112 T. GlLLMAN 



we are presently investigating. Examination of cardiac 

 muscle in this, and in several other cases, thus far available, 

 revealed an extensive, albeit patchy, deposition of iron 

 pigment within the myocardial cells (Figs. 13 and 14) as well 

 as in the liver. It is known from Sheldon's work (1935) that 

 cardiac failure may supervene in relatively young European 

 haemochromatotics. However, at this stage, we still prefer to 

 call this condition in the African nutritional siderosis, with or 

 without cirrhosis. 



There is quite strong evidence to support our view that the 

 siderosis of the liver and other organs is due initially to the 

 liberation of iron within parenchymal cells from their iron- 

 containing enzymes. Thus, at the outset iron is encountered 

 essentially within the hepatic epithelium rather than, as 

 occurs in haemolytic states, mainly in the reticuloendothelial 

 cells. In the later stages of the disease iron again occurs 

 primarily within parenchymal cells such as the heart (Figs. 13 

 and 14), the thyroid epithelium (Fig. 15), etc., in which 

 organs very little iron is observed in the connective tissues 

 even when the parenchymal cells are markedly siderotic. 

 Whatever the underlying cause and pathogenesis of this type 

 of siderosis, in the ultimate analysis, the excessive iron in all 

 the tissues must be derived from the diet. It is our belief that 

 the failure of the normally present alimentary blockade to 

 iron absorption is secondary to some nutritionally based 

 derangement in the iron-containing enzymes within the 

 parenchymal cells in many organs and tissues. The reticulo- 

 endothelial siderosis we consider to occur late in the disease 

 and to follow the liberation of iron consequent on the death 

 and disintegration of iron-laden parenchymal cells. 



Associated with these hepatic lesions we have consistently 

 encountered profound changes in the plasma proteins. The 

 total proteins may be more or less normal but one of the 

 striking and consistent findings in these patients is a profound 

 drop in the plasma albumin associated with a marked increase 

 in the plasma globulin with a consequent complete reversal of 

 the albumin: globulin ratios. These changes, like the siderosis, 



