No abstract

Regardless of modality, findings of liver disease are common among adults with Fontan circulation, even those appearing clinically well. Cirrhosis is present in up to one-third of subjects. Correlations between hepatic fibrosis stage and clinical history or findings on noninvasive testing are few. Further research is needed to identify patients at risk for more severe liver disease and to determine the best methods for assessing liver health in this population.

The risk of HGD increases with the size of PGA, tubulovillous architecture and the presence of AIG as well as mixed immunophenotype. As the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be excised completely if possible, particularly if they are large or show high-grade features.

Aims Immune check‐point inhibitors are frequently used in the treatment of a variety of solid tumours. The mechanism of action of these drugs involves up‐regulation of cytotoxic T cells, which can lead to a lack of self‐tolerance and immune‐related adverse events, including those involving the gastrointestinal tract. This study was performed to characterise the histological features of immune check‐point inhibitor therapy‐associated gastritis. Methods and results Gastric biopsies from patients on immune check‐point inhibitor therapy with clinical suspicion of drug‐associated gastrointestinal injury were identified. The predominant histological pattern of injury, distribution of injury, degree of tissue eosinophilia and prominence of apoptosis were recorded. Presenting symptoms, treatment and follow‐up data were obtained by medical chart review. The 12 patients included in the study group were treated with ipilimumab, nivolumab or pembrolizumab for a variety of tumours. Symptoms at presentation included nausea, vomiting and diarrhoea. Chronic active gastritis with intra‐epithelial lymphocytosis and prominent apoptosis was seen in eight of 12 patients, and was the most useful combination for the diagnosis of drug‐induced gastritis in these patients. Four patients showed focal enhancing gastritis with a lymphohistiocytic cuff around inflamed glands reminiscent of Crohn's disease. One of those four patients was homozygous for the ATG16L1 Crohn's disease‐associated gene variant, but had no history of inflammatory bowel disease. Ten patients responded to medication withdrawal and steroid therapy, while two required treatment with infliximab. Conclusions Awareness of the morphological spectrum of immune check‐point inhibitor therapy‐associated gastritis is important for the accurate diagnosis and prompt management of these patients.