Chronic iron overload and toxicity: Clinical chemistry perspective

Clinical Laboratory Science, Summer 2001 by Kang, Jae O

With early diagnosis and appropriate treatment, the toxicity of chronic iron overload can be effectively treated, and even prevented. For example, a study by Niederau showed that when phlebotomies were initiated before patients developed cirrhosis, hemochromatosis reverted to normal.44 Even among those with cirrhosis, the 10-year survival rate was over 75% which was a remarkable improvement over the 6% 10-year survival rate after diagnosis without the removal of excess iron. Clinical chemistry laboratories can play a vital role in diagnosing and monitoring iron overload, particularly since a non-invasive test for the HFE gene has been developed and commercial reagent kits are now available.97 Some scientists have suggested that screening for the HFE gene in the asymptomatic population be considered.96 Such a widespread screening program, if adopted, would expand the role of clinical laboratory scientists significantly. These professionals must be prepared to accept this important role.

ACKNOWLEDGEMENT

The author acknowledges the assistance of Claire A Archambault in the preparation of this manuscript.

The Focus section seeks to publish relevant and timely continuing education for clinical laboratory practitioners. Section editors, topics, and authors are selected in advance to cover current areas of interest in each discipline. Readers can obtain continuing education credit (CE) through P.A.C.E.(R) by completing the tearout form/examination questions included in each issue of CLS and mailing it with the appropriate fee to the address designated on the form. Suggestions for future Focus topics and authors, and manuscripts appropriate for CE credit are encouraged. Direct all inquiries to Carol McCoy PhD, CLS Continuing Education Editor Department of Clinical Sciences, 343 Cowley Hall, University of Wisconsin, La Crosse WI 54601; (608) 785-6968. cmccoy@mail.uwlax.edu

REFERENCES

1. Harrison PM. Biochemistry of iron. Clin Toxicol 1971; 4:529-44.

2. Crichton RR, Ward RJ. Structure and molecular biology of iron binding proteins and the regulation of "free" iron pools. In: Lauffer RB, editor. Iron and human disease. Boca Raton: CRC Press; 1992. p 23-75.

3. Bothwell TH, Chariton RW, Cook JD, Finch CA. Iron absorption. In: Iron metabolism in man. London: Blackwell Scientific Publications; 1979. p 256-83.

4. Weinberg ED. Cellular iron metabolism in health and disease. Drug Metab Rev 1990;22:531-79.

5. Worwood M. Inborn errors of metabolism: iron. Br Med Bull 1999;55:556-67.

6. Lynch SR. Iron overload: prevalence and impact on health. Nutr Rev 1995;53:255-60.

7. Edwards CQ, Griffen LM, Goldgar D, and others. Prevalence of hemochromatosis among 11,065 presumably healthy blood donors. New Engl J Med 1988;318:1355-63.

8. Feder HN, Gnirke A, Thomas WI and others. A novel MHC class I like gene is mutated in patients with hereditary hemochromatosis. Nat Genet 1996;13:399-408.

9. Voelkerding KV Advances in hereditary hemochromatosis. Clin Lab News March 1998:10-2.

10. Bennett MJ, Lebron JA, Bjorkman PJ. Crystal structure of the hereditary hemochromatosis protein HFE complexed with transferrin receptor. Nature 2000;403:46-53.


 

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