Efficacy of hemostatic powders as monotherapy or rescue therapy in gastrointestinal bleeding related to neoplastic or non-neoplastic lesions.

BACKGROUND: Hemostatic powder (HP) in gastrointestinal bleeding (GIB) is mainly used as rescue therapy after failure of conventional hemostatic procedures (CHP). AIM: To define the best field of application and the efficacy of HP as first choice monotherapy or rescue therapy. METHODS: We compared the efficacy of HP monotherapy, HP rescue therapy, and CHP in the management of active GIB due to neoplastic and non-neoplastic lesions. RESULTS: A total of 108 patients, 43 treated with HP as either first choice or rescue therapy and 65 with CHP, were included in the study. The most frequent sources of bleeding were peptic ulcer and malignancy. Immediate hemostasis rates were: HP monotherapy = 100% in peptic ulcer and 100% in malignancy; HP rescue therapy = 93.2% in peptic ulcer and 85.7% in malignancy; CHP = 77.9% in peptic ulcer and 41.7 in malignancy. Definitive hemostasis rates were: HP monotherapy = 50% in peptic ulcer and 45.5% in malignancy; HP rescue therapy = 73.3% in peptic ulcer and 85.7% in malignancy; CHP = 69.1% in peptic ulcer and 33.3% in malignancy. No difference was found in terms of additional intervention between the three groups. CONCLUSIONS: HP is highly effective as monotherapy and rescue therapy in GIB. GIB related to malignancy may be the best field of application of HP, but confirmatory studies are necessary.

The Pharmacokinetic Profile of a New Gastroresistant Capsule Preparation of Eicosapentaenoic Acid as the Free Fatty Acid.

Supplementation with n-3 polyunsaturated fatty acids (n-3 PUFAs) may be beneficial for patients with inflammatory bowel diseases (IBD). In this study we analyzed the pharmacokinetic profile of eicosapentaenoic acid (EPA), as the free fatty acid (FFA), in an enteric-coated preparation, in 10 ulcerative colitis (UC) and 10 Crohn's disease (CD) patients and 15 healthy volunteers (HV). Subjects received 2 g daily of EPA-FFA for 8 weeks. Plasma phospholipid and red blood cell (RBC) membrane fatty acid content were measured by gas chromatography-mass spectrometry. There was a rapid incorporation of EPA into plasma phospholipids by 2 weeks and a slower, but highly consistent, incorporation into RBC membranes (4% total fatty acid content; coefficient of variation 10-16%). There was a concomitant reduction in relative n-6 PUFA content. Elongation and desaturation of EPA into docosahexaenoic acid (DHA) via docosapentaenoic acid (DPA) were apparent and DHA content also increased in membranes. EPA-FFA is well tolerated and no difference in the pharmacokinetic profile of n-3 PUFA incorporation was detected between IBD patients and HV. Our data support the concept that EPA can be considered the "universal donor" with respect to key n-3 PUFAs and that this enteric-coated formulation allows long term treatment with a high level of compliance.

Clinical application of faecal calprotectin in ulcerative colitis patients.

OBJECTIVE: Faecal calprotectin (FC) is the most relevant noninvasive biomarker for monitoring inflammatory status, response to treatment and for predicting clinical relapse in ulcerative colitis (UC). The aim of this study was to evaluate the role of FC in predicting both clinical/endoscopic activity and clinical relapse in a large UC patient cohort. PATIENTS AND METHODS: A two-phase prospective study was carried out. In the first phase, the relationship between FC and clinical/endoscopic activity was evaluated. In the second phase, a cohort of asymptomatic patients with endoscopic mucosal healing was followed up using clinical and FC level determinations. RESULTS: One hundred and twenty-one UC patients were enrolled. The FC concentrations were directly correlated with both clinical and endoscopic activity (r=0.76 and 0.87, respectively, P<0.05) and were capable of differentiating between different degrees of endoscopic severity (P<0.01). An FC cut-off value of 110 µg/g was highly predictive (95%) of endoscopic activity. Seventy-four patients in clinical remission with mucosal healing were followed up for a year or until relapse and 27% developed a clinical relapse. The FC concentration of nonrelapsed patients (48 µg/g) versus relapsed patients (218 µg/g) was significantly different (P<0.01). An FC cut-off value of 193 µg/g had an accuracy of 89% in predicting clinical relapse. High FC levels were associated with clinical relapse using survival analysis and multivariate analysis. CONCLUSION: Our data strongly support the use of FC for staging the activity of disease, predicting relapse and leading decision-making in a UC setting.

Can fecal calprotectin better stratify Crohn's disease activity index?

BACKGROUND: Crohn's disease (CD) activity index (CDAI) is still widely used for monitoring clinical activity in CD patients, but is of little value as indicator of persistent inflammation in symptomless patients. Fecal calprotectin levels ≥150 µg/g are strongly indicative of endoscopically and/or histologically active disease. Our aim was to study, in a large cohort of CD patients, the relationship between CDAI and fecal calprotectin levels. METHODS: CDAI and fecal calprotectin levels were evaluated in consecutive patients from a CD outpatient clinic. RESULTS: We enrolled 193 CD patients, of whom 38% with CDAI <150 had a calprotectin value ≥150 µg/g, suggestive of active disease. A logistic regression model showed that for CDAI levels between 100 and 150, the estimated logistic probability of calprotectin ≥150 µg/g increased progressively to 76%, reaching 94% where disease activity was localized in the colon. With a CDAI cut-off >120, we found a high diagnostic accuracy of 72%, with 88% specificity and 50% sensitivity (positive predictive value: 76%, negative predictive value: 71%) to identify a calprotectin value ≥150 µg/g. CONCLUSION: CDAI scores between 100 and 150 display an acceptable ability to quantify the risk of persistent inflammation as expressed by the high calprotectin level.

Mycobacterium avium subspecies paratuberculosis in the etiology of Crohn's disease, cause or epiphenomenon?

The origin of inflammatory bowel disease is unknown. Attempts have been made to isolate a microorganism that could explain the onset of inflammation, but no pathological agent has ever been identified. Johne's disease is a granulomatous chronic enteritis of cattle and sheep caused by Mycobacterium avium subspecies paratuberculosis (MAP) and shows some analogies with Crohn's disease (CD). Several studies have tried to clarify if MAP has a role in the etiology of CD. The present article provides an overview of the evidence in favor and against the "MAP-hypothesis", analyzing the methods commonly adopted to detect MAP and the role of antimycobacterial therapy in patients with inflammatory bowel disease. Studies were identified through the electronic database, MEDLINE, and were selected based on their relevance to the objective of the review. The presence of MAP was investigated using multiple diagnostic methods for MAP detection and in different tissue samples from patients affected by CD or ulcerative colitis and in healthy controls. On the basis of their studies, several authors support a close relationship between MAP and CD. Although increasing evidence of MAP detection in CD patients is unquestionable, a clear etiological link still needs to be proven.

A rare case of giant pseudopolyp and colitis cystica profunda coexistence in an ulcerative colitis patient / Un caso raro de coexistencia de un pseudopólipo gigante y colitis cística profunda en un paciente con colitis ulcerosa

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Asymptomatic and persistent elevation of pancreatic enzymes in an ulcerative colitis patient.

Azathioprine has been extensively used in the management of inflammatory bowel diseases. It might cause pancreatic damage in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis. Here we report the case of a 61-year-old patient with ulcerative colitis who had been treated with azathioprine for three years, achieving clinical remission. During treatment he presented an asymptomatic elevation of serum pancreatic enzymes, without any signs of pancreatitis at imaging. This evidence brought us to reassess the drug dosage, without achieving a normalization of biochemical analysis. Autoimmune pancreatitis was excluded. One year after the suspension of azathioprine, we still face persistent high levels of amylase/lipase. Normalization of enzymatic values in patients who develop intolerance to azathioprine, in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis, is usually achieved in about two months after stopping drug intake. Asymptomatic elevation in serum pancreatic enzymes in the absence of pancreatic disease is reported in the literature and defined as "Gullo's syndrome," but nobody of the subjects studied had been treated in the past with pancreatotoxic drugs. Might this case be defined as "benign pancreatic hyperenzymemia"?