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Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide and its prevalence is even higher in patients with risk factors such as type 2 diabetes and obesity. Liver biopsy is the gold standard for diagnosis of non-alcoholic steatohepatitis (NASH), particularly for the assessment of fibrosis stage that is a key prognostic factor. Noninvasive methods for assessment of liver fibrosis are a huge need in contemporary hepatology in order to stratify patient's risk of advanced and progressive liver disease. In this perspective different imaging techniques have been developed in last decades and showed high performance in liver fibrosis evaluation. Strengths and weaknesses of all imaging methods are summarized in this review.

Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease and represent a common finding in highly prevalent metabolic disorders (i.e. type 2 diabetes, metabolic syndrome, obesity). Non-alcoholic steatohepatitis (NASH) requires liver biopsy for grading and staging the liver damage by the assessment of steatosis, inflammation and fibrosis. In parallel with the development of numerous 'liquid' biomarkers and algorithms that combine anthropometric and laboratory parameters, innovative hepatic imaging techniques have increasingly been developed to attempt to overcome the need for biopsy, both in diagnosis and staging of NAFLD, and in possible use in the follow-up of the disease. In this review, we focused on the different imaging techniques trying to highlight the strengths and disadvantages of different approaches, particularly for ultrasound techniques, in stratifying liver injury and fibrosis in patients with NAFLD / NASH.

The clinical and instrumental findings revealed a case of autoimmune polyendocrine syndrome (APS) type 3B+C in a 41-year-old Caucasian woman with unexplained refractory iron-deficiency anaemia secondary to autoimmune atrophic gastritis and a long-term history of two different autoimmune diseases-Hashimoto's disease and vitiligo. Indeed the occurrence in the same patient of three or more autoimmune diseases defines APS. The first classification of APS was suggested by Neufeld and Blizzard in 1980 and it included four main types of APS on the basis of clinical features. The only case of APS type 3B+C was described by Amerio et al in 2006.

To determine whether proliferative patterns in flat rectal mucosal samples can predict the recurrence of adenomatous colorectal polyps, after polypectomy, biopsy specimens from normal looking rectal mucosa were obtained at endoscopy from 55 patients diagnosed for the first time as having adenomatous colorectal polyps. Epithelial cell proliferation was assessed in biopsy specimens through 3H-thymidine autoradiography. After polypectomy, patients were followed for 24 months and underwent complete colonoscopy every 6 months to detect and remove any metachronous lesions. In 40 patients second biopsy specimens were taken during one of the follow up colonoscopies to evaluate the stability of proliferative indices over time. The ratio of labelled (S phase) to total cells (labelling index) for the entire crypt, as well as ratios for each of the five equal compartments into which the crypt had been divided longitudinally, was calculated for each patient. Mean labelling indices for upper crypt compartments 3 and 4 + 5 in the 22 patients in whom polyps recurred were significantly higher (respectively p < 0.05 and p < 0.01) than those of the 33 without recurrence suggesting that an upward shift of the crypt's replicative compartment is associated with polyp recurrence. Labelling indices remained essentially unchanged in those patients who underwent biopsy twice. Reproducible kinetic parameters such as these might be useful in planning follow up of patients with adenomatous polyps after polypectomy.

Franco Trevisani ], Stefania De Notafiis ], Mafia Chiara Cantafinil, Giardudovico Rapaccini 2, Fabio Fafinati 3, Luisa Benvegnu 4, Marco Zoli 1 , Paolo Del Poggio 5, Mafia Anna Di Nolfo 6, Mauro Bernardi 1.1Department of Internal Medicine, Cardioangiology, Hepatology, University of Bologna; 2Unit of Internal Medicine 11, Catholic University of Rome; 3Unit of Gastroenterology, University of Padua; 4Department of Experimental and Clinical Medicine, University of Padua; 5 Unit of Medicine, Treviglio-Caravaggio Hospital, Treviglio; 6Unit of Medicine, Bolognini Hospital, Seriate, Italy