COMMENT:
Metabolic syndrome’s development after transplantation may occur as a consequence of immunosuppression and/or weight gain post-surgery. Indeed, it is estimated that a third of patients develop obesity within a few years after receiving their transplant. Importantly, metabolic syndrome’s development may directly contribute to the onset of recurrent or de novo graft metabolic dysfunction-associated fatty liver disease (MAFLD). MAFLD may itself cause graft dysfunction and fibrosis by exacerbating liver enzyme derangements.
This study aimed to determine the prevalence of graft steatosis and MAFLD measured via non-invasive transient elastography and controlled attenuation parameter (CAP) in a large cohort of post-transplant Chinese patients.
KEY LEARNINGS:
Optimal CAP cut-off levels for diagnosing a minimum of mild (≥ S1) and moderate-to-severe (≥ S2/3) steatosis were found to be 266 and 293 dB/m, respectively, with corresponding AUROCS of 0.740 and 0.954. According to these thresholds and despite none of the cohort’s patients having undergone a liver transplant for cirrhosis, the prevalence of de novo steatosis was found to be 28.9%. Moreover, 95.6% of these patients were estimated to satisfy the criteria for MAFLD. Factors independently associated with the development of moderate-to-severe steatosis included diabetes mellitus, hypertension, HDL-cholesterol, LDL-cholesterol, cryptogenic cirrhosis, and body mass index (BMI). The latter was only relevant at the time of CAP measurement. Indeed, neither BMI nor graft status pre-transplant were identified as independent factors increasing the risks of de novo moderate-to-severe steatosis. Additionally, de novo steatosis was found to be associated with the onset of new hypertension and graft dysfunction, though no link was observed with graft fibrosis. These findings emphasise the significance of routine CAP measurements post-liver transplantation as a preventive measure against de novo MAFLD.
