Diverticular Disease: a Gut Microbiota Perspective.

Gut microbiota composition and functionality are involved in the pathophysiology of several intestinal and extraintestinal diseases, and are increasingly considered a modulator of local and systemic inflammation. However, the involvement of gut microbiota in diverticulosis and in diverticular disease is still poorly investigated. In this review, we critically analyze the existing evidence on the fecal and mucosa-associated microbiota composition and functionality across different stages of diverticular disease. We also explore the influence of risk factors for diverticulosis on gut microbiota composition, and speculate on the possible relevance of these associations for the pathogenesis of diverticula. We overview the current treatments of diverticular disease targeting the intestinal microbiome, highlighting the current areas of uncertainty and the need for future studies. Although no conclusive remarks on the relationship between microbiota and diverticular disease can be made, preliminary data suggest that abdominal symptoms are associated with reduced representation of taxa with a possible anti-inflammatory effect, such as Clostridium cluster IV, and overgrowth of Enterobacteriaceae, Bifidobacteria and Akkermansia. The role of the microbiota in the early stages of the disease is still very uncertain. Future studies should help to disentangle the role of the microbiome in the pathogenesis of diverticular disease and its progression towards more severe forms.

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.

Progressive familial intrahepatic cholestasis.

Progressive familial intrahepatic cholestasis (PFIC) is a heterogeneous group of autosomal recessive childhood cholestasis of hepatocellular origin. PFIC 1, also known as Byler disease, was first described in Amish kindred. It is characterized by cholestasis often arising in the neonatal period and it leads to death due to liver failure. PFIC 1, like Benign Recurrent Intrahepatic Cholestasis (BRIC) which is the benign form of the same disease, recognizes mutations in the ATP8B1 gene. PFIC 2 disease is clinically similar to PFIC 1 but it has a different gene mutation causing a defect in the Bile Salt Export Pump (BSEP), exclusively expressed in the liver and involved in the canalicular secretion of bile acids. PFIC 3 usually appears later in life and it has a higher risk of portal hypertension, gastrointestinal bleeding and liver failure. This particular form of disease (the only one with high serum values of g-glutamil transpeptidase), is associated to a genetic defect in the class III multidrug resistance protein (MDR). External biliary diversion and ursodeoxycholic acid therapy, should be considered as the initial therapy in these patients, even if liver transplantation still seems to be the only solution for most patients.