Background The risk of severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection and clinical outcomes of coronavirus disease (COVID-19) in inflammatory bowel disease are unclear. Methods We searched PubMed and Embase with the keywords: inflammatory bowel disease, Crohn’s disease, ulcerative colitis and COVID-19, novel coronavirus and SARS-CoV-2. We included studies reporting the frequency of COVID-19 infection and outcomes (hospitalisation, need for intensive care unit care and mortality) in patients with inflammatory bowel disease. We estimated the pooled incidence of COVID-19 in inflammatory bowel disease and comparative risk vis-a-vis the general population. We also estimated the pooled frequency of outcomes and compared them in patients who received and did not receive drugs for inflammatory bowel disease. Results Twenty-four studies were included. The pooled incidence rate of COVID-19 per 1000 patients of inflammatory bowel disease and the general population were 4.02 (95% confidence interval (CI) 1.44–11.17) and 6.59 (3.25–13.35), respectively, with no increase in relative risk (0.47, 0.18–1.26) in inflammatory bowel disease. The relative risk of the acquisition of COVID-19 was not different between ulcerative colitis and Crohn’s disease (1.03, 0.62–1.71). The pooled proportion of COVID-19-positive inflammatory bowel disease patients requiring hospitalisation and intensive care unit care was 27.29% and 5.33% while pooled mortality was 4.27%. The risk of adverse outcomes was higher in ulcerative colitis compared to Crohn’s disease. The relative risks of hospitalisation, intensive care unit admission and mortality were lower for patients on biological agents (0.34, 0.19–0.61; 0.49, 0.33–0.72 and 0.22, 0.13–0.38, respectively) but higher with steroids (1.99, 1.64–2.40; 3.41, 2.28–5.11 and 2.70, 1.61–4.55) or 5-aminosalicylate (1.59, 1.39–1.82; 2.38, 1.26–4.48 and 2.62, 1.67–4.11) use. Conclusion SARS-CoV-2 infection risk in patients with inflammatory bowel disease is comparable to the general population. Outcomes of COVID-19-positive inflammatory bowel disease patients are worse in ulcerative colitis, those on steroids or 5-aminosalicylates but outcomes are better with biological agents.

The treatment of inherited metabolic liver diseases by hepatocyte transplantation (HT) would be greatly facilitated if the transplanted normal hepatocytes could be induced to proliferate preferentially over the host liver cells. We hypothesized that preparative hepatic irradiation ( H epatocyte transplantation (HT) is currently being evaluated as a treatment strategy for patients with acute and chronic liver failure and to replace metabolic liver functions in inherited liver diseases. 1 HT has been used in the treatment of inherited metabolic diseases, such as Crigler-Najjar syndrome type I, 2 and for hepatocyte-based ex vivo gene therapy in experimental animals 3-5 as well as in patients with low-density lipoprotein receptor deficiency. 6 However, the clinical application of HT is limited by the availability of human hepatocytes and the number of liver cells that can be transplanted safely at one time. An important consideration is whether a sufficient number of hepatocytes can be engrafted to achieve the desired metabolic correction without causing portal hypertension or other adverse effects. Therefore, a method to induce preferential proliferation of a relatively small number of engrafted hepatocytes in vivo could markedly enhance the applicability of HT.We hypothesized that preparative irradiation of the liver along with a strong mitotic stimulus provided by a maneuver such as partial hepatectomy (PH) should damage the host hepatocyte DNA, causing cell cycle arrest. Subsequently transplanted normal, nonirradiated hepatocytes should proliferate preferentially in response to the

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