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BACKGROUND Although acute graft-vs-host disease (aGvHD) is a rare complication of liver transplantation, it is poorly understood and has an extremely high mortality rate. No standardized diagnostic criteria or treatment regimens currently exist. CASE SUMMARY The present study investigated the etiology, diagnosis, and treatment of aGvHD following liver transplantation. Presentation, diagnosis, disease course, histology, and treatment of an aGvHD case are reported, and associated literature is reviewed. A 64-year-old female required LTx due to primary biliary cirrhosis. The donor was a 12-year-old male. Three weeks following liver transplantation, the recipient developed pyrexia, diarrhea, rashes, and antibiotic-unresponsive pancytopenia. Clinical symptoms together with laboratory investigations suggested a diagnosis of aGvHD, which was confirmed via peripheral blood fluorescent in situ hybridization. Donor XY chromosome fluorescent in situ hybridization indicating early chimerism achieved 93% sensitivity in the detection of GvHD. Existing immunosuppressants were discontinued, and high-dose intravenous methylprednisolone was initiated along with antibiotics. While diarrhea resolved, the patient’s general condition continued to deteriorate until demise due to multi-system organ failure at 37 d post-liver transplantation. This case illustrates the life-threatening nature of aGvHD. CONCLUSION Herein, we have summarized a post-LTx aGvHD case and reviewed associated literature in order to increase awareness and provide potentially risk-mitigating recommendations.

Objective Prevalence of hepatopulmonary syndrome (HPS) ranges from 4% to 47% in patients with cirrhosis. This study aimed to explore possible relationship between CX3CR1 and angiogenesis or macrophage accumulation in pathological process of HPS. Material and methods Wide-type C57Bl/6 mice were divided into WT-sham, WT-common bile duct ligation (WT-CBDL), WT-CBDL plus antibody (WT-CBDL + Ab) and WT-CBDL plus Bevacizumab. The CX3CR1GFP/GFP mice were grouping into CX3CR1 GFP/GFP-sham, CX3CR1 GFP/GFP-CBDL and CX3CR1 GFP/GFP-CBDL + Bevacizumab group. Intrapulmonary expression of Akt, pAkt, ERK, pERK, iNOS, VEGF, PDGF was measured using biological technology. Hematoxylin-eosin (H&E) staining and immunohistochemical analysis were used to evaluate changes of pulmonary tissues including pathological abnormality, angiogenesis and macrophage accumulation. Results Blockade CX3CR1 pathway inhibited angiogenesis, macrophage accumulation and pathological changes of lung tissues. Blockade of CX3CR1 pathway reduced pAkt, pERK, iNOS, PDGF and VEGF activation. CX3CR1 contributed to the process of angiogenesis and activate the pro-angiogenic factors. CX3CR1 deficiency obviously reduced the macrophage accumulation. Inhibition of VEGF by Bevacizumab improved intrapulmonary angiogenesis and pathological changes of lung tissues. Inhibition of VEGF by Bevacizumab retarded the production of pAKt, PDGF, and iNOS. Inhibition of VEGF by Bevacizumab reduced CX3CL1 production. Conclusion CX3CR1 could regulate the angiogenesis and activation of pro-angiogenic factors, including pAKT, pERK, iNOS, VEGF and PDGF in the process of hepato-pulmonary syndrome. Moreover, CX3CR1 could also contribute to the macrophage accumulation.