Sensitivity and specificity of magnetic resonance enterography in the clinical management of fistulizing Crohn's disease.

BACKGROUND: High diagnostic accuracy is reported for magnetic resonance enterography (MRE) in Crohn's disease (CD), but few studies have evaluated its role in abdominal fistulae. The primary aim of this study was to assess the reliability of MRE in the identification of internal fistulae in CD. METHODS: One hundred and eighty-six patients with moderate CD (CD Activity Index : 250-400) were prospectively selected from the inflammatory bowel disease clinic of Parma University Hospital. Eligible patients had already undergone nutritional screening, pancolonoscopy, and computed tomography enterography (CTE) in the month before enrollment. MRE was performed according to the study protocol. Additional fluoroscopic contrast-enhanced studies or surgical evaluation were used for discordance between CTE and MRE results. A consensus committee resolved equivocal findings. Surgical findings and/or fluoroscopic contrast-enhanced studies together with the clinical data were considered the composite "reference standard" to which the results of MRE were compared. RESULTS: MRE identified 22 internal fistulae in 21 patients (11%), of whom 4 (19%) also had perianal fistulae and found 7 abscesses (33%). Forty-one (22%) additional patients with perianal fistulae were identified. Thirteen patients (57%) with internal fistulae required enteral nutrition support. No statistically significant differences were found between MRE and CTE in fistula detection. There was also no significant difference between MRE and the composite diagnosis in those who underwent surgery (n = 8) and/or contrast-enhanced studies (n = 7). CONCLUSIONS: CTE and MRE accurately detect internal fistulae in CD. MRE is preferable because it avoids radiation. Reliable identification of internal fistulae by MRE should permit earlier and improved treatment.

Long-term treatment with mesalazine in patients with symptomatic uncomplicated diverticular disease.

The aim of this work was to compare the recurrence of diverticulitis during a 5-year follow-up in a population of patients affected by symptomatic uncomplicated diverticular disease (SUDD), taking either 800 mg of mesalamine b.i.d for 10 days every month or no 5-ASA. Sixty-seven consecutive patients affected by SUDD followed-up every 6 months for 5 years. All patients in this group (M-group) were requested to consume mesalamine 800 mg b.i.d for 10 days every month. A control group (C-group) of 82 subjects with SUDD allocated in an institution for the elderly and taking no 5-ASA medications was also followed-up for the same period. As a result in the M-group 14.9% of patients did not complete the follow-up, and diverticulitis developed in two patients (4%; 95% CI 1.1-13.5). In the C-group 6.1% patients did not complete the follow-up, and diverticulitis developed in 8 patients (10.4%; 95% CI 5.4-19.2). The difference between the two groups was not significant (difference = -6.4%; 95% CI -15.6 to 4.3; log rank test: p = 0.1256). Cyclic treatment with mesalazine seems to be clinical, although not statistically effective in reducing the incidence of diverticulitis. In future well-designed RCTs are necessary to demonstrate the therapeutic gain of the use of mesalazine, if any, in the management of patients with SUDD.

Helicobacter pylori eradication: are we really all equal? A controlled study in native and immigrant population.

Italy's shift to a tertiary economy has modified the working market, concentrating demand also on unqualified one, which includes most immigrants. It is also well established that low socio-economical conditions are associated with an increased prevalence of H. pylori infection. The aims of this study were to compare: (1) the efficacy of a 7 days triple therapy in immigrant and in Italian patients; (2) the prevalence of PUD between these two groups of patients. A total of 116 consecutive immigrant and 112 Italian H. pylori infected patients were recruited between 2007 and 2008. Patients underwent (13)C-UBT, endoscopy with biopsies, and were offered a 7-day triple therapy. Eradication rate (ER) was assessed 8 weeks after the end of the treatment using (13)C-UBT. The two populations differed for median age (p < 0.01), prevalence of PUD (p < 0.01), and smoking status (p < 0.01). The ER according to the ITT analysis was 70% for Italian and 48.3% for immigrant (p < 0.01). Multivariate analysis including country of origin, sex, age, PUD, smoking, and alcohol status found that immigrant had an adjusted OR for not eradicating of 2.14 (p = 0.03). In immigrant patients resident in Italy, performance of triple therapy was lower than expected. Further studies are demanded to confirm and clarify these intriguing results.

Quantification of serum levels of pepsinogens and gastrin to assess eradication of Helicobacter pylori.

BACKGROUND & AIMS: We investigated whether serum levels of pepsinogen (sPG)I and sPGII, the ratio of sPGI to sPGII, or serum levels of gastrin-17 (sG17), can be used to assess eradication of Helicobacter Pylori 8 weeks after treatment. METHODS: We performed a prospective study of 228 consecutive patients with H pylori infections. At the start of the trial (baseline), patients were assessed using the (13)C-urea breath test ((13)C-UBT) and endoscopy, and serum levels of pepsinogens and gastrin levels were measured. Patients were offered a 7-day triple therapy and asked to return 8 weeks after treatment for another (13)C-UBT and measurements of serum levels of sG17, sPGI, and sPGII (175 patients completed the study). RESULTS: The eradication rate of H pylori was 67%. Percentage variation in levels of sPGI and sPGII, the ratio of sPGI to sPGII, and in levels of sG17 resulted in area under the curve values of 0.858, 0.973, 0.940, and 0.810, respectively, for H pylori eradication. A decrease of 22.7% or greater in the level of sPGII detected H pylori eradication with 100% sensitivity and 96.6% specificity. Spectrum analysis did not identify differences in accuracy. CONCLUSIONS: Percentage variation of sPGII levels 8 weeks after therapy for H pylori infection correlates with eradication. Additional studies are needed to confirm these results.

Evaluation of CD10 positivity in colorectal polyps in neoplastic transformation.

BACKGROUND: CD10 is a metalloprotein that is potentially associated with greater tumour growth. MATERIALS AND METHOD: We have correlated CD10 positive in carcinomatous polyps with tumour size, grade, patient age and sex, postoperative TNM staging and Asler-Coller classification. We have matched these cases with a control group that showed presence of polypoid adenomatous tissue with mild to moderate dysplasia. RESULTS: We have divided these in a group of 39 cases, characterised by the presence of carcinoma arising in adenomatous polyps, and a control group of 16 cases, characterised by the presence of colorectal polyps with mild to moderate dysplasia. In the first group, we have discarded three cases for incomplete data. In the remaining 36 cases we have identified 28 patients testing positive for CD10 with positivity values and 8 cases negative for CD10. In CD10 positive cases, we have confirmed the presence of increased incidence of lymph node involvement compared to CD10 negative cases, with high specificity and high predictive value and a higher incidence of cases attributable to group C (Asler-Coller) and grading 3. CONCLUSIONS: CD10 positivity should be assessed in terms of increased progression.

Plasma citrulline as a quantitative biomarker of HIV-associated villous atrophy in a tropical enteropathy population.

BACKGROUND & AIMS: Studies have shown that the circulating citrulline concentration is decreased in patients with proximal small bowel villous atrophy from coeliac disease and more so in patients with extensive damage to the intestinal mucosa, but there have been few data on HIV enteritis and tropical enteropathy (TE). Our primary aim was to correlate serum citrulline with the degree of reduction of the enterocyte mass in HIV-infected patients with TE. METHODS: Postabsorptive fasting serum citrulline was measured in 150 TE pts, 44 of whom had HIV infection, using reverse phase, high performance liquid chromatography. Absorptive capacity and permeability were measured after intrajejunal instillation of 4 sugars (5 g lactulose, 1 g L-rhamnose, 0.5 g D-xylose, 0.2 g 3-O methyl D glucose) with assay by thin-layer chromatography. Morphometric analysis was carried out on jejunal biopsies. RESULTS: In HIV positive patients, the median serum citrulline was significantly lower (median 19, interquartile range (IQR) 17-24 µmol/L) than in HIV negative patients (median 27, IQR 23-33 µmol/L; p < 0.001). There were statistically significant correlations (p < 0.005) between citrulline and: crypt depth; villous height/crypt depth ratio; Shenk-Klipstein score; and xylose absoption, only in the HIV positive. CONCLUSIONS: Serum citrulline concentration appears to be a quantitative biomarker of small bowel mass integrity in HIV positive enteropathy and deserves assessment as a surrogate for monitoring anti-retroviral therapy.

Connections between genetics and clinical data: Role of MCP-1, CFTR, and SPINK-1 in the setting of acute, acute recurrent, and chronic pancreatitis.

OBJECTIVES: Acute, acute recurrent, and chronic pancreatitis are inflammatory diseases with multifactorial pathogenic mechanisms. Genetic mutations and polymorphisms have been correlated with pancreatitis. The aim of this study was to investigate the association of cystic fibrosis transmembrane conductance regulator (CFTR) and serine protease inhibitor Kazal type 1 (SPINK-1) gene mutations and monocyte chemoattractant protein 1 (MCP-1) -2518A/G polymorphism with acute pancreatitis (AP), acute recurrent pancreatitis (ARP), and chronic pancreatitis (CP), and to associate genetic backgrounds with clinical phenotype in these three conditions. METHODS: One hundred eighteen AP, 64 ARP, 142 CP patients, and 88 normal controls were enrolled consecutively. We analyzed MCP-1 serum levels using enzyme-linked immunosorbent assay. Polymorphism -2518 of MCP-1 and SPINK-1 N34S gene mutations were determined by PCR-restriction-fragment length polymorphism. Sequence analysis was performed when necessary. Thirty-three CFTR mutations were analyzed in CP and ARP patients using multiplex DNA testing. RESULTS: Serum MCP-1 levels were significantly higher in all patients affected by pancreatic inflammatory diseases. Moreover, we found a significant over-representation of the MCP-1G allele in ARP patients. We found a statistically significant association of CFTR gene mutations with ARP, but not with CP. We did not find a statistically significant association of ARP or CP with the N34S SPINK-1 gene mutation. Interestingly, 39 of 64 ARP patients (61%) carried at least one genetic mutation and/or polymorphism. Five of 64 ARP patients had pancreas divisum and four of these five also carried the G allele. CONCLUSIONS: Analysis of a comprehensive range of potential susceptibility variants is needed to support modeling of the effects of genes and environment in pancreatitis. As such, beyond gene mutations, the context within which those mutations exist must be considered. In pancreatitis the context includes the inflammatory response, clinical features, and exogenous factors.

Usefulness of a serological panel test in the assessment of gastritis in symptomatic children.

BACKGROUND: Non-invasive methods are advisable for the detection of Helicobacter pylori-related chronic gastritis in pediatric patients. Serum pepsinogens I and II (sPGII and sPGII), gastrin-17 (G-17) and anti-H. pylori antibodies (IgG-Hp) have been proposed as a 'serological gastric biopsy'. AIM: To assess H. pylori infection and to evaluate gastric mucosa status in a pediatric population by means of serological parameters such as sPGI, sPGII, G-17 and IgG-Hp. METHODS: 45 consecutively children evaluated for upper gastrointestinal symptoms were analyzed. All children were submitted to upper gastrointestinal endoscopy with biopsies. Serum samples were analyzed for IgG-Hp, sPGII, sPGI and G-17 (Biohit, Helsinki, Finland). RESULTS: 18 children had H. pylori-related mild or moderate non-atrophic chronic gastritis. They presented significantly higher mean levels of sPGII and of IgG-Hp than negative ones, either under or up to 10 years. sPGI showed significantly increased levels in H. pylori-positive patients only over 10 years. G-17 levels were not different between H. pylori-positive and -negative ones. The best cut-offs of IgG-Hp, sPGII and of product IgG-Hp x sPGII, to identify H. pylori infection, were 30 IU/l, 9 microg/l, and 241 IU/l x microg/l, respectively. The product IgG-Hp x sPGII identified H. pylori infection with a 100% sensitivity, 92% specificity, 90% positive predictive value and 100% negative predictive value. IgG-Hp and IgG-Hp showed a correlation (r = 0.94; p < 0.001). CONCLUSIONS: Combined analysis of sPGII and IgG-Hp antibody levels could be recommended as a non-invasive panel for the assessment of H. pylori-related histological alterations of gastric mucosa in childhood.

Quality of life in uncomplicated symptomatic diverticular disease: is it another good reason for treatment?

BACKGROUND: Quality of life (QoL) is becoming a major issue in the evaluation of any therapeutic intervention. AIMS: To assess the QoL in patients with uncomplicated symptomatic diverticular disease (DD) and to elucidate the influence of two different treatments either on symptoms or QoL. MATERIALS AND METHODS: 58 outpatients affected by uncomplicated symptomatic DD, admitted in our Gastroenterological Unit from October 2003 to March 2004, were enrolled. Patients were randomly assigned to two different treatments consisting of rifaximin or mesalazine for 10 days every month for a period of 6 months. QoL was evaluated by means of an SF-36 questionnaire and clinical evaluation was registered by means of a global symptomatic score (GSS) at baseline and after 6 months. RESULTS: At baseline, lower values in all SF-36 domains were confirmed in patients with DD. Both rifaximin and mesalazine groups showed a significant reduction of their mean GSS (p < 0.01 and p < 0.001, respectively) and improvement of SF-36 mean scores after therapy, even though treatment with mesalazine showed better results. CONCLUSIONS: DD has a negative impact on QoL. Cyclic treatment with poorly absorbable antibiotics or anti-inflammatory drugs relieves symptoms and improves QoL.

Diverticular disease in the elderly.

There are few diseases whose incidence varies as greatly worldwide as that of diverticulosis. Its prevalence is largely age-dependent: the disease is uncommon in those under the age of 40, the prevalence of which is estimated at approximately 5%; this increases to 65% in those > or =65 years of age. Of patients with diverticula, 80-85% remain asymptomatic, while, for unknown reasons, only three-fourths of the remaining 15-20% of patients develop symptomatic diverticular disease. Traditional concepts regarding the causes of colonic diverticula include alterations in colonic wall resistance, disordered colonic motility and dietary fiber deficiency. Currently, inflammation has been proposed to play a role in diverticular disease. Goals of therapy in diverticular disease should include improvement of symptoms and prevention of recurrent attacks in symptomatic, uncomplicated diverticular disease, and prevention of the complications of disease such as diverticulitis. Diverticulitis is the most usual clinical complication of diverticular disease, affecting 10-25% of patients with diverticula. Most patients admitted with acute diverticulitis respond to conservative treatment, but 15-30% require surgery. Predictive factors for severe diverticulitis are sex, obesity, immunodeficiency and old age. Surgery for acute complications of diverticular disease of the sigmoid colon carries significant rates of morbidity and mortality, the latter of which occurs predominantly in cases of severe comorbidity. Postoperative mortality and morbidity are to a large extent driven by patient-related factors.

A curcumin-based 1-week triple therapy for eradication of Helicobacter pylori infection: something to learn from failure?

BACKGROUND: Curcumin is the principal element of turmeric powder extracted from the root of Curcuma longa. Studies on curcumin have demonstrated some anti-Helicobacter pylori activity as well as immunomodulating properties. N-acetylcysteine and lactoferrin with their respective mucolytic and antibacterial activities might also be effective in H. pylori eradication therapy. AIM: To determine if a 7-day non-antibiotic therapy comprised of curcumin, lactoferrin, N-acetylcysteine, and pantoprazole was effective for eradication of H. pylori infection and reduction of gastric inflammation, assessed by serum pepsinogens and relief of symptoms. SUBJECTS AND METHODS: Twenty-five consecutive H. pylori-positive patients (12 males, mean age 50 +/- 12 years, range 31-76) with functional dyspepsia were enrolled. Patients were administered for 7 days curcumin 30 mg b.i.d., bovine lactoferrin 100 mg b.i.d., N-acetylcysteine 600 mg b.i.d., and pantoprazole 20 mg b.i.d. H. pylori status and upper gastrointestinal symptoms were assessed by (13)C-urea breath test and a scale of upper gastrointestinal symptoms intensity (absent, mild, moderate, and severe), as well as a blood test for serum pepsinogens (sPGI, sPGII), gastrin-17 (G-17), and anti-H. pylori IgG (IgG-Hp) at baseline (T0) and after 2 months (T1). RESULTS: Three of 25 patients (12%) were cured of H. pylori infection. A significant decrease in the overall severity of symptoms (T0: 6, interquartile range [IQR]: 4.5-8; T1: 2, IQR: 2-3; p < or = .001), and sPGII (T0: 16 microg/L, IQR: 13-22; T1: 10 microg/L, IQR: 8-16; p < or = .001) and sPGI (T0: 82 microg/L, IQR: 67-97; T1: 74 microg/L, IQR: 62-94; p = .02) levels were observed after 2 months of the treatment. IgG and G-17 values did not significantly decrease after 2 months. CONCLUSIONS: This novel therapy was not effective for H. pylori eradication. However, despite the bacterium persistence, significant improvement of dyspeptic symptoms and reduction of serologic signs of gastric inflammation were observed after 2 months at the end of the 7-day treatment schedule.

Prevention of complications and symptomatic recurrences in diverticular disease with mesalazine: a 12-month follow-up.

In uncomplicated diverticular disease, treatment is aimed at relieving symptoms. The aim of the present study was to evaluate the efficacy of mesalazine for symptomatic relief of uncomplicated diverticular disease of the colon. Two hundred sixty-eight consecutive eligible outpatients (122 male, 146 female; age, 66.1 years; range, 31-81 years) were enrolled in four treatment schedules in a randomized fashion: Group R1 (66 patients), rifaximin, 200 mg bid; Group R2 (69 patients), rifaximin, 400 mg bid; Group M1 (67 patients), mesalazine, 400 mg bid; and Group M2 (66 patients), mesalazine, 800 mg bid. Treatments were administered for 10 days every month for 12 months. Clinical evaluations were performed at admission and at 3-month intervals for 12 months considering 12 clinical variables (upper and lower abdominal pain/discomfort, tenesmus, diarrhea, abdominal tenderness, fever, bloating, general illness, nausea, emesis, dysuria, bleeding) graded as 0 = no symptoms, 1 = mild, 2 = moderate, and 3 = severe. The Global Symptomatic Score (GSS) was calculated using the sum of each symptom score. Two hundred forty-four patients completed the 12- month study; 24 were discontinued (14 treated with rifaximin and 10 treated with mesalazine) either as voluntary dropouts or because they developed side effects and/or complications. Group M2 demonstrated a lower frequency of many symptoms after 6 and 12 months of treatment; the mean GSS was significantly lower in Group M2 after 6 and 12 months of therapy by both intention-to-treat and per-protocol analyses. Patients treated with mesalazine (Groups M1+M2) had a lower GSS than subjects treated with rifaximin (Groups R1+R2) during the 12-month follow-up period. We conclude that cyclic administration of mesalazine is effective for symptomatic relief of uncomplicated diverticular disease of the colon. Some symptoms showed greater improvement with mesalazine, 800 mg bid, than with the other treatment schedules.

Role of gut microflora and probiotic effects in the irritable bowel syndrome.

BACKGROUND: Even though the cause of irritable bowel sindrome (IBS) is not yet known, alterations of the intestinal microflora may be important in its pathogenesis. AIM: To evaluate the efficacy of rifaximine alone or in association with the probiotic strain of Bifidobacterium longum W11 in reducing symptoms in patients with IBS. METHODS: We performed a monocentric, prospective, randomized open trial including 70 patients randomized in to two groups: Group A (41 patients) receiving rifaximin 200 (2 cp bid for ten days in a month) followed by a formulation of the probiotic strain of Bifidobacterium longum W11(one granulated suspension for 6 days on alternate weeks ) and Group B (29 patients) receiving only rifaximin 200 (2 cp bid for ten days in a month). The clinical evaluation was performed at admission and after 2-months, taking into account the method of visual analogous. RESULTS: At the 2-month follow-up, Group A patients reported a greater improvement of symptoms compared to patients in group B (p = 0.010) even if the physician's opinion at T1 did not confirm these results (p = 0.07). CONCLUSION: The increased colonisation by Bifi-dobacterium longum W11, after the cyclic administration of rifaximin, which eradicates the bacterial overgrowth of the small intestine, may reduce symptoms, especially those related to bowel habit and stool frequency in patients with IBS. The abnormalities observed in the colonic flora of IBS suggest, in fact, that a probiotic approach will ultimately be justified.

Use of mesalazine in diverticular disease.

Diverticular disease includes a spectrum of conditions sharing the underlying pathology of acquired diverticula of the colon: symptomatic uncomplicated diverticular disease, recurrent symptomatic uncomplicated diverticular disease, and complicated diverticular disease. Goals of therapy in diverticular disease should be to improve symptoms and to prevent recurrent attacks in symptomatic uncomplicated diverticular disease, and to prevent the complications of disease such as diverticulitis. Inflammation seems to play a key role in all forms of the disease. This is the rationale for the use of anti-inflammatory drugs such as mesalazine. Inflammation in such diseases seems to be generated by a heightened production of proinflammatory cytokines, reduced anti-inflammatory cytokines, and enhanced intramucosal synthesis of nitric oxide. The mechanisms of action of mesalazine are not yet well understood. It is an anti-inflammatory drug that inhibits factors of the inflammatory cascade (such as cyclooxygenase) and free radicals, and has an intrinsic antioxidant effect. Some recent studies confirm the efficacy of mesalazine in diverticular disease both in relief of symptoms in symptomatic uncomplicated forms and in prevention of recurrence of symptoms and main complications.

Effects of chronic therapy with non-steroidal antiinflammatory drugs on gastric permeability of sucrose: a study on 71 patients with rheumatoid arthritis.

AIM: To evaluate the gastric permeability after both acute and chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) and to assess the clinical usefulness of sucrose test in detecting and following NSAIDs- induced gastric damage mainly in asymptomatic patients and the efficacy of a single pantoprazole dose in chronic users. METHODS: Seventy-one consecutive patients on chronic therapy with NSAIDs were enrolled in the study and divided into groups A and B (group A receiving 40 mg pantoprazole daily, group B only receiving NSAIDs). Sucrose test was performed at baseline and after 2, 4 and 12 wk, respectively. The symptoms in the upper gastrointestinal tract were recorded. RESULTS: The patients treated with pantoprazole had sucrose excretion under the limit during the entire follow-up period. The patients without gastroprotection had sucrose excretion above the limit after 2 wk, with an increasing trend in the following weeks (P = 0.000). A number of patients in this group revealed a significantly altered gastric permeability although they were asymptomatic during the follow-up period. CONCLUSION: Sucrose test can be proposed as a valid tool for the clinical evaluation of NSAIDs- induced gastric damage in both acute and chronic therapy. This technique helps to identify patients with clinically silent gastric damages. Pantoprazole (40 mg daily) is effective and well tolerated in chronic NSAID users.

Does Helicobacter pylori infection eradication modify peptic ulcer prevalence? A 10 years' endoscopical survey.

AIM: To compare peptic ulcer prevalence in patients referred for upper gastrointestinal endoscopy in two Italian hospitals in pre-Helicobacter era and ten years after the progressive diffusion of eradication therapy. METHODS: We checked all the endoscopic examinations consecutively performed in the Gastroenterology Unit of Padova during 1986-1987 and 1995-1996, and in the Gastroenterology Unit of Parma during 1992 and 2002. Chi Square test was used for statistic analysis. RESULTS: Data from both the endoscopic centers showed a statistically significant decrease in the prevalence of ulcers: from 12.7% to 6.3% (P<0.001) in Padova and from 15.6% to 12% (P<0.001) in Parma. The decrease was significant both for duodenal (from 8.8% to 4.8%, P<0.001) and gastric ulcer (3.9% to 1.5%, P<0.001) in Padova, and only for duodenal ulcer in Parma (9.2% to 6.1%, P<0.001; gastric ulcer: 6.3% to 5.8%, NS). CONCLUSION: Ten years of extensive Helicobacter pylori (H pylori) eradication in symptomatic patients led to a significant reduction in peptic ulcer prevalence. This reduction was particularly evident in Padova, where a project for the sensibilization of H pylori eradication among general practioners was carried out between 1990 and 1992. Should our hypothesis be true, H pylori eradication might in the future lead to peptic ulcer as a rare endoscopic finding.

Usefulness of serum pepsinogens in Helicobacter pylori chronic gastritis: relationship with inflammation, activity, and density of the bacterium.

We sought to study the relationship between serum pepsinogens and different histopathologic features of Helicobacter pylori-related chronic gastritis. One hundred forty-nine consecutive dyspeptic patients underwent endoscopy with biopsies; serum pepsinogens I and II were measured by immunoassay. Serum levels of pepsinogens (sPG) were significantly correlated with H. pylori density both of the corpus (sPGI: r = 0.32, P < .001; sPGII: r = 0.56, P < .001) and antrum (sPGI: r = 0.41, P < .001; sPGII: r = 0.43, P < .001) as well as with chronic inflammation (sPGI: r = 0.26, P < .001; sPGII: r = 0.49, P < .001) and activity (sPGI: r = 0.38, P < .001; sPGII: r = 0.50, P < .001) in the antrum. Only sPGII was correlated with chronic inflammation (r = 0.44, P < .001) and activity (r = 0.40, P < .001) in the corpus. SPGI was inversely correlated with atrophy (r = -0.33, P < .001) and intestinal metaplasia (r = -0.37, P < .001) in the corpus. sPGII levels could be considered as markers of gastric inflammation all over in the stomach. sPGI levels are inversely related to atrophic body gastritis.

Recovery of gastric function after Helicobacter pylori eradication in subjects with body atrophic gastritis: prospective 4-year study.

BACKGROUND: The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level. AIM: To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels. METHODS: Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy. RESULTS: Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years. CONCLUSION: After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.

Influence of antisecretory treatment with proton pump inhibitors on serum pepsinogen I levels.

It has been reported in literature that serum pepsinogen levels rise during omeprazole and lansoprazole administration. However, the influence of pantoprazole and esomeprazole on serum pepsinogens levels is still to be assessed. The aim of this study was to evaluate the influence of proton pump inhibitor (PPI) therapy on pepsinogen I (PGI) levels. PGI and gastrin (G17) levels (EIA; Biohit, Helsinki, Finland) in 126 consecutive patients (M 57; F 69, mean age 53, range 15-91), with upper gastrointestinal symptoms at baseline condition and after 2 months of PPI treatment, were evaluated. Patients underwent a therapy schedule based on: omeprazole 20 mg b.i.d. (20 patients), pantoprazole 40 mg b.i.d. (27 patients), esomeprazole 40 mg b.i.d. (29 patients), lansoprazole 30 mg b.i.d. (21 patients) and rabeprazole 20 mg b.i.d. (26 patients) for 2 months. A significant increase in serum PGI (sPGI) levels was found after a 2-month treatment for all five different PPIs: omeprazole, pantoprazole, esomeprazole, lansoprazole and rabeprazole (P < 0.05). The effect of rabeprazole on sPGI was less pronounced as compared with other PPIs, whereas esomeprazole achieved superior sPGI levels, with no overall statistically significant difference among the five groups (P > 0.05). However, a comparison within a single group of PPIs showed a statistical significance when the esomeprazole group was compared with the rabeprazole group (P = 0.007). sPGI levels are significantly influenced by antisecretory therapy, rising under PPI treatment. Moreover, a statistically significant difference in sPGI levels between the rabeprazole and esomeprazole groups has been demonstrated.