Excessive deposition of Fe in the organs and tissues of Sub-Saharan African
s was first described in South Africa in 1929. Fe overload, or siderosis, w
as initially attributed to infections and to metallic poisoning (Cu, Sn, Zn
), and then to malnutrition. In 1953 it was hypothesized that it was due pr
imarily to excessive Fe intake derived from foods and drinks prepared in Fe
vessels. Recently, in 1992 it was advanced that a gene distinct from any H
LA-linked locus may also play a role. As to sequelae, in early research on
series of hospital patients, the condition was linked to scurvy, osteoporos
is, diabetes, cirrhosis, and latterly, to hepatocellular cancer and tubercu
losis. Accordingly, many have concluded that Fe overload is responsible for
considerable morbidity and mortality, that adventitious Fe intake should b
e reduced, and that phlebotomy be recommended for those severely affected.
However, there are numerous limitations in the evidence. There are also pro
blems in interpretation, since levels of Fe in the serum are affected addit
ionally by a variety of factors: infection, inflammation, certain cancers a
nd alcohol intake. These considerations complicate attempts to assess to wh
at extent the associations described denote causation, and whether Fe overl
oad has significant ramifications for ill in the general African population
. While the adverse sequelae of overload may be less of significance than m
any believe, the precise pathogenicity of the phenomenon will remain uncert
ain until further investigations, including prospective studies, are undert
aken.