Kayali Zeid, Ranguelov Rostislav, Mitros Frank, Shufelt Chrisandra, Elmi Farshad, Rayhill Stephen C, Schmidt Warren N, Brown Kyle E
Division of Gastroenterology and Hepatology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Liver Int. 2005 Feb;25(1):41-8. doi: 10.1111/j.1478-3231.2005.01022.x.
Although hepatic iron deposition unrelated to hereditary hemochromatosis is commonly observed in cirrhosis, its clinical significance is unclear. The aim of this study was to examine the outcomes of cirrhotic patients with and without hemosiderosis.
Patients with an initial liver biopsy demonstrating cirrhosis between January 1993 and December 1997 were identified using the Department of Pathology database. Based on iron staining, patients were characterized as siderotic or nonsiderotic. Charts were reviewed to determine outcomes.
Siderotic patients had significantly higher Child-Pugh (CP) and model for end-stage liver disease (MELD) scores. Their median survival without transplant was 23 months vs. 85 months in the nonsiderotics (P<0.0001, confidence interval: 95%). On univariate analysis, siderosis was associated with a hazard ratio of 2.74 (P<0.0001). On multivariate analysis, the effect of siderosis was reduced but remained significant after correction for the CP or MELD score (hazard ratios 1.82 and 2.06, P=0.05 and 0.02, respectively). Child's A cirrhotics with hemosiderosis decompensated more rapidly and had shorter median survival than those without siderosis (P=0.007 and P=0.01, respectively).
The presence of siderosis is associated with more advanced liver dysfunction. Even when the effects of baseline liver function are taken into account, siderosis is associated with decreased survival and more rapid decompensation in cirrhosis.
