Inflammatory bowel disease (IBD) refers to a group of chronic inflammatory diseases that targets mainly the gastrointestinal tract. The clinical presentation of IBD includes both gastrointestinal manifestations and extraintestinal manifestations (EIM). The reported cardiovascular manifestations in IBD patients include pericarditis, myocarditis, venous and arterial thromboembolism, arrhythmias, atrioventricular block, heart failure, endocarditis, valvulopathies, and Takayasu arteritis. The aim of this article is to review the available literature about the possible pathogenic mechanisms and determine preventive measures capable of reducing the incidence and severity of the cardiovascular manifestations. In IBD patients, the incidence of cardiovascular manifestations is low, but higher than that in the general population. Therefore, clinicians should pay attention to any new modification that might indicate cardiovascular involvement in IBD patients, and they should consider chronic inflammatory diseases in patients with cardiac conditions without an evident cause. Considering the role of inflammation in the development of cardiovascular manifestations, the management should include prevention of flares and maintenance of remission for as long as possible. Preventive measures should also include active screening and strict control of the cardiovascular risk factors in all IBD patients.

At present, irritable bowel syndrome (IBS) is a common medical problem all over the world that implies considerable social burden and high costs. Considering the different pathophysiological pathways, unitary management for IBS is not possible. Of the therapeutic approaches that have been proposed so far, only a few have been demonstrated to have beneficial effects in IBS patients. The implication of gut microbiota in IBS is obvious, similarly to the therapeutic effect of pro-/prebiotics, which is reflected by the latest publications. The intake of inulin seems to regulate the bowel peristalsis and colonic transit, the consistency and frequency of the stools, as it changes the composition of gut microbiota. The beneficial effect of inulin in patients with IBS-constipation form (IBS-C) is obvious, but still, more randomized controlled clinical trials involving large samples of patients are needed in order to provide more evidence. Contents

Artificial intelligence, a computer-based concept that tries to mimic human thinking, is slowly becoming part of the endoscopy lab. It has developed considerably since the first attempt at developing an automated medical diagnostic tool, today being adopted in almost all medical fields, digestive endoscopy included. The detection rate of preneoplastic lesions (i.e., polyps) during colonoscopy may be increased with artificial intelligence assistance. It has also proven useful in detecting signs of ulcerative colitis activity. In upper digestive endoscopy, deep learning models may prove to be useful in the diagnosis and management of upper digestive tract diseases, such as gastroesophageal reflux disease, Barrett’s esophagus, and gastric cancer. As is the case with all new medical devices, there are challenges in the implementation in daily medical practice. The regulatory, economic, organizational culture, and language barriers between humans and machines are a few of them. Even so, many devices have been approved for use by their respective regulators. Future studies are currently striving to develop deep learning models that can replicate a growing amount of human brain activity. In conclusion, artificial intelligence may become an indispensable tool in digestive endoscopy.

Gardner syndrome is a neoplasic disease that associates intestinal polyposis and colorectal adenocarcinoma with osteomas and soft tissue tumors determined by germline mutations in the APC gene. The early diagnosis and identification of high-risk individuals are important because patients have a 100% risk of colon cancer. We present the case of a family with Gardner syndrome. Cephalometric, panoramic X-rays and CBCT of the proband and her brother showed multiple osteomas affecting the skull bones, mandible and paranasal sinuses. The detailed family history showed an autosomal dominant transmission with the presence of the disease in the mother and maternal grandfather of the proband. Both had the typical signs of disease and died in the fourth decade of life. Based on these aspects the clinical diagnosis was Gardner syndrome. By gene sequencing, a novel pathogenic variant c.4609dup (p.Thr1537Asnfs*7) in heterozygous status was identified in the APC gene in both siblings. We reviewed literature data concerning the correlation between the localization of mutations in the APC gene and the extracolonic manifestations of familial adenomatous polyposis as well as their importance in early diagnosis and adequate oncological survey of patients and families based on abnormal genomic variants.