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Background: Patients with substance use disorders present with many risk factors for liver disease-including alcohol, hepatitis C virus infection, and obesity-and should thus be screened for compensated advanced chronic liver disease (cACLD). Such screening could potentially be performed by outpatient addiction clinics. In this study, we aimed to assess the feasibility, acceptability, and results of cACLD screening using transient elastography (TE) among all patients attending routine follow-up visits at addiction clinics, regardless of their liver disease risk factors., Methods: Liver fibrosis evaluation using TE was offered to every patient consulting two different addiction clinics in France, between December 2020 and September 2021, during dedicated half-day screening sessions. The screening was proposed during the patient's routine care and was performed immediately after the scheduled consultation. Patients with a liver stiffness measurement over 8 kPa were referred to a hepatology visit in the addiction clinic within 2-4 weeks., Results: Screening was offered to 227 patients and was accepted by 116 (51%) patients. Twelve patients had a liver stiffness over 8 kPa, and nine of these patients attended the recommended specialist hepatology visit. Five patients (4.3% of those screened) were diagnosed with cACLD. Patients' acceptance of the screening was associated with older age, being on one's own or professionally inactive, and presenting with alcohol use disorder., Conclusion: Overall, our results demonstrated that opportunistic cACLD screening using TE in outpatient addiction clinics was feasible and acceptable, with good results., (© 2024 The Author(s). Alcohol, Clinical and Experimental Research published by Wiley Periodicals LLC on behalf of Research Society on Alcohol.)

Aim: To determine the evolution of transient elastography (TE) in patients with alcoholic liver disease according to alcohol cessation or continuation., Methods: We retrospectively selected in our local database all patients who had two TE between June 2005 and November 2010 with chronic alcohol excessive consumption and excluded those with associated cause of liver disease. TE was performed at least one week apart by senior operator. TE examinations with less than ten successful measures or with an interquartile range above 30% were excluded. We retrospectively reviewed file of all patients to include only patient followed up by trained addictologist and for which definite information on alcohol consumption was available. Concomitant biological parameters [aspartate amino transferase (AST), alanine amino transferase and gamma-glutamyl transpeptidase (GGT)] within 4 wk of initial and final TE were recorded. Putative fibrosis score according to initial and final TE were determined with available cut-off for alcoholic liver disease and hepatitis C. Initial and final putative fibrosis score were compared according to alcohol consumption during follow-up., Results: During the study period 572 patients had TE examination for alcoholic liver disease and 79 of them had at least two examinations. Thirty-seven patients met our criteria with a median follow-up of 32.5 wk. At the end of the study, 13 (35%) were abstinent, and 24 (65%) relapsers. Eight patients had liver biopsy during follow-up. TE decreased significantly during follow-up in 85% of abstinent patients [median (range): -4.9 (-6.1,-1.9)], leading to a modification of the putative fibrosis stage in 28%-71% of patient according to different cut-off value. In relapsers TE increased in 45% and decreased in 54% of patient. There was no statistical difference between initial and final TE in relapsers. In the overall population, using 22.6 kPa as cut-off for cirrhosis, 4 patients had cirrhosis at initial TE and 3 patients had cirrhosis at final TE. Using 19.5 kPa as cut-off for cirrhosis, 7 patients had cirrhosis at initial TE and 5 patients had cirrhosis at final TE. Using 12.5 kPa as cut-off for cirrhosis, 16 patients had cirrhosis at initial TE and 15 patients had cirrhosis at final TE. Evolution of biological data was in accordance with the relapse or abstinent status: abstinence ratio (duration of abstinence/duration follow-up) was correlated with AST ratio (r = -0.465, P = 0.007) and GGT ratio (r = -0.662, P < 0.0001). GGT was correlated with initial (r = 0.488, P = 0.002) and final TE (r = 0.49, P < 0.005). Final TE was correlated with AST (r = 0.362, P < 0.05). Correlation between TE ratio and AST ratio (r = 0.44, P = 0.01) revealed that TE varied proportionally to AST for all patients irrespective of their alcohol status. The same relationship was observed between TE ratio and GGT ratio (r = 0.65, P < 0.0001). Evolution of TE was significantly correlated with the ratio of time of abstinence to observation time (r = -0.387, P = 0.016) and the evolution of liver enzymes., Conclusion: TE significantly decreased with abstinence. Results of TE in alcoholic liver disease cannot be interpreted without taking into account alcohol consumption and liver enzymes.

Iron overload diseases of genetic origin are an ever changing world, due to major advances in genetics and molecular biology. Five major categories are now established: HFE-related or type1 hemochromatosis, frequently found in Caucasians, and four rarer diseases which are type 2 (A and B) hemochromatosis (juvenile hemochromatosis), type 3 hemochromatosis (transferrin receptor 2 hemochromatosis), type 4 (A and B) hemochromatosis (ferroportin disease), and a(hypo)ceruloplasminemia. Increased duodenal iron absorption and enhanced macrophagic iron recycling, both due to an impairment of hepcidin synthesis, account for the development of cellular excess in types 1, 2, 3, and 4B hemochromatosis whereas decreased cellular iron egress is involved in the main form of type 4A) hemochromatosis and in aceruloplasminemia. Non-transferrin bound iron plays an important role in cellular iron excess and damage. The combination of magnetic resonance imaging (for diagnosing visceral iron overload) and of genetic testing has drastically reduced the need for liver biopsy. Phlebotomies remain an essential therapeutic tool but the improved understanding of the intimate mechanisms underlying these diseases paves the road for innovative therapeutic approaches.

Iron overload diseases are a quickly and deeply changing world, due to major advances in genetics and molecular biology. Five main entities are concerned: a frequent one, namely HFE-related or type1 haemochromatosis, and four rare or exceptional diseases which are types 2, 3 and 4 haemochromatosis and aceruloplasminemia. Increased duodenal iron absorption and enhanced macrophagic iron recycling, both due to hypo-hepcidinemia, account for the development of cellular excess in types 1, 2, 3 haemochromatosis whereas decreased cellular iron egress is the main explanation for type 4 haemochromatosis and aceruloplasminemia. Non-transferrin bound iron plays an important role in cellular iron excess and damage. Phlebotomies remain an essential therapeutic tool but the improved understanding of the intimate mechanisms underlying these diseases open the road for innovative therapeutic approaches.

We describe a case of Whipple's disease confirmed by clinical, histological, bacteriological and molecular criteria. The duodenal involvement was associated with the presence of an endoscopic and histological enterocolitis. Final diagnosis of small bowel and colonic involvement by Whipple's disease was confirmed by histology and molecular biology. We review the literature on extra duodenal involvement. We underline the fact that enterocolitis in Whipple's disease is non-specific. We also discuss the other causes of intestinal mucosal infiltration by macrophages.