Accuracy of a new monoclonal stool antigen test in post-eradication assessment of Helicobacter pylori infection: comparison with the polyclonal stool antigen test and urea breath test.

BACKGROUND AND AIM: The enzyme immunoassay based on polyclonal antibodies (HpSA) represents a valid method for the detection of Helicobacter pylori antigens in stool specimens, but some controversial results were reported in post-eradication setting. A new monoclonal enzyme immunoassay (FemtoLab H. pylori, Connex) has been developed. The present study compares the diagnostic accuracy of the two tests after eradication therapy. PATIENTS AND METHODS: Stool samples were collected and urea breath test and endoscopy performed in 325 patients (161 F, 164 M, age 17-78 years), 4-8 weeks after standard triple eradication therapy. The FemtoLab and HpSA tests were performed in accordance with the manufacturer's protocol. H. pylori infection was confirmed if culture alone or both urease test and histology were positive and was considered absent if all three tests were negative. RESULTS: H. pylori was eradicated in 231 patients (71.1%). Urea breath test showed the best performances with sensitivity 98.9% and specificity 99.5%. The sensitivity of FemtoLab was 88.3%, specificity 94.8%, positive and negative predictive values 87.4% and 95.2%. Corresponding HpSA values were 73.4%, 97.8%, 93.2% and 90%. Sensitivity and negative predictive value of FemtoLab were significantly better than HpSA. Adjusting the cut-offs according to a ROC curve improved not significantly the sensitivity of the two tests. CONCLUSIONS: Urea breath test shows the best accuracy in the assessment of H. pylori infection. Between the stool tests, the FemtoLab due to its higher sensitivity is to prefer in the post-eradication assessment of H. pylori infection.

Twice-daily standard dose of omeprazole achieves the necessary level of acid inhibition for Helicobacter pylori eradication. A randomized controlled trial using standard and double doses of omeprazole in triple therapy.

Antibiotic resistances and level of acid inhibition may affect the outcome of eradicating regimens for H. pylori. To evaluate the impact of different degrees of acid inhibition on the efficacy of triple treatment, we treated 323 patients with H. pylori infection with clarithromycin and tinidazole plus omeprazole, either 20 mg bid or 40 mg bid. Gastric biopsies and antimicrobial susceptibility testing were performed. Eradication was evaluated by means of breath test. Eradication rates were (intention to treat and per protocol) 83.3 and 84.3% in patients receiving 40 mg omeprazole and 81.9 and 84.1% in those receiving 80 mg omeprazole. Culture was successful in 218 patients (68.7%). Resistance to clarithromycin and metronidazole were found in 13.7 and 20.6%, respectively. Eighteen further patients (8.2%) presented double resistance. Resistance was comparable across the two groups. In resistant patients the eradication rate was significantly lower (66.6% [95% CI, 56-76%], vs 86% [95% CI, 78-91%]; P = 0.001). Antibiotic resistance (OR, 2.73; 95% CI, 1.4-5.3) and smoking (OR, 2.68; 95% CI, 1.4-5.2) were independent predictors of eradication failure. Omeprazole, 20 mg bid, achieves the optimal acid inhibition in H. pylori eradication. Increasing antisecretory activity does not significantly enhance cure rates.

Relationship between intestinal metaplasia of the gastro-oesophageal junction, Helicobacter pylori infection and gastro-oesophageal reflux disease: a prospective study.

BACKGROUND: The role of Helicobacter pylori infection and/or gastro-oesophageal reflux disease in pathogenesis of intestinal metaplasia in gastric cardia is still unclear. AIMS: To prospectively evaluate prevalence of inflammation and intestinal metaplasia of cardia in relationship to Helicobacter pylori infection in patients with gastro-oesophageal reflux disease and in healthy controls. PATIENTS: A total of 122 consecutive patients with gastro-oesophageal reflux disease and 49 control subjects were included. METHODS: During endoscopy, a total of six biopsies were taken from antrum, corpus and cardia. Helicobacter pylori infection was assessed by histology and rapid urease test. Degree of chronic gastritis, inflammatory activity and Helicobacter pylori colonization were scored from 0 to 3. RESULTS: No difference in prevalence was observed between gastro-oesophageal reflux disease patients and controls as far as concerns Helicobacter pylori (41% vs 38%), inflammation of cardia (59.5% vs 70%) and intestinal metaplasia of cardia (18% vs 19%). Inflammation of cardia was significantly (p<0.001) associated with Helicobacter pylori irrespective of gastro-oesophageal reflux disease symptoms. Cardial intestinal metaplasia was more frequently (p=0.03) found in infected subjects ((27%) than in uncolonized subjects (13%). No relationship was observed between gastro-oesophageal reflux disease and carditis and cardial intestinal metaplasia. Cardial intestinal metaplasia was more frequently detected in association with carditis (26% vs 6%, p=0.001). CONCLUSIONS: Inflammation and intestinal metaplasia of the gastric cardia are not markers of gastro-oesophageal reflux disease but are related to Helicobacter pylori.

Omeprazole-based dual and triple therapy for the treatment of Helicobacter pylori infection in peptic ulcer disease: a randomized trial.

OBJECTIVES: It was our goal to evaluate the efficacy and safety and patient compliance with omeprazole-based dual and triple therapy for eradication of Helicobacter pylori in peptic ulcer disease. MATERIALS AND METHODS: One hundred seventy-five consecutive patients with H. pylori infection and associated active peptic ulcer were included. H. pylori infection was assessed by rapid urease test and histological analysis. Patients were randomized among three treatments: group 1 (56 patients): omeprazole, 20 mg bid, and amoxicillin, 1 gm bid, for 2 weeks; group 2 (61 patients): omeprazole, 20 mg bid, plus amoxicillin, 1 gm bid, and metronidazole, 500 mg bid, for 1 week; and group 3 (58 patients): omeprazole, 20 mg bid, plus amoxicillin, 1 gm bid, and clarithromycin, 500 mg bid, for 1 week. Ulcer healing and cure of infection were evaluated at 4 to 6 weeks after cessation of therapy. Eradication rate was calculated per-protocol and by an intention-to-treat analysis. RESULTS: At posttreatment endoscopy, duodenal ulcer was healed in 98.3% of patients. Eleven patients (6%) were lost to follow-up. H. pylori infection was treated successfully in 55% (95% confidence interval [CI] = 41%-69%) of patients of group 1; 86% (95% CI = 77%-95%) of group 2 (p < .001 vs. group 1); and 93% (95% CI = 85%-100%) of group 3 (p < .001 vs. group 1). On intention-to-treat analysis, eradication was 52%, 80%, and 86% in groups 1, 2, and 3, respectively. A good compliance was observed in more than 90% of patients of all groups. Side effects were reported by 7% of patients in group 1, 9% in group 2, and 11% in group 3. None of the patients stopped therapy because of side effects. CONCLUSIONS: Dual-therapy omeprazole-amoxicillin for 2 weeks is associated with significantly lower eradication rate than is 1-week omeprazole-based triple therapies. Triple therapy is well-tolerated and produces side effects similar to those of dual therapy. The highest cure rate of H. pylori infection was achieved with triple therapy of omeprazole, amoxicillin, and clarithromycin for 1 week.

Gastric hypersensitivity in nonulcer dyspepsia: an inconsistent finding.

Visceral hypersensitivity is claimed to be involved in the pathogenesis of nonulcer dyspepsia (NUD). We evaluated whether gastric hypersensitivity is a consistent finding in an unselected group of NUD patients. In 11 patients and 20 healthy controls, a standardized gastric distension was performed using a gastric barostat. Perception was scored by a questionnaire and compared between the two groups. There was a linear pressure/volume relationship during gastric distension in both groups. The pain threshold in NUD patients was significantly lower compared to controls [5.5 +/- 4.0 mm Hg above minimal distending pressure (mdp) and 10.2 +/- 2.2 mm Hg above mdp, respectively, P < 0.004], irrespective of the H. pylori status. However, more than 50% of the NUD perception scores were in the control range at most distension levels. Gastric hypersensitivity could be confirmed in NUD patients as a group. However, there is a considerable overlap concerning perception in response to distension between unselected NUD patients and controls.

Proximal gastric motility functions are normal in severe obesity.

The role of altered gastric motor functions for the development of obesity is still unclear. In this study, we investigated whether severe obesity is related to gastric dysfunctions or to abnormal perception in response to distension. 31 obese patients and 20 healthy volunteers were studied using an electronic barostat. Basal gastric tone, gastric accommodation, and perception in response to distension were not altered in obese patients. The median minimal distending pressure, reflecting the intra-abdominal pressure, was significantly elevated in obese patients, being 12 versus 7 mm Hg, respectively (p < 0.0001). We conclude that the proximal gastric motility, including perception and accommodation in response to intragastric distension, is not impaired in severe obesity. Whether disturbances of gastric reflex relaxation in response to a meal are involved in the pathogenesis of obesity remains to be established.

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.

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.

Exocrine pancreatic function in the early phase of human acute pancreatitis.

BACKGROUND: Little is known about exocrine pancreatic function during human acute pancreatitis. We aimed to evaluate interdigestive exocrine pancreatic secretion and pancreatic polypeptide (PP) release during the early phase of acute pancreatitis in humans. METHODS: Eight patients with acute pancreatitis (six biliary, one alcoholic, and one idiopathic acute pancreatitis) were studied within 72 h from the onset of symptoms. Four patients had necrotizing and four had edematous acute pancreatitis. Normal values were obtained from 26 normal subjects matched by sex and age. Interdigestive pancreatic secretion was studied by a duodenal intubation perfusion technique. Enzyme output was calculated for consecutive 15-min periods over 3-4 h and expressed as units per hour within a secretion cycle and units per hour around a secretion peak. Plasma PP concentrations were measured by radioimmunoassay in 15-min intervals. RESULTS: All variables studied were similar in patients with acute pancreatitis and in controls. PP release in acute pancreatitis was maintained in a normal cyclical pattern closely related to the secretory cycles. CONCLUSIONS: Interdigestive exocrine pancreatic secretion in the early phase of mild to moderate acute pancreatitis in humans remains within the normal range. This finding provides a rational basis for early therapeutic inhibition of pancreatic secretion in human acute pancreatitis.

Effect of pancreatic ductal and parenchymal changes on exocrine function in chronic pancreatitis.

The effect of pancreatic ductal and parenchymal changes on exocrine pancreatic function was analyzed prospectively in 75 patients with chronic pancreatitis (CP). Endoscopic retrograde pancreatography (ERP), computed tomography (CT), and serum pancreolauryl test (PLT) were performed to evaluate the degree of ductal, parenchymal, and functional changes, respectively. Results were evaluated by stepwise multivariate logistic regression and are expressed as the odds ratio (OR). A strong association was found between the degree of ductal changes in ERP and the degree of exocrine functional impairment (OR = 5.8). However, the association between the degree of parenchymal changes in CT and the degree of pancreatic dysfunction was weaker and was clearly confounded by the degree of ductal changes. On the basis of these findings, we suggest that the development of exocrine pancreatic functional impairment in patients with CP depends primarily on the degree of ductal changes, while parenchymal abnormalities play a less important role.

Is increased pancreatic pressure related to pain in chronic pancreatitis?

In this study, we investigated the relationship between pain and pancreatic pressure in patients with chronic pancreatitis (CP). We studied 12 patients with CP undergoing surgery and five controls with cancer of the pancreatic tail. CP was staged on the basis of morphological (ERP) and functional (serum-pancreolauryl test) criteria. Patients kept daily records of the intensity of pain on a linear analog scale. Intraoperatively, pressure within the pancreas was assessed by the introduction of a fine needle into the pancreatic parenchyma connected to a pressure transducer. In controls, pressure was determined in macroscopically normal tissue in the head of the pancreas. Pancreatic pressure was significantly higher in CP than in controls (29.9 +/- 3.1 vs 7.2 +/- 1.1 mmHg, p < 0.001). No relationship was found between the pain score and the pancreatic pressure. Pressure was positively correlated with ductal changes (r = 0.831; p < 0.001), but not with exocrine function of the pancreas. Postoperatively, pancreatic pressure fell by 15.3% in four patients with CP in whom pressure assessment was repeated after surgical decompression. We conclude that pancreatic parenchyma pressure is not closely related to pain in CP.

Postprandial release of cholecystokinin and pancreatic polypeptide in health and in gallstone disease: relationships with gallbladder contraction.

OBJECTIVES: The present study investigated endogenous postprandial release of cholecystokinin (CCK) and pancreatic polypeptide (PP) in relation to gallbladder dynamics in healthy subjects and patients with gallstones. METHODS: Gallbladder volume (by ultrasonography) and plasma concentrations of CCK and PP (by radioimmunoassay) were evaluated in 18 patients with gallstones and 14 healthy controls before and after administration of a semi-liquid test meal (250 ml, 1450 kJ). Gallbladder contractility was previously assessed on a separate day by intravenous infusion of ceruletide (2.5 ng/kg/min). RESULTS: Basal gallbladder volume was not different in patients (32 +/- 5.9 cm3) and controls (26 +/- 2.7 cm3). Postprandial gallbladder contractility was impaired in gallstone patients, who showed a reduced integrated response (-3718 +/- 349 vs. -5251 +/- 376 cm3/2 h, p < 0.01) and a delayed time to maximal gallbladder contraction (67 +/- 7.4 min vs. 37 +/- 2.4 min, p < 0.002). Maximal gallbladder contraction after ceruletide infusion was also reduced (44.1 +/- 5.0% vs. 72.5 +/- 3.2%, p < 0.001), but not delayed (15.8 +/- 2.4 vs. 15.7 +/- 1.4 min) in gallstone patients. Basal CCK and PP plasma levels were similar in both groups. Postprandial CCK release was impaired in gallstone patients, predominantly due to a decreased response over the first 30 min (3.8 +/- 1.8 vs. 20.0 +/- 4.9 pmol/L/30 min, p < 0.005). Postprandial PP release was not different between groups. A direct linear correlation between postprandial release of CCK and PP was found in healthy controls but not in patients with gallstones. Postprandial gallbladder volume at any moment was inversely correlated with CCK plasma levels in healthy subjects, but not in gallstone patients. No correlation between postprandial PP response and gallbladder dynamics was observed. CONCLUSIONS: Based on a multivariate logistic approach, a reduced and delayed postprandial gallbladder contractility and an impaired CCK release in the early postprandial phase are significantly associated with gallstone disease. Our data provide further evidence for the predominant role of endogenous postprandial CCK release in gallbladder contraction. A role for PP in modulating postprandial gallbladder dynamics is not supported.

Impaired interdigestive pancreatic polypeptide release. Early hormonal disorder in chronic pancreatitis?

The purpose of this study was to investigate interdigestive cycling and postprandial release of pancreatic polypeptide (PP) in relation to exocrine pancreatic function in chronic pancreatitis (CP). We investigated nine patients with mild-moderate CP (MCP), eight patients with severe CP and steathorrea (SCP), and 17 healthy subjects as controls. Interdigestive antroduodenal motility was monitored by means of manometry. Following two consecutive motility cycles, a standard test meal was administered. Plasma samples were drawn for PP determinations every 15 min throughout the entire study, which concluded 2 hr after ingestion of the meal. Mean interdigestive PP plasma concentrations during phase III motor activity were lower in MCP (146 +/- 46 pg/ml) than in controls (270 +/- 42 pg/ml) and lower still in SCP (55 +/- 8 pg/ml). Accordingly, the percent increase in PP concentrations during phase III over those in phase I was progressively decreased from controls (112%) to MCP (62%) to SCP (19%). Mean interdigestive PP concentrations were also lower during phase I and II in SCP than in controls or MCP. None of the postprandial parameters for PP release was affected in the early stage of disease, while mean, peak, and integrated postprandial values were significantly lower in SCP than in controls or MCP. Thus, we observed a progressive diminution of both interdigestive and postprandial PP release with increasing severity of disease. Interdigestive release parameters, in particular, were tightly correlated with exocrine function. CP appears to alter interdigestive PP release to a greater extent than postprandial PP release; this effect is already apparent in early stages of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical utility of the serum pancreolauryl test in diagnosis and staging of chronic pancreatitis.

Indirect pancreatic function tests are frequently used in the clinical routine as complementary tools for the diagnosis of chronic pancreatitis (CP) because of their noninvasiveness and simplicity. We analyzed the clinical efficacy and routine application of a modified serum pancreolauryl test (PLT) in the diagnosis and staging of CP. We studied a total of 90 patients with CP diagnosed by endoscopic retrograde pancreatography and 54 patients with extrapancreatic gastrointestinal disorders as controls. Sensitivity and specificity of the serum PLT in the diagnosis of CP were 82% and 91%, respectively, using a value of 4.5 micrograms/ml as cutoff. In the diagnosis of patients with mild to moderate morphological changes of CP, the sensitivity of the serum PLT (52%) was improved by the concomitant analysis of serum pancreatic amylase in a logistic model (70%). Serum PLT closely correlated with the degree of pancreatic ductal abnormalities (p < 0.001), and showed a sensitivity of 81% and specificity of 89% in the staging of CP (mild-moderate vs. marked CP; cutoff 2.5 micrograms/ml). We conclude that the modified serum PLT is a reliable test which should be considered as a first-line option for the diagnosis and follow-up of patients with CP.

Gastric emptying of solids and liquids in obesity.

The purpose of this study was to determine whether obese patients have different rates of solid and liquid gastric emptying compared to healthy controls. Twenty-four obese patients (7 males, 17 females) were investigated prior to dietary restriction. The patients had a weight excess above ideal weight ranging from 25% to 216% (mean weight 118.1 +/- 6.5 kg). The control group consisted of 8 healthy subjects (4 males, 4 females), within 10% of the ideal weight. The solid phase of the test meal consisted of 40 g bread, 30 g ham, 10 g margarine, and two scrambled eggs labeled with 99mTc. For the liquid phase, 200 ml orange juice was labeled with 201Tl. Three-minute counts of both tracers were taken for 106 min using a large field-of-view gamma camera. In obese patients, a significantly shortened lag phase for the emptying of solids was observed (27.0 +/- 3.3 versus 38.4 +/- 4.1 min; P < 0.05). Half-emptying time (105.9 +/- 6.7 versus 100.7 +/- 5.7 min), emptying rate (0.60 +/- 0.04 versus 0.71 +/- 0.07%/min), and total emptying of solids (49.4 +/- 3.6 versus 50.5 +/- 5.0%) were not different from controls. Obese subjects had a trend to slowed liquid emptying (half-time 82.7 +/- 4.8 versus 69.9 +/- 6.9 min; emptying rate 0.59 +/- 0.03 versus 0.65 +/- 0.03%/min; total emptying 59.8 +/- 2.9 versus 66.0 +/- 3.3%), but this was not statistically significant. There was no correlation between weight or body surface area and rate of solid or liquid gastric emptying.(ABSTRACT TRUNCATED AT 250 WORDS)

Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release.

Gallbladder dynamics, cholecystokinin (CCK), and pancreatic polypeptide (PP) release were studied in 14 patients with chronic pancreatitis (CP) (2 females, 12 males; age range 24-56 years) and 12 control subjects (4 females, 8 males, 21-50 years). On day 1, gallbladder contractility was investigated after ceruletide intravenous infusion (2.5 ng/kg/min for 10 min). On day 2, a mixed standard test meal (1450 kJ) was administered orally. Gallbladder volume was assessed at three time intervals before (-30, -15, 0 min) and at 5, 10, 20, 30, 40, 50, 60, 80, 100 and 120 min after stimulation by means of ultrasonography. CCK and PP plasma levels were determined at each time interval. Exocrine pancreatic function was assessed using the pancreolauryl serum test (PLT). Six patients with CP had severe exocrine pancreatic insufficiency (EPI) (PLT < 1.8 micrograms/ml) with steatorrhea, eight patients had mild-moderate EPI. Fasting gallbladder volume was increased in CP (32.3 +/- 3.1 cm3) as compared to controls (20.5 +/- 1.2 cm3) (P < 0.01). Peak gallbladder contraction (percent of initial volume) in CP ranged from 5 to 55% (controls: 8-46%) following ceruletide and from 17 to 86% (controls: 27-80%) following the test meal (NS). There was no correlation between the degree of EPI according to PLT and peak gallbladder contraction. Gallbladder emptying in CP patients was not different from controls, although the postprandial CCK response was significantly impaired (P < 0.01). Postprandial PP response in CP was correlated with the PLT result (r = 0.78; P < 0.01) but not with gallbladder emptying or refilling time.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastrointestinal motility in patients with non-ulcer dyspepsia: a role for Helicobacter pylori infection?

Motor disorders of the upper gastrointestinal tract are a frequent finding in patients with non-ulcer dyspepsia (NUD). In this study we attempted to assess whether Helicobacter pylori infection contributes to gastrointestinal motor disorders in NUD. Interdigestive and post-prandial gastrointestinal motility was studied in 46 consecutive patients with NUD and in eight healthy control subjects. Abdominal complaints were assessed by means of a symptom score. Chronic gastritis and H. pylori infection were assessed and graded by histology. Accordingly, patients with NUD were divided into two sub-groups: 18 patients with H. pylori infection and chronic active gastritis and 28 patients without H. pylori infection. The length of the interdigestive motor cycle was not different in patients with NUD (139 +/- 6 min, mean +/- SEM), compared with controls (128 +/- 5.5 min). There was also no difference in the duration of individual phases I, II, and III, either between NUD and controls or between H. pylori-positive and -negative patients. The motility index (MI) of antral phase II also was not changed in NUD patients. Postprandial antral motility was decreased in patients with NUD (MI 6.96 +/- 0.4 vs. 9.7 +/- 0.3 controls; p < 0.025), with no difference between H. pylori-positive and -negative subgroups. It therefore appears unlikely that H. pylori infection plays a primary role in the pathophysiology of antroduodenal motor disorders in NUD.

Ratios of different serum pancreatic enzymes in the diagnosis and staging of chronic pancreatitis.

The aim of this study was to define an optimum serum enzyme ratio for the diagnosis of chronic pancreatitis (CP) and for the evaluation of the stage of the disease. With this goal in mind, a simultaneous and interrelated analysis of different serum pancreatic enzymes was performed in 296 consecutive patients with clinically suspected CP. A total of 167 patients were finally diagnosed with CP and 129 with other digestive diseases (used as controls). Serum values of pancreatic amylase, lipase, immunoreactive trypsin, and their ratios were determined in every patient before final diagnosis was established. Stepwise logistic regression analysis was performed. As expected, abnormally low values of individual serum pancreatic enzymes in the diagnosis of CP were highly specific (92-98%) but very insensitive (20-32%). Their diagnostic usefulness was neither improved by calculation of their ratios nor by the use of multivariate logistic regression analysis. A low pancreatic amylase/lipase ratio correlated with advanced CP (p < 0.01), and had a high degree of accuracy (80.5%) in the evaluation of the stage of the disease (assessed by endoscopic retrograde pancreatography). In conclusion, while serum pancreatic enzymes have limited usefulness in the diagnosis of CP, the pancreatic amylase/lipase ratio could be a simple method for staging the disease.