aging decreases GMSH. PATIENTS: One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). METHODS: Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. RESULTS: Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). CONCLUSIONS: A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence.
Adult↗
M1-muscarinic mechanisms regulate interdigestive cycling of motor and secretory activity in human upper gut.
We determined the influence of M1-muscarinic pathways in modulating temporal cycling of motor and secretory activity in the fasting upper gut. Eight healthy subjects were studied on two separate days, following a double-blind, randomized protocol. Antroduodenal motility (migrating motor complex, MMC), pancreatic exocrine secretion (amylase, lipase, trypsin, chymotrypsin), and plasma levels of associated hormones [motilin, pancreatic polypeptide (PP)] were monitored for two consecutive cycles during background infusion of placebo or telenzepine, a selective M1-muscarinic receptor antagonist. On placebo days, pancreatic enzymes and hormones cycled in synchrony with motor activity, as expected. During M1 blockade, duodenal output of each enzyme was decreased by 85-90% in phase I and by > 90% in phase III. Similarly, plasma concentrations of hormones were decreased during all phases and cycling was absent. Despite the loss of these putative influences, intestinal motility continued to cycle, albeit in an altered fashion. Intermittent phase II activity was replaced by phase I quiescence, while phase III-like fronts were diminished (contraction frequency, amplitude, propagation velocity reduced 30-60%, duration not altered) but recurred at expected intervals (cycle length 105 +/- 14 min vs 109 +/- 12 in placebo). Gastric motor activity was virtually abolished. These data suggest or extend several working hypotheses: (1) Motilin is released and/or acts via cholinergic (M1-muscarinic) pathways to initiate antral, but not duodenal, phase III activity. (2) M1 receptors mediate all components of the gastric MMC and phase II activity throughout the gut, but intestinal phase III activity arises via alternate pathways. (3) M1-muscarinic mechanisms regulate interdigestive cycling of pancreatic enzymes and PP. (4) Secretions from the endocrine/exocrine pancreas are not primary mediators of intestinal motility.
Adult↗
Interdigestive cycling in chronic pancreatitis: altered coordination among pancreatic secretion, motility, and hormones.
BACKGROUND & AIMS: Secretions from the exocrine and endocrine pancreas may modulate interdigestive motility. To test this hypothesis in humans, we investigated interdigestive cycling in patients with chronic pancreatitis (CP) as a model of impaired pancreatic function. METHODS: Antroduodenal motility, pancreatic enzyme output, and pancreatic polypeptide release were monitored for two consecutive interdigestive cycles in 13 controls and 9 patients with CP. RESULTS: Interdigestive enzyme output was severely impaired in patients with CP (> 80% decrease); however, secretory cycling was still evident in most patients. All parameters describing interdigestive motility were similar in controls and patients with CP (duration of the migrating motor complex [MMC] was 107 +/- 19 minutes in patients with CP vs. 114 +/- 15 minutes in controls). The time between cyclic peaks of enzyme secretion (76 +/- 4 minutes vs. 101 +/- 4 minutes in controls) and pancreatic polypeptide (63 +/- 4 minutes vs. 106 +/- 7 minutes in controls) was shortened in patients with CP, and peaks were no longer temporally related to the MMC. Only 56% of phase III activity fronts were associated with a concomitant secretory peak in patients with CP compared with 92% in healthy subjects. CONCLUSIONS: CP not only decreases pancreatic secretion but interrupts the coordination among interdigestive cyclic phenomena. Our findings in several animal and human models refute the concept that pancreatic mechanisms exert a major regulatory influence on interdigestive motor activity.
Adult↗
Relationship between postprandial release of CCK and PP in health and in chronic pancreatitis.
The aim of this study was to investigate the relationship between postprandial release of cholecystokinin (CCK) and pancreatic polypeptide (PP) in healthy subjects and patients with chronic pancreatitis (CP). 14 patients with CP and 14 age-matched healthy subjects were studied. Diagnosis of CP was confirmed by standardized imaging modalities (ERCP and CT). Exocrine pancreatic function was assessed in all 28 subjects using the pancreolauryl serum test (PLT). An oral test meal was administered to stimulate endogenous hormone release. Plasma samples were taken before and at several time points after the test meal. CCK and PP plasma levels were measured by specific radioimmunoassays. Basal CCK and PP plasma levels were not different between patients with CP and controls, and were not correlated in either group. However, a direct linear correlation between integrated postprandial release of CCK and PP was found in healthy subjects (r = 0.74, P < 0.005). This postprandial coupling was not evident in patients with CP (r = 0.16; n.s.). Peak fluorescein serum concentration in patients with CP and steatorrhea (SCP) (n = 6) was < 2.5 micrograms/ml, and CCK and PP responses to the meal were significantly impaired (CCK response = 61 +/- 14 pmol/l/120 min in SCP vs. 110 +/- 14 in controls, P < 0.05; PP response = 3920 +/- 1773 pg/ml/120 min in SCP vs. 13418 +/- 3299 in controls, P < 0.05). In patients with mild/moderate exocrine insufficiency, CCK and PP responses varied greatly and were not different from controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Hyperlipidemia in acute pancreatitis. Relationship with etiology, onset, and severity of the disease.
Serum lipid (triglycerides and cholesterol) concentrations were studied in 49 patients with acute pancreatitis (AP). The aims of the study were to investigate the prevalence of hyperlipidemia (HL) in patients with AP according to etiology and to evaluate whether HL precedes or is a consequence of AP. Moreover, we analyzed the relationship between HL and the development of pancreatic necrosis. At admission, 23 patients (47%) had HL: 9 of 19 patients with alcoholic pancreatitis, 5 of 18 patients with biliary pancreatitis, and 9 of 12 patients with AP of miscellaneous etiologies (p less than 0.05). Severe HL (serum triglycerides greater than 20 mmol/L) was observed in five patients. Serum lipid levels in patients with AP and HL decreased markedly during the first 72 h of evolution, but remained slightly above the upper normal limit in most of them after 15 d. The prevalence of HL was similar in edematous and necrotizing pancreatitis. Necrotizing pancreatitis was significantly associated with the presence of hypertriglyceridemia in conjunction with hypercholesterolemia (p less than 0.05). The observations that a) hyperlipidemia is an early event in acute pancreatitis, (b) serum lipid values decrease during the acute phase of the disease, (c) hyperlipidemia has a different prevalence in different etiologies, and (d) high serum lipid levels are not always associated to pancreatic necrosis suggest that HL is a preexistent metabolic abnormality with respect to AP. On the other hand, HL may play a role in aggravating AP.
Acute Disease↗