Background and Aims Elevated serum ferritin is common in NAFLD, and is associated with more advanced disease and increased mortality. Hyperferritinaemia in NAFLD is often attributed to inflammation, while in other conditions ferritin closely reflects body iron stores. The aim of this study was to clarify the underlying cause of hyperferritinaemia in NAFLD. Methods Ferritin levels were examined with markers of iron status, inflammation and liver injury across the clinical spectrum of NAFLD using blood, tissue and magnetic resonance (MR) imaging. A separate larger group of NAFLD patients with hepatic iron staining and quantification were used for validation. Results Serum ferritin correlated closely with the iron regulatory hormone hepcidin, and liver iron levels determined by MR. Furthermore, ferritin levels reflected lower serum adiponectin, a marker of insulin resistance, and liver fat, but not cytokine or CRP levels. Ferritin levels differed according to fibrosis stage, increasing from early to moderate disease, and declining in cirrhosis. A similar pattern was found in the validation cohort of NAFLD patients, where ferritin levels were highest in those with macrophage iron deposition. Multivariate analysis revealed liver iron and hepcidin levels as the major determinants of serum ferritin. Conclusions While hyperferritinaemia is associated with markers of liver injury and insulin resistance, serum hepcidin and hepatic iron are the strongest predictors of ferritin levels. These findings highlight the role of disordered iron homeostasis in the pathogenesis of NAFLD, suggesting that therapies aimed at correcting iron metabolism may be beneficial.

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ObjectivesThere is a critical need to develop robust biomarkers for Parkinson's diasease (PD) research. We aimed to determine whether a serum biomarker could be used: to predict cognitive decline in PD or a diagnosis of PD. Five of the most promising serum biomarkers were identified based on recent and current evidence: Vitamin D, Apolipoprotein A1 (ApoA1), Uric Acid, C-reactive protein and Epidermal Growth Factor.MethodA peripheral blood sample was taken at baseline, spun in a centrifuge and then stored at −80°C. PD patients (n=641) diagnosed within 3.5 years, a control population (n=146) and patients with REM sleep behaviour disorder (n=74) were included at baseline. 3 year follow up data was available from 229 PD patients. Serum analysis was conducted either using Abbott systems or ELISA techniques. Age, gender, disease duration and seasonality (for vitamin D) were adjusted for using statistical models. Results: There was no strong evidence that the potential biomarkers predicted either baseline or change in cognition. Uric acid was lower in the PD group compared to controls (p=0.008), though this effect was not replicated in the RBD group. EGF (p<0.001) and ApoA1 (p=0.04) were both lower in RBD cases compared to controls, and Vitamin D levels were higher (p=0.009). These results should be viewed with caution however as they were not replicated in the PD group so may relate to type I errors and require further replication.Conclusion: None of the biomarkers predicted cognitive decline in the PD group. This may be because there is not yet enough follow up data to detect a signal, but they do not predict baseline cognition. EGF, Vitamin D and ApoA1 show some differences in the RBD group compared to controls, while Uric Acid was lower in the PD group. Individually, the candidate biomarkers did not predict cognitive decline or patient group. Additional data will be available by the time of the conference as data collection is.