An increase in the iron content of food may be harmful to people with genetic hemochromatosis. We studied the prevalence of this disorder in Sweden, which is the country with the world's highest iron fortifhtion of food. Serum ferritin and transferrin (TIBC) saturation levels were used as initial screening methods. Three (0.5 %) of 623 males aged 30-39 years were found to have genetic hemochromatosis. Family studies revealed 10 additional homozygotic family members. A prevalence of 0.5 % of homozygotes (47 implies a gene frequency (4) of 6.9% or a heterozygote frequency ( 2 x q ) of 13.8%. The high gene frequency may be explained by a possible genetic advantage of heterozygotes in the past. We conclude that idiopathic hemochromatosis is not as rare as previously thought. Affected persons should be detected and treated before irreversible organ damage occurs. This study demonstrates that serum ferritin levels together with TIBC saturation levels are adequate methods for screening populations. Abbreviations:TIBC= transferrin, HLA= histocompatibility antigen, DF=desferrioxamine. S-ALAT= serum alanine aminotransferase. N Engl J Med 1979; 301: 1291. 24. Bezwoda WR, Bothwell TH. Derman DP et al. Effect of diet on the rate of iron accumulation in idiopathic haemochromatosis. S Afr Med J 1981; 5 9 219-22. ASSW J 1976; 114 417-21. Acra Med Scand 213

Three hundred forty-seven (96.4%) of all persons aged 30 to 39 years were screened with serum iron and iron binding capacity measurements to determine the incidence of hemochromatosis in a population. No women had signs of iron overload; however, nine men (5%) had persistenly elevated serum iron levels. In four men (2%), increased iron stores was found with a distribution like that in the early stages of hemochromatosis. In combination with recent findings of clinical hemochromatosis at our hospital, this study suggests that this condition is not as rare as has been reported earlier.

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People with parenchymal iron overload exhibit an elevated serum iron concentration and a raised transferrin (TIBC) saturation early in the course of the disease. They can therefore be detected by simple laboratory tests before organ damage has occurred. In this study running for 2 months, 10512 samples from approximately 8750 patients and blood donors were examined in a county hospital in Central Sweden. Abnormal TIBC saturation (>70%) was found in 1.7% of the samples. This abnormality was caused by physiological fluctuations in serum iron in 44%, liver disease in 22%, blood disorder in 10%, iron therapy in 10.5% and parenchymal iron overload in 11.5%. The diagnosis of iron overload was confirmed by measuring the serum ferritin concentration and by performing the desferrioxamine test, liver biopsy, quantitative phlebotomy and family studies including HLA typing. We found a prevalence of iron overload of 0.24%. This figure is almost certainly too low because some affected patients were probably lost because of TIBC desaturation induced by inflammatory conditions.

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