Cognitive Impairment in Liver Transplant Recipients ≥3 Months After Transplant
Ketura Berry1, Fawzy Barry1, Amy Shui1, Randi Wong1, Sri Seetharaman1, Dorothea Kent1, Jessica Ruck2, Lawren Vandvrede1, Jennifer Lai1
1UCSF, 2Johns Hopkins
Objective:
Characterize prevalence of cognitive impairment after liver transplant
Background:
Liver transplant (LT) recipients have a high burden of factors known to lead to cognitive impairment (CI) in other populations, yet little work has explored cognitive function in this population. We aimed to characterize the prevalence of CI in LT recipients ≥3 months post-LT.
Design/Methods:
We enrolled ambulatory adults with cirrhosis at the UCSF LT center. Patients with hepatic encephalopathy on pre-LT exam (Numbers Connection Test A>45 seconds) or who did not receive LT were excluded. CI was assessed with the Montreal Cognitive Assessment (MoCA) pre-LT and ≥3 months post-LT (CI=MoCA<24). Demographics, comorbidities, history of hepatic encephalopathy and months since LT were abstracted from hepatology notes on day of study visit. Logistic regression associated CI and co-variables.
Results:
Of 98 participants, median age was 58 years (Q1-Q3 50-63), 72% had ≥12years education, 42% were female, 14% had diabetes, 34% had hypertension, and 51% had a history of hepatic encephalopathy. Median time between LT and post-LT MoCA was 7 months (Q1-Q3 5-12). Median post-LT MoCA score was 26 (Q1-Q3 23-27). 30% of all subjects had CI post-LT. 27% of those evaluated ≥12 months post-LT had CI. Compared to those without post-LT CI, those with post-LT CI had lower median pre-LT MoCA score (22(19-25) vs. 25(24-27), p<0.001); no other differences in co-variables were found. In multivariable analyses, controlling for age, education, and time since LT, for each point increase in pre-LT MoCA score, odds of CI post-LT decreased by 27% (OR 0.73, 95%CI 0.61-0.86, p<0.001).
Conclusions:
CI is highly prevalent (30%) in LT recipients ≥3 months after LT, despite this population having a median age far younger than those with CI from the general population. Furthermore, our data raise the possibility that neither classical risk factors for CI nor past hepatic encephalopathy explain CI in this population.