Circulating miR-122 in patients with non-toxic acute acetaminophen ingestions.

Introduction: MicroRNA-122 (miR-122) is a novel biomarker of liver injury and has been proposed as an early predictor of acetaminophen-associated hepatotoxicity. However, there is little data on miR-122 in patients with nontoxic acute acetaminophen ingestions.Methods: This was an observational study of patients with a history of acute acetaminophen ingestion and measured acetaminophen concentrations below the treatment nomogram and who did not receive antidotal treatment. Fold increase in miR-122 expression was measured from the remnant sample corresponding with the timed serum acetaminophen concentration used to determine need for antidotal treatment.Results: Ten patients met inclusion criteria with a four-hour acetaminophen concentration below the nomogram line (mean: 73.4 µg/mL). There was no significant difference in mean fold change of miR-122 expression between the acetaminophen exposed patients and negative controls [(0.82, IQR: 0.27, 0.77) vs (1.24, IQR: 0.54, 1.98), p = 0.33].Conclusion: miR-122 was not elevated in patients with acute acetaminophen ingestions with timed acetaminophen concentrations below the nomogram line. These data help to further characterize patterns of miR-122 in patients with acute acetaminophen exposures.

Serum iron concentrations in non-iron induced acute liver injury.

Acute liver injury (ALI) is seen in conjunction with elevated iron concentrations in the setting of acute iron toxicity. However, occult or delayed presentations of iron toxicity can be difficult to identify clinically and there is limited data describing iron concentrations in ALI without a confirmed history of iron overdose. This was a single center observational before-and-after study of adult patients who developed acute liver injury during hospitalization. Patients with a serum ALT > 500 U/L were identified by a daily hospital laboratory report and met inclusion if the ALT< 80 U/L at the time of admission, no history of overdose (iron, acetaminophen, or other ingestion), and no underlying liver disease. Serum AST, iron, and ferritin concentrations were obtained from blood samples at the time of admission and at peak serum ALT. Ten patients met inclusion criteria. The median age was 69 years old and 60% were male. There was a significant difference in serum AST (p = 0.005), serum ALT (p = 0.005), and ferritin (p = 0.005) before and after development of ALI. Serum iron concentrations were not clinically or significantly different (median: 23 mcg/dL vs 27 mcg/dL, p = 0.8). In this cohort of patients with non-iron induced acute liver injury, serum iron concentrations did not significantly change with the observed rise in aminotransferases. These data help to further characterize patterns of serum iron concentrations in patients with ALI.