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.

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.

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.

TRH-immunoreactivity in chronic pancreatitis.

Thyrotropin-releasing hormone (TRH) is abundantly present in the pancreas. We studied the circulating TRH-immunoreactivity (IR) in 27 patients with chronic pancreatitis (CP) and different degrees of exocrine pancreatic insufficiency (EPI), as well as in 23 normal subjects. Furthermore we examined the effect of oral administration of 100 g glucose on peripheral TRH-IR in normal subjects (n = 5) and in patients with severe exocrine insufficiency (SEI, n = 5). Basal TRH-IR plasma levels in the CP group (20.8 +/- 7 fmol/ml, mean +/- SD) were significantly lower (p < 0.005) as compared with the normal subjects (38 +/- 14). TRH-IR plasma levels in patients with CP and SEI (15.8 +/- 3) were significantly lower (p < 0.05) than in patients with normal pancreatic function (28.1 +/- 8), but were no different from those in patients with CP and moderate exocrine insufficiency (18.7 +/- 5). In normal controls TRH-IR rose 120-180 min after glucose ingestion from 33 +/- 5 to 64 +/- 20 fmol/ml, while no increase in TRH-IR levels was observed in patients with SEI. We conclude that circulating TRH-IR levels are mainly of pancreatic origin. Patients with SEI have very low peripheral TRH-IR, indicating that CP does indeed influence TRH-release.

[Pain in chronic pancreatitis: recent pathogenetic findings]. / Il dolore nella pancreatite cronica: recenti acquisizioni patogenetiche.

Pain is the major symptom in chronic pancreatitis. Its intensity frequently necessitates partial or complete pancreatectomy. The mechanisms of pain are not yet fully understood and, thereby, the therapeutic management is still controversial. Possible causes of pain include outflow obstruction with increased ductal and parenchymal pressure within the pancreas, and inflammatory involvement of intrapancreatic nerve fibres. Possible extrapancreatic causes are common bile duct and duodenal stenosis. The first theory has recently been substantiated by the demonstration of a definite relationship between intrapancreatic pressure, as measured intraoperatively, and intensity of pain. Infiltration of inflammatory cells around the nerves together with an increase in the number of nerve fibres in the fibrotic pancreatic tissue has been proposed as a possible cause of pain in chronic pancreatitis. Moreover, immunohistological studies have shown that the amount of neurotransmitters, such as substance P, is increased in afferent pancreatic nerves. Stenosis of the common bile duct and duodenum has been reported to be associated with severe abdominal pain. Common bile duct and duodenal stenosis in chronic pancreatitis may be caused by extension of fibrosis and active inflammation of the pancreas within the wall of duodenum and bile duct. This article updates the different pathogenetic mechanisms in pancreatic pain and the current therapeutic possibilities with their advantages and shortcomings.

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.

[Relations between gastrointestinal interdigestive motility and secretion]. / Beziehungen zwischen gastrointestinaler interdigestiver Motilität und Sekretion.

The motility of the upper gastrointestinal tract in the interdigestive state shows a cycling pattern called Migrating Motor Complex (MMC) and is composed by phases I, II and III. Gastric, biliary and pancreatic secretion show cyclical fluctuations during fasting closely associated with the motor activity. The motor and secretory interdigestive activity is regulated by a complex interplay of nerval and humoral mechanisms. Among them, motilin, a gastrointestinal hormone mainly secreted from the duodenum, is supposed to play a central role in the initiation of phase III. Gastric acid secretion, directly or by means of motilin release, may modulate the duration of the MMC and the propagation of phase III in the small intestine. Pancreatic secretion does not initiate phase III but may exert a control on gastric interdigestive motility probably by means of pancreatic polypeptide release. Biliary interdigestive secretion seems to play a little or no role in the control of these phenomena. The coordination of motor and secretory events is likely to be under control of the duodenum.

[The H2-lactulose breath test in the diagnosis of intestinal transit time]. / Der H2-Laktulose-Atemtest in der Diagnostik der intestinalen Transitzeit.

The H2-Lactulose breath test is used to detect small bowel bacterial overgrowth but mainly to evaluate the orocoecal transit time (OCTT) in man. The result of the H2-breath test is influenced by several intestinal and extraintestinal factors that cause a large variability of normal values. By reviewing the possible influencing factors of the breath tests we try to make a contribution to a better judgement of the results as the H2-lactulose breath-test is a simple noninvasive and non-expensive screening in the investigation of gastrointestinal disorders. For evaluating the better dosage of lactulose in gastroenterological routine diagnostic we designed a prospective study. The test was performed in 12 healthy volunteers by ingestion of 10 g and 20 g lactulose to quantitate the OCTT and to evaluate it in normal conditions. We found that the length of transit is related to the dose of lactulose. OCTT was 97.1 +/- 22.4 min. after ingestion of 10 g lactulose, and significantly shorter, 57.1 +/- 16.6 min. after ingestion of 20 g lactulose (p less than or equal to 0.01). The lower dose of lactulose is more suitable for routine diagnostic because of better acceptance despite slower transit time.

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.

Relationship between pancreatic function and pain in chronic pancreatitis.

The association between pain and exocrine pancreatic function was re-evaluated in 56 patients with chronic pancreatitis to see if residual function of the gland may evoke outflow obstruction resulting in pain. No significant differences were found in the degrees of pancreatic dysfunction among three groups with different degrees of pain (no pain, n = 7; moderate pain, n = 21; and severe pain, n = 28), but patients with more impairment of exocrine pancretic function tended to have less pain. In patients with no pain the mean (SD) peak serum concentration of fluorescein was 2.0 (0.2) micrograms/l, in those with moderate pain it was 2.6 (0.1), and in those with severe pain it was 3.4 (0.1). No significant differences were found between the degree of pain and the duration of the disease, which was 5.5 (0.3) years in the group with no pain, 3.5 (0.2) in patients with moderate pain, and 3.8 (0.1) in those with severe pain. We conclude that outflow obstruction may affect some patients, but is not the only cause of pain. Patients with severe pancreatic dysfunction and steatorrhoea often present with pain, so either obstruction of the residual secretions, or inflammatory activity impinging on nerve endings in fibrotic tissue, may also cause pain. The causes vary, and there is often more than one, so optimal management implies thorough investigation of each patient and long term follow up.

[Simultaneous sonographic study of postprandial gastric emptying and gallbladder contraction]. / Simultane sonographische Untersuchung der postprandialen Magenentleerung und Gallenblasenkontraktion.

Postprandial gastric emptying and gallbladder contraction were assessed in 14 healthy subjects by means of ultrasonography after oral administration of a semi-liquid test meal (250 ml, 1450 kJ). For this purpose, cross-sectional areas of the gastric antrum and gallbladder volume were calculated and recorded over a period of 120 minutes using an annular-array-transducer. The semi-liquid test meal allowed suitable sonographic measurement of cross-sectional areas of the antrum in all 14 subjects. Mean half-time of gastric emptying was 47 minutes (range 17-72 minutes). Mean peak gallbladder contraction was 36% (range 17-60%) of initial volume and mean time to peak contraction was 65 minutes (range 20-120 minutes). The method described was found to be a practical and reliable procedure for the investigation of postprandial gastric emptying and gallbladder contraction. It is therefore of potential interest for application to a variety of clinical questions. A minor drawback involves the relative length and variability of time required for testing, owing to the wide range in the time-course of gastric emptying and gallbladder contraction across subjects. Normal ranges for defined test meals must be established in large control groups.

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)

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.

Effect of ketanserin, a selective antiserotoninergic drug, on human anal canal pressure.

The effect of Ketanserin, a new antiserotoninergic drug, on human anal pressure in vivo was investigated. Anal pressure was recorded continuously in 14 normal subjects by a low-compliance water perfused probe with two recording points at the sphincter level. After a 30-min basal tracing Ketanserin (10 mg IV as bolus) or placebo was administered in a double blind manner, and the recording continued for 1 h. The results show that Ketanserin induced a 30% fall in anal pressure soon after its administration which was statistically significant when compared with the placebo (p less than 0.01). This effect lasted up to 40 min of recording and was followed by a return to control values within 1 h.

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)

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.

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.

Interdigestive gastroduodenal motility and cycling of putative regulatory hormones in severe obesity.

The aim of the present study was to evaluate interdigestive gastrointestinal motility and its coordination with plasma concentrations of motilin and pancreatic polypeptide (PP) in 14 patients with severe obesity and in 10 control subjects with normal body weight. Motor activity of the stomach, duodenum, and proximal jejunum was recorded by using an eight-lumen catheter. Blood samples were drawn for determination of interdigestive motilin and PP plasma concentrations. We observed no difference in total duration of the migrating motor complex (MMC) or of phases I, II, or III of the MMC. Gastric phase-III activity occurred less frequently in severely obese patients (only 15% originating in the stomach) than in controls (65%; p less than 0.01). Plasma motilin concentrations were decreased in obese patients in phase I (127 +/- 17 pg/ml in controls versus 87 +/- 10 pg/ml in obese), in phase II (189 +/- 26 pg/ml controls versus 134 +/- 15 obese) and in phase III (195 +/- 29 pg/ml controls versus 153 +/- 28 pg/ml obese). Peak motilin release occurred in synchrony with phase-III activity and was greater in controls than in obese patients. Plasma PP concentrations did not differ from those of controls during any phase of the MMC. These results further suggest a potential role for motilin in regulating gastrointestinal motor activity and indicate a potential defect in this regulatory mechanism in severe obesity. Whether the relationship between disordered motor activity and motilin release is etiologic with regard to the pathophysiology of obesity remains to be determined.

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.