抄録
I. Pathophysiology of sideropenic symptoms were dicussed from the standpoints of the ferrous and iron-flavin enzymes. The sideropenic asthenia was ascribed to a slowdown of TCA-cycle, due to a decrease of aconitase and SDH activities, and a disturbance of the electron transport system, especially in muscles. The lowered cell renewal rate as supposed from a decrease of DPNH-diaphorase activity together with a decreased 32P-uptake by DNA-fraction of the intestinal epithelium might be one of causative factors of the epithelial lesions including spoon nails.
The iron deficiency from early childhood may cause a retardation of physical and mental growth, and the deficiency during the fetal life might possibly cause malformations in a similar mechanism as seen in ariboflavinosis and in hypoxia
II. The hyposideremia with low TIBC in active pulmonary tuberculosis was ascribed to the accumulation of iron in the lesions and in RES, and that with a relatively high TIBC in the inactive tuberculosis with poor pulmonary functions was due to increased consumption of iron for erythropoiesis induced by tissue hypoxia. The low TIBC in case of infection or inflammation could be ascribed to
i) an increased catabolism of transferrin (examined by means of the labelled protein)
ii) a decreased synthesis of transferrin (14C-glycine uptake by the liver homegenate) and
iii) a maldistribution or accumulation of transferrin together with iron to the focus and to RES-tissue (semiquantitative determination by means of Ouchterlony's method).
III. Pathophysiology in iron excess: a case of anemia refractoria sideroblastica was presented with special reference to iron, transferrin and porphyrin metabolism.
