Serum ferritin in ascorbic acid deficiency.

Abstract

Summary Serum ferritin levels were monitored in guinea‐pigs rendered scorbutic by dietary deprivation of ascorbic acid (AA). Hepatic and splenic concentrations of AA fell rapidly during the first 8 d of deprivation, and then declined more slowly to reach approximately 10% of control values after 14 d. Normal levels of serum ferritin (geometric mean, 324 μg/1) were observed for 20 d but a significant fall occurred between days 20 and 23 of deficiency (143 γg/1; P<0·05).Intramuscular administration of iron dextran to scorbutic animals (75 mg Fe per kg body weight) resulted in a non‐significant elevation of serum ferritin levels (geometric mean, 470 μg/1; P>0·1). In control animals, the same dose of iron dextran caused a 10‐fold rise in serum ferritin levels (3400 μg/1). A single subcutaneous dose of AA (75 mg/kg weight) given to scorbutic animals caused a significant rise in serum ferritin levels to 599 μg/1 (P<0·001) but had no effect in control animals. The same dose of AA given to iron loaded, scorbutic animals elevated serum ferritin levels from 554 μg/1 to 1297 μg/1 (P<0·025).Thus, AA deficiency in guinea‐pigs caused serum ferritin levels to fall and blocked the rise in serum ferritin levels observed in response to acute iron loading in control animals. Adequate tissue concentrations of AA appeared to be necessary for the maintenance of a quantitative correlation between tissue iron stores and serum ferritin levels. The mechanisms by which AA influences serum ferritin levels are at present unknown.