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Summary Background : Certain evidence suggests that Helicobacter pylori strains expressing genes for cytotoxin production show a higher sensitivity than non-cytotoxic organisms to eradication treatment. No data are available on the involvement of bacterium-related lesions in different therapeutic outcomes. Aims : (i) To investigate whether differences in eradication rates may be related to the different expression of virulent strains (cagA, vacA, iceA) in patients undergoing proton pump inhibitor-based triple therapy, and (ii) to evaluate whether therapeutic outcome may be affected by bacterium-induced gastric lesions. Methods : One hundred and ten H. pylori-positive subjects were enrolled. H. pylori was genotyped by polymerase chain reaction. Treatment consisted of lansoprazole–amoxicillin–clarithromycin, twice daily for 1 week. Eradication was checked by urea breath test. Results : The eradication rate was 70%, and the absence of cagA was associated with unsuccessful treatment. No difference between the groups with successful and unsuccessful eradication was found with regard to vacA and iceA. Lympho-epithelial lesions and fibrosis were associated with unsuccessful treatment. Conclusions : The present data confirm the importance of cagA (but not vacA and iceA) as a predictor of successful eradication. When fibrosis and lympho-epithelial lesions are present, therapy appears to be less effective. Therefore, these histological features may be involved in an unsuccessful therapeutic outcome.

Helicobacter pylori (HP) related inflammation is mediated by tumour necrosis factor alpha (TNFalpha), which "in vitro" increases epithelial apoptosis in response to infection. In the early stages of HP gastritis, a raised epithelial apoptosis occurs; this phenomenon becomes less evident with progression towards intestinal metaplasia. Aim of our study was to analyze "in vivo" mucosal TNFalpha in relation to epithelial apoptosis in the progression of HP related histological damage. Antral biopsies from 20 HP positive patients were retrospectively studied: 10 with and 10 without intestinal metaplasia (IM and CG group respectively); samples of 10 dyspeptics with normal HP negative stomach (N) were used as control. The following parameters were evaluated by immunohistochemistry: 85 kDa caspase-cleaved fragment (p85) of human poly (ADP-ribose) polymerase (PARP) labelling index (LI) as marker of apoptosis and TNFalpha LI in stromal cells as marker of inflammatory response. Both epithelial apoptosis and mucosal TNFalpha expression were higher in chronic active gastritis compared to intestinal metaplasia and controls (PARP and TNFalpha LI: CG > IM > N; ANOVA & Student-Neumann-Keuls; p < 0.05 and p < 0.01, respectively). Pearson's coefficient showed a significant correlation between PARP and TNFalpha LI in IM and CG groups. Our data show that mucosal TNFalpha, similarly to what suggested "in vitro", may be related "in vivo" to epithelial apoptosis thus suggesting a possible mechanism for immune system involvement in the control of gastric epithelial turnover.

Knowledge on the role of Helicobacter pylori (HP) infection is continually evolving, and treatment is becoming more challenging due to increasing bacterial resistance. Since the management of HP infection is changing, an update of the national Italian guidelines delivered in 2007 was needed. In the III Working Group Consensus Report 2015, a panel of 17 experts from several Italian regions reviewed current evidence on different topics relating to HP infection. Four working groups examined the following topics: (1) “open questions” on HP diagnosis and treatment (focusing on dyspepsia, gastro-oesophageal reflux disease, non-steroidal anti-inflammatory drugs or aspirin use and extra-gastric diseases); (2) non-invasive and invasive diagnostic tests; (3) treatment of HP infection; (4) role of HP in the prevention of gastric cancer. Statements and recommendations were discussed and a consensus reached in a final plenary session held in February 2015 in Bologna. Recommendations are based on the best current evidence to help physicians manage HP infection in Italy. The guidelines have been endorsed by the Italian Society of Gastroenterology and the Italian Society of Digestive Endoscopy.

The diagnosis of Celiac Disease (CD) relies on the concordance of pathological, serological, genetic and clinical features. For this reason, the diagnosis of CD is often a challenge. Seronegative celiac disease (SNCD) is defined by the negativity of anti-tissue transglutaminase antibodies in the presence of a positive histology on duodenal biopsy samples, i.e. inflammatory infiltrate of intra-epithelial lymphocytes (IELs > 25/100 enterocytes), mild villous atrophy and uneven brush border associated to human leukocyte antigen (HLA) haplotype DQ2 and/or DQ8. SNCD is characterized by mucosal deposits of tissue transglutaminase (tTG)/anti-tTG immuno-complexes. These may counteract the passage of anti-tTG into the bloodstream, thus explaining seronegativity. Another reason for seronegativity may be found in an incomplete maturation of plasma cells with a consequent failure of antibodies production. This condition often characterizes immunoglobulin deficiencies, and, indeed, SNCD is common in subjects with immunoglobulin deficiencies. The management of SNCD still remains debated. The treatment option for SNCD may be represented by gluten free diet (GFD), but the usefulness and appropriateness of prescribing GFD are controversial. Some evidences support its use only in SNCD subjects showing CD clear clinical picture and compatible HLA status. The choice of GFD administration could be linked to an investigation able to diagnose SNCD in no doubt even if a reliable test is not currently available. On these bases, a test helping the diagnosis of SNCD is justifiable and desirable.

To assess the evolution of duodenal lymphocytosis (DL), a condition characterized by increased intraepithelial lymphocytes (IELs), over 2 years of follow-up.Consecutive patients undergoing upper endoscopy/histology for abdominal pain, diarrhea, weight loss, weakness or other extraintestinal features compatible with celiac disease (CD) were included. Evaluation of IELs infiltrate in duodenal biopsy samples was carried out by CD3-immunohistochemistry and expressed as number of positive cells/100 enterocytes. Diagnostic agreement on the IELs count was tested by calculating the weighted k coefficient. All patients underwent serological detection of autoantibodies associated with CD: IgG and IgA anti-tissue transglutaminase and endomysium. Each patient underwent further investigations to clarify the origin of DL at baseline and/or in the course of 2 years of follow-up every six months. Autoimmune thyroiditis, intestinal infections, parasitic diseases, bacterial intestinal overgrowth, hypolactasia and wheat allergy were detected. Colonoscopy and enteric magnetic resonance imaging were performed when necessary. Risk factors affecting the final diagnosis were detected by multinomial logistic regression and expressed as OR.Eighty-five patients (16 males, 69 females, aged 34.1 ± 12.5 years) were followed up for a mean period of 21.7 ± 11.7 mo. At baseline, endoscopy/duodenal biopsy, CD3 immunohistochemistry revealed:25 IELs/100 enterocytes in 22 subjects, 15-25 IELs in 37 and15 IELs in 26. They all had negative serum anti-transglutaminase and anti-endomysium, whilst 5 showed IgG anti-gliadin positivity. In the course of follow-up, 23 developed CD seropositivity and gluten sensitivity (GS) was identified in 19. Other diagnoses were: 5 Helicobacter pylori infections, 4 jejunal Crohn's disease, 1 lymphocytic colitis and 1 systemic sclerosis. The disease in the remaining 32 patients was classified as irritable bowel syndrome because of the lack of diagnostic evidence. At multivariate analysis, the evolution towards CD was associated with an IELs infiltrate25 (OR = 1640.4) or 15-25 (OR = 16.95), human leukocyte antigen (HLA) DQ2/8 (OR = 140.85) or DQA1*0501 (OR = 15.36), diarrhea (OR = 5.56) and weakness (OR = 11.57). GS was associated with IELs 15-25 (OR = 28.59), autoimmune thyroiditis (OR = 87.63), folate deficiency (OR = 48.53) and diarrhea (OR = 54.87).DL may have a multifactorial origin but the IELs infiltrate and HLA are strong predictive factors for CD development and a clinical diagnosis of GS.

Intestinal microbiota is a “dynamic organ” influencing host metabolism, nutrition, physiology and immune system. Among its several interactions, the role of a phosphatidylcholine metabolite derived by gut flora activity, i.e., trimethylamine-N-oxide (TMAO), allows perceiving a novel insight in the cardiovascular risk scenario, being a strong predictor of this condition. Based on current reports, including the paper of Tang et al., we describe here: the possible role of intestinal microbiota in cardiovascular risk as well as potential interventions to reduce gut flora TMAO production by diet, probiotics and antibiotics. Finally, we highlight the possibility of evaluating, monitoring and modulating TMAO in order to use its serum levels as a marker of cardiovascular risk in the next future, when the need of controlled studies on large series will be satisfied.

Background: H. pylori antibiotic resistance is an important factor in the treatment failure, therefore is important to know the local pattern of this resistance. Material and Methods: A total of 111 patients were studied. Ninety- one H. pylori strains isolated from patients, including 12 from children, having previous repeated treatment failure and 20 strains were isolated from naive patients, were studied. Antibiotic susceptibility including those to tigecycline, was determinated by E-Test. Results: In treated adult and children patients the resistance rates were respectively 81% and 91.6% for clarithromycin; 27.8% and 41% for amoxicillin; 67.1% and 16.7% for metronidazole; 38% and 8.3% for levofloxacin; 5.1% and 0% for tetracycline. Primary resistance, in naive adult patients was 50% for clarithromycin, 10% for amoxicillin, 20% for metronidazole, 30% for levofloxacin and 0% for tetracycline. Tigecycline has shown good activity, in vitro, against H. pylori (MIC90 = 0.064 mg/L). Conclusion: The resistance rates found in H. pylori, in our area, are very high both in naive and treated patients. Few papers have reported the tigecycline susceptibility in H. pylori. The good activity and the lack of resistance to tigecycline found in our study, may consider this antibiotic a “rescue” therapy, saving the use of other antibiotics such as rifabutin, a drug used for the treatment of tuberculosis.

Atherosclerosis is a systemic inflammatory disease able to deeply worsen the outcome of patients because of its serious clinical consequences. The complex inflammatory background underlining such a disease makes atherosclerosis linked to several systemic inflammatory conditions able to impair endothelial function and morphology. Inflammatory bowel diseases are a group of gastrointestinal diseases including Crohn's disease and ulcerative colitis, that is, syndromes characterized by changes in mucosal immunity and gastrointestinal physiology, which could negatively influence the vascular endothelial function and structure. Hepatitis (i.e. inflammatory diseases of the liver mainly due to viral infections) and nonalcoholic fatty liver disease could be aligned to inflammatory bowel disease in such an induction of atherosclerosis disease.Many studies tried to point out the relationship between bowel and liver inflammatory diseases and early vascular changes, considered the first step for atherosclerosis development.The aim of such a narrative review is to explain the relationship between inflammatory bowel disease, hepatitis and nonalcoholic fatty liver disease and their role in increasing cardiovascular risk profile due to early impairment in vascular function and morphology.

It is well known that complicated diverticular disease (DD), which includes Acute Uncomplicated Diverticulitis (AUD), Acute Complicated Diverticulitis (ACD) and Chronic Diverticulitis (CDiv), is characterised by profound structural changes in the colonic tissue, varying from tissue disruption to fibrosis; it has been hypothesised that an unbalanced expression of matrix metalloproteinases (MMP) and their inhibitors (TIMP) protein expression in the bowel wall might, at least in part, mediate this process.1 However, there is limited knowledge about the role of MMPs in the pathogenesis of diverticulitis. It has been reported that altered concentrations of MMPs and TIMPs may explain the structural changes found in diverticulitis.1 Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract characterised by chronic, multifocal transmural inflammation potentially affecting the whole gastrointestinal tract, particularly in the ileocolonic segment. Altadill et al 2 recently hypothesised that CD and complicated DD seem to share the same destiny: a chronic inflammation evolving towards fibrosis. Adhesion molecules containing heparan sulfate (syndecan family) are proteo-glycans, and play a significant role in tissue repair.3 Basic fibroblast growth factor (bFGF) is a peptide able to …

Background/Aims : Alpha-interferon (α-IFN) and lamivudine are the two licensed drugs for patients with chronic hepatitis B, however, their efficacy in precore mutant chronic hepatitis B is limited. The aim of this study was to investigate the efficacy of 1 year α-IFN–lamivudine combination therapy for anti-HBe/hepatitis B virus- (HBV)-DNA positive patients. Methods : Between 1997 and 1999, 29 consecutive anti-HBe/HBV-DNA positive patients entered this prospective pilot study. Patients received 100mg lamivudine orally daily and α-IFN 6 million units (MU) three times weekly for 52 weeks. All patients were followed-up for 12 months after stopping therapy. Primary end points were loss of serum HBV-DNA and alanine transaminase normalization at week 52. Results : Overall, the end-treatment biochemical and virological response was 93% while the sustained response at week 104 was 14%. HBV-DNA negative patients did not experience a viral breakthrough during treatment; no tyrosine–methionine–aspartate–aspartate amino acid motif of HBV polymerase (YMDD) variant emerged. At week 52, 46% of patients with paired liver biopsies slides available, showed an histological improvement (histological activity index ≥2). Conclusions : Combination of lamivudine and interferon for 1 year is followed by high end-treatment virological and biochemical response rates, by improvement of liver histology and by the prevention of the emergence of YMDD mutation; however, the sustained response rate remains low.

Several studies have found a fairly low Helicobacter pylori eradication rate using a standard 7-day triple therapy in Italy. Recently, two new therapeutic schedules have been proposed with an eradication rate higher than 90%. This study compared the efficacy of these two treatment regimens.A total of 131 patients with Helicobacter pylori infection and either non-ulcer dyspepsia (73 patients] or peptic ulcer (58 patients) were enrolled. Helicobacter pylori infection was assessed by rapid urease test and histology on gastric biopsies. Patients were randomised to receive either a 5-day course of ranitidine bismuth citrate 400 mg bid, clarithromycin 500 bid, and tinidazole 500 bid, or a 10-day course of omeprazole 20 mg bid plus amoxycillin 1 g bid for the first 5 days, and omeprazole 20 mg bid, clarithromycin 500 mg bid and tinidazole 500 mg bid for the remaining 5 days. Eradication was assessed by endoscopy 4-6 weeks after therapy.Overall, 4 patients (2 for each treatment group) were lost to follow-up. Helicobacter pylori eradication rates were 67.2% (95% confidence interval: 55.7-78.7) and 65.2% (95% confidence interval: 53.7-76.6) at per protocol and intention-to-treat analyses, respectively, after the 5-day regimen, and 96.8% (95% confidence interval: 92.5-100) and 93.8% (95% confidence interval: 88-99.7) after the 10-day regimen (p0.05). Both treatments were well tolerated, and no major side-effects were reported.The 5-day regimen gave disappointing results, while the eradication rate after the 10-day regimen was very high.

In ulcerative colitis (UC), epithelial proliferation plays a role in crypt repair and neoplastic evolution. Proliferative status is predominantly connoted in active disease, but not defined in remission. Histologically, remission is characterized by normalization of the picture or development of atrophy. Mutation of the ras oncogene is involved in intestinal carcinogenesis. Aim of this work was to assess the proliferative pattern of rectal epithelium in UC during disease activity and in remission and correlate it with ras oncoprotein p21. The study was performed retrospectively in rectal biopsies from four groups each of 10 patients: active ulcerative colitis (AUC), remission with a normal histology (RUC), remission with rectal atrophy (ARUC), and irritable bowel syndrome (C, control group). In all, immunohistostain was employed to evaluate the proliferation cell nuclear antigen labeling index (PCNA LI) and ras p21. Statistical analysis was performed by ANOVA and Student-Neumann-Keuls tests. PCNA LI was significantly higher in AUC and ARUC than in RUC and C. Positive cells were predominant in the lower zone of crypts in RUC and C, while a significant expression of PCNA was also observed in the upper areas in AUC and ARUC. Oncoprotein p21 was expressed on the apical surface of the epithelium in 3/10 AUC patients, in all 10 ARUC patients and in none of RUC and C. The persistently increased epithelial proliferation associated with ras p21 expression in ARUC may be due to the action of an abnormal, mutated ras gene that could play a role in UC-related tumorigenesis.

Objective To evaluate the usefulness of a commercial serological enzyme immunoassay (EIA) for detecting salivary immunoglobulin (Ig) G to Helicobacter pylori. Design Prospective, multicentre study. Setting The study was conducted at 11 gastroenterology hospital centres throughout Italy. Participants and interventions Two hundred and thirteen dyspeptic patients underwent gastroscopy with antral biopsies. At each centre, two of the following three tests for H. pylori diagnosis were performed: urease quick test, histology, and 13 C-urea breath test. Samples of unstimulated saliva and venous blood were collected from each patient. Salivary and serum H. pylori IgG were determined with the EIA Helori-test IgG (Eurospital, Trieste, Italy). Main outcome measures Sensitivity, specificity, positive and negative predictive values, and accuracy of the salivary and serum ElAs. Results By using a receiver operating characteristic curve, salivary EIA yielded 81% (95% confidence interval 73-87%) sensitivity, 73% (62-83%) specificity, 84% (76-90%) positive predictive value, 69% (58-79%) negative predictive value, and 78% (72-84%) accuracy. At the cut-off suggested by the manufacturer, serum EIA had 90% (84-95%) sensitivity, 78% (67-86%) specificity, 88% (81 -93%) positive predictive value, 82% (71-90%) negative predictive value, and 86% (81 -91%) accuracy. Conclusion In this large multicentre study, detection of salivary H. pylori IgG with a commercial serological EIA was a fairly accurate diagnostic method. Data confirm that saliva testing does not compare favourably with serology in the assessment of H. pylori status.

Tumor necrosis factor alpha (TNFalpha) in intestinal mucosa plays a key role in the inflammation characterizing Crohn's disease (CD). Moreover, adhesion molecule syndecan-1 mediates the maintenance of mucosal integrity and supports tissue repair. Therefore, our aim in this study was to correlate simultaneous expression of TNFalpha and syndecan-1 in patients affected by CD. Biopsies from 10 patients with CD of large bowel and 10 subjects with irritable bowel syndrome (controls) were studied by immunohistochemical detection of both TNFalpha and syndecan-1 on successive serial sections. Overall labeling index (OLI) was indicated by the percentage of positive stromal (i.e., nonepithelial) cells/1000 counted in randomized fields, whereas selected labeling index (SLI) was represented by the simultaneous evaluation of both molecules in a same single selected field of each specimen. TNFalpha and syndecan-1 OLI were significantly higher in CD compared with controls, while SLI showed an inverse relationship between the molecules in CD which was not observed in controls. Epithelial syndecan-1 cytoplasmatic staining of superficial epithelium was associated with loss of basolateral staining in the crypts and high stromal TNFalpha in CD. In conclusion, TNFalpha and syndecan-1 expression is increased in the intestinal mucosa of patients with CD. However, the expression of the two molecules is inversely related when a single field is considered, these data supporting the possibility of a downregulation exerted by TNFalpha.

Two cases of gastric anisakiasis have been documented in two Italian women who had consumed raw anchovies (Engraulis encrasicolus). The first patient was a 49-year-old woman presenting with epigastric pain and bloody vomiting after ingestion of marinated (vinegar) raw anchovies. During the esophagogastroduodenoscopy (EGDS) a white color worm was detected and extracted from cardia by means of biopsy forceps. The second patient was a 59-year-old woman with irritable bowel syndrome and gastritis, who underwent to periodical EGDSs. In the course of the last EGDS, a white color round worm on antrum and a small polyp on the fundus of the stomach were observed. The two nematodes have been identified as L3 larvae of the genus Anisakis by a light microscope, and as Anisakis pegreffi by polymerase chain reaction-restriction fragment length polymorphism. The molecular identification of the etiological agent at the species level allows to identify what Anisakidae species play a zoonotic role and which are the fish host species.

Objectives: The frequency of primary clarithromycin resistance in Helicobacter pylori strains is increasing worldwide, and its presence significantly reduces the treatment efficacy of infection. This study aimed to evaluate whether the progression of the prevalence of clarithromycin resistance over a 15 year period has increased and whether a possible change in the distribution of the three most frequent point mutations, which account for the large majority of clarithromycin resistance cases, has taken place. Methods: Antral biopsies of consecutive H. pylori-positive patients observed between January 1989 and December 1990 and between January 2004 and December 2005 were retrieved. A TaqMan real-time PCR was performed in all cases to assess point mutations involved. Results: Primary clarithromycin resistance was assessed for 147 patients observed in the first period 1989‐90 and 178 cases observed in the second period 2004‐05. The overall frequency of clarithromycin resistance increased from 10.2% (15 patients) to 21.3% (38 patients) during the study period (P 5 0.01). The increase was more evident in females [4 out of 55 patients (7.2%) versus 24 out of 103 patients (23.3%); P 5 0.01] and in non-ulcer dyspepsia patients [13 out of 106 patients (12.2%) versus 37 out of 140 (26.4%) patients; P 5 0.009]. A2143G was the most frequent point mutation observed in both study periods, and its prevalence rate remained unchanged [11 out of 15 (73.3%) patients versus 27 out of 38 (71%) patients; P 5 1]. Conclusions: A 2-fold increase in primary clarithromycin resistance in H. pylori strains occurred during the last 15 years in Italy. A2143G remains the most prevalent point mutation involved, thus suggesting that new therapeutic strategies are needed.

With the aim of investigating a possible relationship between "objective" halitosis (established by sulfide levels in the breath) and Helicobacter pylori, we performed a study in 58 dyspeptic patients reported to suffer from "bad breath." Furthermore, we evaluated the effects on halitosis of eradication therapy (only for H. pylori-positive patients) and chlorhexidine antiseptic mouth rinses (in all patients). Sulfide compound assay indicated objective halitosis in 52/58 patients, 30 of whom were positive and 22 negative for H. pylori. In 19/30 eradication by double therapy provoked a decrease to below the cutoff value of sulfide levels in 15. In the other 11 of the 30 subjects, in whom H. pylori positivity persisted, halitosis parameters did not change. Chlorexidine reduced sulfides to below the cutoff value in 16/22 H. pylori-negative patients, but did not provoke any change in the 11 unsuccessfully treated H. pylori-positive subjects. In these, objective halitosis disappeared only after a successful eradication by triple therapy (9/11). Our results show a possible association between halitosis and H. pylori since bacterial eradication may resolve the symptom. Antiseptic mouthwashes may be effective only in absence of H. pylori, when halitosis may be due to oral putrefactive microbial activity. In a small number of subjects the cause and treatment of halitosis need to be clarified.

Intestinal microbiota is composed by a community of microorganisms, which regulate intestinal functions and affect the global health. It is presumable that the well-known intestinal damages induced by Non Steroidal Antiinflammatory Drugs (NSAIDs) mirror on the homeostasis of microbiota, as confirmed by studies investigating this aspect. This review reports the evolving knowledge in this field taking into account both intestinal damage and microbiota involvement. In addition, we analyze a recent study reporting how NSAIDs change intestinal bacterial composition and, on this basis, hypothesize further possible interactions. Indeed, NSAIDs are responsible for a marked reduction of Lactobacilli, which act in the maintenance of luminal pH, mucosal permeability, enterocyte adhesion, mucus production, and immune system modulation. Moreover, Bifidobacteria are involved in the modulation of intestinal motility and local immunity and the demonstrated dangerous effect of NSAIDs could operate through an interference with these functions. A participation of microbiota in mesalazine and salycilate prevention of intestinal cancer may be supposed through their ability to stimulate bacterial production of molecules interfering with cell cycle on the basis of scanty available data. Finally, a supplementation with probiotics in chronic users of NSAIDs may help microbiota remodeling in a damaged intestine, but the poor current knowledge does not allow setting a clear indication for their use despite few evidences of a beneficial effect. In conclusion, it is presumable that the multiple effects of NSAIDs on the lower gastro-intestinal tract may involve microbiota alterations and this consideration suggests further investigations.

Objective: We hypothesized that remifentanil continuous infusion during colonoscopy in spontaneous respiration may give benefits in terms of quality of sedation and recovery compared to propofol, and that patients’ ventilatory drive and consciousness could be accurately evaluated by the continuous measurement of end-tidal CO2 (EtCO2), and of Bispectral Score (BIS) respectively. Methods: One-hundred and eighty patients scheduled for colonoscopy were randomized in two groups: 76 patients were included in Groupcontrol (propofol 0.5 mg/kg bolus plus infusion 1 mg/kg/h) and 78 patients in Gruopremi (0.5 mcg/Kg/1 min bolus plus infusion 0.08 mcg/kg/min, progressively reduced to 0.03 mcg/kg/min). Cardiovascular and respiratory variables were measured before induction and every 3 min throughout the procedure. Sedation level was estimated by BIS and Observer’s Assessment of Alertness/Sedation Scale (OAA/S). Respiratory function was evaluated by arterial oxygen saturation (SaO2) and EtCO2. Recovery from sedation and hospital discharge criteria were assessed by Modified Aldrete Score System (APRS) 30 min after colonoscopy completion. Results: Remifentanil was effective and well tolerated during colonoscopy. Hemodynamic parameters remained stable throughout the study steps in both groups. In Groupremi OAA/S and BIS score were higher (p

Cirrhosis has always been regarded as hemorrhagic coagulopathy caused by the reduction in the hepatic synthesis of procoagulant proteins. However, with the progression of liver disease, the cirrhotic patient undergoes a high rate of thrombotic phenomena in the portal venous system. Although the progression of liver failure produces a reduction in the synthesis of anticoagulant molecules, a test able to detect the patients with hemostatic balance shifting towards hypercoagulability has not yet been elaborated. The need of treatment and/or prophylaxis of cirrhotic patients is demonstrated by the increased mortality, the risk of bleeding from esophageal varices, and the mortality of liver transplantation, when portal vein thrombosis (PVT) occurs even if current guidelines do not give indications about PVT treatment in cirrhosis. In view of the general feeling that the majority of cirrhotic patients at an advanced stage may be in a procoagulant condition (suggested by the sharp increase in the prevalence of PVT), it is presumable that a prophylaxis of this population could be of benefit. The safety and the efficacy of prophylaxis and treatment with enoxaparin in patients with cirrhosis demonstrated by a single paper suggest this option only in controlled trials and, currently, there are no sufficient evidences for a recommendation in the clinical practice.

Goals: The goals of this study were to investigate the role of a new probiotic preparation (Lactobacillus reuteri DSM 17938 and L. reuteri ATCC PTA 6475) in Helicobacter pylori infection. Background: Specific probiotic strains play a role in H. pylori infection for their ability to decrease bacterial load and gastritis, prevent antibiotic-associated side effects, and increase the eradication rate. Study: This is a prospective, double-blind, randomized, placebocontrolled study in a tertiary care setting. A total of 100 H. pylori– positive naive patients received either L. reuteri combination (2� 108 Colony Forming Units) or placebo during a 3-phase study (pre-eradication, eradication, and follow-up). All underwent 13C urea breath test (13C-UBT), blood assessments of gastrin-17 (G17), endoscopy, and the Gastrointestinal Symptom Rating Scale. Eradication was confirmed by 13C-UBT 8 weeks after the completion of therapy. Results: Fifty patients were allocated in each group. During preeradication period, 13 C-UBT d decreased by 13% in L. reuteri combination as compared with a 4% increase in placebo (� 13.2 ± 34% vs. 4.3 ± 27%; P < 0.03). During eradication, GSRS increased significantly in placebo as compared with L. reuteri combination (6.8 ± 2.9 vs. 4 ± 3.1; P < 0.01). Significantly less patients in L. reuteri combination as compared with placeboreported side effects (40.9% vs. 62.8%; P < 0.04). An abnormal G17 value was found in patients receiving placebo as compared with L. reuteri combination (28% vs. 12%; P < 0.02). Eradication rate was 75% in L. reuteri combination and 65.9% in placebo (P = NS). L. reuteri combination increased eradication rate by 9.1% (odds ratio: 1.5). Conclusions: L. reuteri combination alone is able to exert an inhibitory effect on H. pylori growth, and when administered with eradication therapy, it determines a significant reduction in antibiotic-associated side effects. Moreover, L. reuteri combination was able to decrease serum G17 levels and to (not significantly) increase the H. pylori–eradication rate.

Conventional triple therapies for Helicobacter pylori (H. pylori) eradication have recently shown a disappointing reduction in effectiveness in many countries. The main reason for failure was found to be bacterial resistance to one of the most commonly used antibiotics, clarithromycin. An additional problem for conventional triple therapy is the high rate of resistance to metronidazole found in Europe, America and Asia. In Italy, in the last 15 years a 2-fold increase in resistance has occurred. A recent study of the whole of Italy included about 20 patients from each region at the first endoscopic diagnosis of H. pylori infection. The most surprising result was the patchy distribution of resistance, which was almost absent in two regions (one northern and one southern), although the highest prevalence was found in some regions of the South. In the paediatric population we found a 25% prevalence of resistance in a sample of H. pylori positive children observed between 2002 and 2007, mirroring data obtained in southern European countries. Clarithromycin resistance assessment is currently based on phenotypic detection performed after culture the agar dilution method or E-test, and genotypic methods based on polymerase chain reaction (PCR). In a recent comparative study we found a 71.2% agreement between the two methods. Culture-free techniques are highly accurate in finding even minimal traces of genotypically resistant strains. Moreover, PCR-based tools are accurate in detecting a heteroresistant status, defined as the co-existence of some strains that are susceptible and some resistant to the same antibiotic in an individual patient. Three point mutations, namely A2143G, A2142G and A2142C, are responsible for 90% of cases of primary clarithromycin resistance in H. pylori strains isolated in Western countries, although we previously demonstrated that the presence of the A2143G mutation, but not A2142G or A2142C, significantly lowered the H. pylori eradication rate. Treatment failure has considerable cost/benefit implications because of "waste" of National Health System and patient resources, in terms of drugs, further diagnostic tests and medical examination expenses. Therefore, in future it would be very useful to be able to test for clarithromycin resistance before starting conventional triple therapy. Hopefully, fast, effective non-invasive tests may soon be devised to determine this condition.

To assess the safety and effect of the supplementation of a patented blend of dietary phytoestrogens and insoluble fibers on estrogen receptor (ER)-β and biological parameters in sporadic colonic adenomas.A randomized, double-blind placebo-controlled trial was performed. Patients scheduled to undergo surveillance colonoscopy for previous sporadic colonic adenomas were identified, and 60 eligible patients were randomized to placebo or active dietary intervention (ADI) twice a day, for 60 d before surveillance colonoscopy. ADI was a mixture of 175 mg milk thistle extract, 20 mg secoisolariciresinol and 750 mg oat fiber extract. ER-β and ER-α expression, apoptosis and proliferation (Ki-67 LI) were assessed in colon samples.No adverse event related to ADI was recorded. ADI administration showed a significant increases in ER-β protein (0.822 ± 0.08 vs 0.768 ± 0.10, P = 0.04) and a general trend to an increase in ER-β LI (39.222 ± 2.69 vs 37.708 ± 5.31, P = 0.06), ER-β/ER-α LI ratio (6.564 ± 10.04 vs 2.437 ± 1.53, P = 0.06), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (35.592 ± 14.97 vs 31.541 ± 11.54, P = 0.07) and Ki-67 (53.923 ± 20.91 vs 44.833 ± 10.38, P = 0.07) approximating statistical significance. A significant increase of ER-β protein (0.805 ± 0.13 vs 0.773 ± 0.13, P = 0.04), mRNA (2.278 ± 1.19 vs 1.105 ± 1.07, P0.02) and LI (47.533 ± 15.47 vs 34.875 ± 16.67, P0.05) and a decrease of ER-α protein (0.423 ± 0.06 vs 0.532 ± 0.11, P0.02) as well as a trend to increase of ER-β/ER-α protein in ADI vs placebo group were observed in patients without polyps (1.734 ± 0.20 vs 1.571 ± 0.42, P = 0.07).The role of ER-β on the control of apoptosis, and its amenability to dietary intervention, are supported in our study.

To investigate tumor necrosis factor-α (TNF-α), syndecan 1 and basic fibroblast growth factor (bFGF) balance in Crohn's disease (CD) strictures.Our study was performed on 24 surgical specimens of CD fibrotic stenosis. Ten histological normal surgical samples were retrieved for both the large and small bowel from patients with benign conditions and healthy tissue represented control collection. Sex and age in controls did not differ from CD group. Three endoscopic biopsy specimens taken after informed consent in subjects with normal colon were also used as negative controls. TNF-α, syndecan 1 and bFGF were detected by both reverse transcriptase reverse transcriptase polymerase chain reaction after mRNA extraction (results expressed as fold-change) and immunohistochemistry.TNF-α did not show any significant difference between CD and control specimens (1.54 ± 1.19; P0.05). Very high levels of bFGF were observed in CD (11.76 ± 4.65; P0.001) unlike syndecan 1 which showed a moderate increase (5.53 ± 2.18; P0.005). analysis of variance (ANOVA) plus Student-Neumann-Keuls showed: bFGFsyndecan 1TNF-α = control. Immunoreactivity for bFGF was observed in epithelial, stromal, endothelial cells and even in the muscular layer, whilst in normal tissue it was almost unexpressed. Syndecan 1 and TNF-α staining was confined to mucosal epithelial and stromal cells, while in controls syndecan 1 was found in its normal site, i.e., basolateral area of the crypts and TNF-α very poorly expressed.Fibrotic stenosis of CD may be the final result of an irreversible transformation of different cells into fibrogenic phenotype no longer inhibited by post-transcriptional regulation.

Helicobacter pylori (HP) infection is the main etiopathogenetic agent responsible for inflammatory and ulcerative changes in gastroduodenal mucosa and the basis for both intestinal and diffuse types of gastric carcinoma. In this latter case, intestinal metaplasia is the intermediary between gastritis and cancer. In this study we describe the proliferative activity of gastric epithelium in the progressive stages of HP infection. The expression of proliferating cell nuclear antigen (PCNA), which has proven to be a reliable method for this evaluation, was used as a marker. The study was performed on endoscopic biopsies of the gastric antrum of 40 patients, who were divided into five groups, eight in each group: normal histology and endoscopy, HP-; histological HP+ gastritis with normal endoscopy; histological HP+ gastritis with endoscopic evidence of chronic erosions; complete and incomplete intestinal metaplasia in a HP+ stomach. PCNA was detected by immunohistochemistry and expressed as labeling index, ie, percentage of positive nuclei either in the whole or upper third of foveolae. Our data show a progressive increase of epithelial proliferation in the successive stages of HP infection ranging from gastritis alone to the development of incomplete intestinal metaplasia, a well-known precancerous condition. The proliferative pattern tended to expand towards the upper foveolar third, which in normal conditions does not represent a site of epithelial renewal. These alterations may be related to the development of neoplastic transformations of gastric epithelium. It is well known that genetic mutations are facilitated in proliferating cells. Therefore, our results indicate that the high epithelial turnover, expressed by PCNA LI, may be an indicator of increased risk of neoplastic changes in long-standing untreated HP+ chronic gastritis.

Background A link between small intestinal bacterial overgrowth (SIBO) and celiac disease (CD) has been hypothesized. Methods Literature search was performed in main medical databases. Methods of analysis/inclusion criteria were based on Preferred Reporting Items for Systematic reviews and Meta-Analyses recommendations. The end-point was to estimate, by a pooled-data analysis, SIBO prevalence in CD. Proportions/percentages and their 95% confidence intervals (CI) were calculated by inverse variance method, whereas odd ratios (OR) and their 95% CI were estimated, where available, based on the Mantel-Haenszel method. Data were entered into the RevMan 5.3 software. Key Results Eleven articles fulfilled considered criteria. The pooled mean prevalence of SIBO in CD was 20% (95% CI of 10%-30%). In comparison to asymptomatic controls, CD was associated to higher risk of SIBO, with an OR of 10.52 (95% CI 2.69-41.21, P=.0007). Jejunal aspirate culture assessed SIBO prevalence of 11% (95% CI 3%-19%) in CD, whereas breath tests detected a higher value (23%, 95% CI 10%-37%). The pooled prevalence of SIBO in CD patients who were symptomatic despite a GFD was 28% (95% CI 10%-47%), higher than in asymptomatic celiac patients (pooled prevalence of 10%, with a 95% CI of 3%-16%), despite not statistically significant (P=.06). When GFD-unresponsive CD was defined only by clinical persistence of symptoms, the prevalence of SIBO was higher than in the case of villous atrophy association (31% vs 16% P=.33). Conclusions The heterogeneity of available studies may not support a relationship SIBO-CD. Nevertheless, SIBO could be more common in CD when symptoms do not improve after GFD.

We evaluated the incidence and risk factors of duodenal ulcer (DU) in a cohort of patients who had undergone esophagogastroduodenoscopy in our institution from 1978 to 1982, without then finding a gastric or duodenal ulcer. Six hundred and twenty-one subjects entered the study, and 526 (84.7%) were traced in 1992. Forty-one cases of DU were found, an incidence rate of 6.7 per 1,000 person-years; the male/female ratio was 2:1. The diagnoses of peptic ulcer (PU) were validated by means of medical documentation. The odds ratio of DU was 2.3 (95% confidence interval 0.8-6.3) and 3.5 (1.4-9.0) in the II and III tertile of basal acid output (BAO) compared with the I tertile, and 2.6 (0.8-8.3) and 7.0 (2.3-20.7) in the II and III tertile of maximal acid output (MAO) compared with the I tertile. Cigarette smoking and the presence of PU among siblings of DU patients were risk factors for DU. Multiple logistic regression confirmed only the association of DU with MAO, cigarette smoking, and family history. By means of a nested case-control study, the risk of developing DU was assessed in subjects with Helicobacter pylori (HP) at the biopsy of gastric mucosa performed before the ulcer diagnosis. The odds ratio of DU in HP-positive subjects was 5.0 (95% confidence interval 0.6-45). The results of this study confirm the influence of gastric acid secretion, cigarette smoking, and family history in the pathogenesis of DU and suggest that HP infection not only favors relapse but could have an important role in the onset of the disease.

Interest in the possibility that diet might help to reduce the risk of colorectal cancer dates back to 1970 based on both the large variation in rates of specific cancers in different countries and the impressive changes observed in the incidence of cancer in migrants from low- to high-risk areas. Here, we report the state of art of literature data about this topic. Three sections have been separately considered: chemoprevention of first tumor onset, chemoprevention of recurrence after surgery, and chemoprevention of polyp recurrence in the course of the follow-up of subjects with elevated risk. A particular attention has been pointed to dietary factors and survival, whose relevance is showing a growing interest. The relationship between diet and colorectal cancer has been extensively studied about the onset, sometimes with controversial results. Its influence on recurrence and survival has been examined in only few studies. Literature data are convincing for a protective role on the onset of preneoplastic and neoplastic lesions for some foods such as fibers, vitamin A and D, folic acid, calcium, antioxidants, and promising perspectives for some substances such as phyto-estrogens. Less evidence-based data are available on the possibility to avoid the recurrence of the disease or to affect its mortality with dietary habits. Future perspectives will be directed be not only to identify new dietary style able to prevent the onset of neoplastic lesion of the colon but also to realize an effective chemoprevention.

Terminal ileum adenocarcinoma is a rare tumour. Its incidence or prevalence among the other sites of gastro-intestinal tract is unknown, since it has been only sporadically described. Since contrast enhanced ultrasonography has been recently used to study bowel alterations in the course of neoplastic or inflammatory disorders, we report here a case of a rare tumour (terminal ileum poorly differentiated adenocarcinoma) in which the investigation played a pivotal role to obtain a defined diagnosis. MATERIALS AND METHODS (CASE REPORT): Here we report the case of a 62 year old male patient. Due to intestinal occlusive symptoms and body weight decrease of about 8 Kg, he performed an abdominal computed tomography, intestinal magnetic resonance with double contrast medium, colonoscopy and contrast enhanced ultrasonography using a second generation medium.In our case the peculiar aspect is that no arterial enhancement was observed and the finding remained unchanged for about 2.48 minutes as well as after a further administration of 1.5 ml of contrast medium. This aspect was not suggestive of an active inflammation such as Crohn's disease, where a marked contrast medium enhancement should be expected.At present it is too speculative to emphasize contrast enhanced ultrasonography as usefulness tool in the diagnosis of terminal ileum tumors. Nevertheless, our preliminary experience strongly encourages the diffusion of the method.

Dr. De Francesco. A 28-year-old male farmer, complaining of mild, recurrent right upper quadrant and chest pain was referred to gastroenterology. The patient had received sporadic and unsuccessful NSAID-based therapy during the prior 2 years. Bowel movements were regular and no fever was present. He smoked ten cigarettes daily. Physical examination was unrewarding, but abdomen palpation revealed exacerbation of tenderness in the liver area with modest hepatomegaly. An abdominal ultrasonography was performed showing a round mass, 8 cm in diameter, localized in the right hepatic lobe, with a heterogeneous ultrasound signal in the central area. Laboratory tests found elevated levels of alanine aminotransferase (91.5 normal value), alkaline phosphatase and c-glutamyltranspeptidase (both 9 1.3 normal value) and increased values of erythrosedimentation rate (48 mm/h), C-reactive protein (95.5 normal value), cholesterol level (91.2 normal value) and triglycerides level (92 normal value); all other biochemical tests, including a-fetoprotein, were in the normal range. Computed tomography (CT scan) confirmed the presence of a round mass (11 9 10 cm) in the right hepatic lobe, compressing the right hepatic vein. The lesion appeared heterogeneous and hypodense, with a peripheral enhancement in the arterial phase and low enhancement in the portal and delayed phase. A pseudo-capsule was evident with a small interruption in the proximity of a satellite nodule of 1 cm (Fig. 1).

Probiotics survive in gastric environment competing with H. pylori. We studied probiotic “multistrain” administration in dyspeptics with H. pylori (placebo-controlled study). Forty patients with H. pylori (urea breath test – UBT - and IgG) were treated for 10 days with a mixture of 8 species of probiotics. Control group represented by 40 positive subjects received placebo. A second UBT and H. pylori stool antigen (HpSA) detection were performed after 1 month. Patients who remained infected were treated with triple therapy undergoing another UBT after 30 days. A second line therapy was administered in remaining positive patients. Statistics: Fisher’s exact probability and Student’s t tests. Thirteen out 40 patients using probiotics became negative, while controls remained positive, irrespectively of the initial UBT delta value. No difference in the eradication rates between the two groups was found (68%-71%). After second line therapy two patients remained positive.Thirteen out 40 patients using probiotics became negative, while controls remained positive, irrespectively of the initial UBT delta value. No difference in the eradication rates between the two groups was found (68%-71%). After second line therapy two patients remained positive. An adequate supplementation with probiotics might eradicate H. pylori.

Helicobacter pylori (H. pylori) plays a crucial role in the pathogenesis of chronic active gastritis, peptic ulcer and gastric mucosa-associated lymphoid tissue-lymphoma, and is also involved in carcinogenesis of the stomach. H. pylori treatment still remains a challenge for physicians, since no current first-line therapy is able to cure the infection in all treated patients. Several factors may help in the eradication of therapy failure. We reviewed both bacterial and host factors involved in therapeutic management of the H. pylori infection. In addition, we evaluated data on the most successful therapy regimens - sequential and concomitant therapies - currently available for H. pylori eradication.

Complex and conflicting relationships between epidermal growth factor (EGF), estrogens (E), androgens (A), and related receptors (EGF-R, E-R, A-R) have been reported in different biological situations associated with cell proliferation. There is also evidence that EGF and sex hormone receptors may be involved in normal and neoplastic growth of the gastrointestinal mucosa. In this study, we investigated the behavior of EGF receptors and sex hormone and related receptors, during N-methyl-N'-nitro-N-nitrosoguanidine (NG)-induced gastric carcinogenesis in Sprague-Dawley male rats. Four groups of 15 rats each (10 NG-treated and five controls) were sacrificed after 1, 20, 30, and 40 weeks of treatment. Gastric tissue from each rat was processed for receptor status (number and affinity) and proliferative activity. A significant and progressive decrease of A-R and EGF-R was observed starting from the 20th week, while no change of E-R occurred throughout the experiment. Cell proliferation in the gastric mucosa of NG-treated rats increased after 30 weeks of treatment. These data indicate that NG treatment is able to modify the receptor status of gastric mucosa in rats.

Tumour necrosis factor-α (TNF-α) expression may be increased in segmental colitis associated with diverticulosis (SCAD). Our aim was to assess TNF-α expression in SCAD in relationship to the treatment.10 patients affected by severe (type B and D) SCAD were studied (6 males, 4 females, mean age 60.54 years, range 43-85 years). All patients were treated with beclomethasone dipropionate 10 mg/day plus a probiotic preparation VSL#3 for 8 weeks. At that time, clinical, endoscopic and histological reassessment was performed. Controls were 5 patients with active ulcerative colitis (UC).After treatment, all SCAD B and no SCAD D patients were in remission. The TNF-α expression dropped from 42.7% (+/-7.58) to 15.7% (+/-2.6) in SCAD B patients (p=0.001), and from 40% (+/-5.9) to 28.6% (+/-5.3) in SCAD D patients (p=0.005). In UC patients, the TNF-α expression dropped from 45.5% (+/-5.09) to 22.5% (+/-2.5) (p=0.001). Neither SCAD B nor SCAD D patients showed a significant difference in TNF-α expression compared to UC after treatment. Finally, TNF-α was significantly overexpressed in SCAD D than in SCAD B at the end of treatment (p=0.048).TNF-α expression in SCAD down regulates after treatment, and seems to be related to the clinical response to therapy. This behaviour, similar to that of Inflammatory Bowel Diseases (IBD), confirms that this disease should be considered as a subtype of IBD.

It is known that syndecan 1 in inflammatory bowel diseases is able to migrate from epithelial basolateral site to the stromal area and apical surface of epithelium with a consequent activation and modulation of basic fibroblast growth factor (bFGF), and this process sustains mucosal healing of ulcers. On the other hand, tumour necrosis factor (TNF) α mucosal levels are directly related to the entity of the damage in these disorders. Aim of the study A 'post-hoc' retrospective study was performed to estimate mucosal TNF α in rectal biopsies of subjects with ulcerative colitis (UC) before and after effective infliximab therapy and its relationship with syndecan 1, bFGF and endoscopic mucosal healing.Paraffin-embedded rectal samples from 12 patients with UC responders to infliximab were analysed for TNF α, syndecan 1 and bFGF before and 6 months after therapy using a real-time reverse transcriptase polymersase chain reaction. Additionally, syndecan 1 location was evaluated by immunohistochemistry. Samples from 12 subjects with irritable bowel symptoms without endoscopic/histological abnormalities represented the control group. Mucosal healing induced by the treatment was defined by an endoscopic Mayo subscore changing from 2-3 to 0. ANOVA plus Student-Newman-Keuls was used for statistical analysis.The authors found that in the active disease, an increase in TNF α (p0.001) is accompanied by raised levels of both syndecan 1 (p0.005) and bFGF (p0.005) compared with the control group. Infliximab-induced TNF α decrease to levels similar to controls is associated with both endoscopic mucosal healing and adhesion molecule/growth factor significant reduction. Additionally, syndecan 1 location, which is predominant in the stromal cells and apical epithelium in the active disorder, is quite exclusively located at the basolateral epithelial area in both healed mucosa and controls.Balanced interaction among TNF α inhibition by infliximab, syndecan 1 migration, bFGF repair modulation and final adhesion molecule reversal to its normal location might represent a suitable molecular pathway of endoscopic mucosal healing in UC.

The aim of the work was to compare H. pylori clarithromycin-resistance according two methods. Etest was performed on H. pylori isolated from gastric biopsy samples. TaqMan Real-Time-PCR (RT-PCR) was performed on paraffin-embedded gastric biopsy samples of the same patients. Forty-seven out of 88 strains were resistant to clarithromycin by Etest, whereas RT-PCR detected this resistance on paraffin-embedded specimens of 50 patients. RT-PCR performed on paraffin-embedded biopsy specimens of 47 patients infected with H. pylori resistant to clarithromycin as detected by Etest, revealed the presence of a resistant strain only in 40 samples. RT-PCR performed on samples of 41 patients harbouring clarithromycin-susceptible H. pylori strains showed the presence of 31 susceptible and 10 resistant strains. RT-PCR detected 18 cases with heteroresistant status. The difference between the two tests in detecting clarithromycin-resistance was not statistically significant even if RT-PCR detected more resistant cases. The genotyping resistance on paraffin-embedded gastric biopsy specimens may be used to establish resistance to clarithromycin before the treatment when culture and susceptibility testing are not available. In case of failure of an empirical clarithromycin-based triple antimicrobial treatment, RT-PCR performed on paraffin-embedded biopsy sample will establish the primary resistance to clarithromycin. In addition, this test can be useful for epidemiological investigation as well as for monitoring the evolution of clarithromycin resistance along the time.

Albumin constitutes approximately one half of the proteins in the plasma and plays a pivotal role in modulating the distribution of fluid between body compartments. Hence it is commonly employed in cirrhotic patients in association with diuretics for the treatment of ascites. Nevertheless, its usefulness is controversial in this condition and well-stated only in some circumstances. The item of safety of the drug appears to be convincing due to the accurate cautions in the course of its preparation. Side effects are described in literature only as sporadic events. Indeed, albumin administration is effective to prevent the circulatory dysfunctions after large-volume paracentesis and renal failure and after Spontaneous Bacterial Peritonitis (SBP). Finally albumin represents, associated with vasoconstrictors, the therapeutic gold standard for the hepatorenal-syndrome (HRS). Physiopathological bases of the therapeutic use of albumin in hepatic cirrhosis consist in both hypoalbuminemia and portal hypertension consequences. In fact, cirrhotic patient with ascites, in spite of hydrosaline retention, shows an effective hypovolemia with peripheral arterial vasodilatation and increase in heart rate. Therefore the effectiveness of albumin administration in the treatment of ascites is due to its plasma volume expander property as well as its efficacy in restoring plasmatic oncotic pressure. Trials are in progress in order to define the effectiveness of the prolonged home-administration of human albumin in the treatment and prevention of ascites. Finally, it has been recently demonstrated that the binding, transport and detoxification capacities of human albumin are severely reduced in cirrhotics and this impairment correlates with the degree of liver failure. Therefore, the next challenge will be to determine whether the alterations of non-oncotic properties of albumin are able to forecast mortality in cirrhotics with ascites and exogenous albumin chronic administration will be effective in predicting and preventing such alterations.

Background: Tumour necrosis factor- expression may be increased in segmental colitis associated with diverticulosis. Aims: To assess tumour necrosis factor- expression in segmental colitis associated with diverticulosis in relation with the severity of the endoscopic damage. Methods: 21 patients affected by segmental colitis associated with diverticulosis were studied (15 M, 6 F, mean age 58.87 years, range 43–85 years). Segmental colitis associated with diverticulosis was graduated as mild-moderate (patterns A and C) and severe (patterns B and D). Ten patients with moderate-to-severe ulcerative colitis, 10 patients with moderate-to-severe Crohn’s disease, and 10 patients with irritable bowel syndrome served as control groups. Results: Tumour necrosis factor- expression was significantly higher in segmental colitis associated with diverticulosis B (42.7%) and segmental colitis associated with diverticulosis D (40%) than in segmental colitis associated with diverticulosis A (19.1%) and segmental colitis associated with diverticulosis C (21.1%).Tumour necrosis factor- expression was lower in segmental colitis associated with diverticulosis A and C than in ulcerative colitis and Crohn’s disease, whilst no different tumour necrosis factorexpression was found between segmental colitis associated with diverticulosis B and D and both ulcerative colitis and Crohn’s disease.Finally, tumour necrosis factor- expression was significantly lower in irritable bowel syndrome (8% ± 4) than in every type of segmental colitis associated with diverticulosis. Conclusions: Tumour necrosis factor- expression in segmental colitis associated with diverticulosis seems to be related to the severity of the endoscopic damage. This behaviour, similar to that of the inflammatory bowel diseases (IBD), confirms that this disease should be considered as a subtype of IBD. © 2010 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.