Clinical Chemistry
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Clinical Chemistry 46: 885-886, 2000;
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(Clinical Chemistry. 2000;46:885-886.)
© 2000 American Association for Clinical Chemistry, Inc.

Letters

Plasma Ferritin in Acute Hepatocellular Damage

Chotoo I. Bhagata, Stephen Fletcher, John Joseph and John P. Beilby

Department of Clinical Biochemistry, PathCentre, Hospital Avenue, Nedlands 6009, Western Australia, Australia
a Author for correspondence. Fax 61-8-9346-3882; e-mail Chotoo.Bhagat{at}health.wa.gov.au


To the Editor:

Plasma ferritin concentrations are increased in iron overload, liver diseases, infections, inflammatory conditions, and malignancy. Very high concentrations (>10 000 µg/L) have been described in Still disease (1) and less commonly in hemochromatosis. There are very few reports of ferritin concentrations in patients with acute hepatocellular damage (AHD). A review of extreme increases in ferritin found that liver disease was the cause of 20% of cases but did not specify actual concentrations seen and did not differentiate acute and chronic liver disease (2). We have determined ferritin concentrations in AHD patients.

Plasma ferritins were measured in eight patients who had plasma alanine aminotransferase (ALT) values <100 U/L pre-AHD and >1000 U/L post-AHD. ALT, iron, and transferrin were measured on a Hitachi 917 (Roche Diagnostics), and ferritin was measured on the ACS:180 (Bayer Diagnostics).

The results for individual patients are shown in Table 1 . In one patient, serum ferritin did not exceed the upper limit of the reference interval during AHD. This patient was iron-deficient with a basal ferritin of 22 µg/L.


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  		Table 1. Plasma ferritin in AHD.1

The plasma ALT increased from a basal mean (SD) of 45 (29) U/L to 2970 (1540) U/L during AHD, and ferritin increased from 200 (130) µg/L to 18 260 (17 860) µg/L. The mean plasma iron increased from 12 (11) µmol/L to 16 (19) µmol/L, transferrin decreased from 27 (11) µmol/L to 22 (7) µmol/L, and transferrin saturation increased from 18% (7%) to 31% (30%).

The rapid increase in ferritin in AHD suggests that ferritin is present in the cytosol of the hepatocytes. There was significant (P <0.01) correlation between the increase in ALT and ferritin in AHD. Despite the marked increase in ferritin in five of six patients in whom iron and transferrin were measured, the transferrin saturation increased above the reference interval in only one of these patients.

In conclusion, ferritin concentrations were markedly increased after AHD and are of no diagnostic value during this time. These data imply that ferritin and ALT are present in the cytosol of the hepatocytes.


References

  1. Schwarz-Eywill M, Heilig B, Bauer H, Breitbart A, Pezzutto A. Evaluation of serum ferritin as a marker for adult Still’s disease activity. Ann Rheum Dis 1992;51:683-685. [Abstract/Free Full Text]
  2. Lee MH, Means RT. Extremely elevated serum ferritin levels in a university hospital: associated diseases and clinical significance. Am J Med 1995;98:566-571. [Medline] [Order article via Infotrieve]



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This Article
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