Ferritin is the main intracellular protein involved in iron storage, and its synthesis is regulated by body iron stores. Although the liver, spleen, and bone marrow contain the highest concentrations of stored iron, variable amounts are present in many other organs, including serum. It is now generally accepted that serum ferritin concentrations reflect the amount of body iron stores since concentrations below 12 |ug/L are always associated with depletion of body iron stores, whereas those above 300 (ig/L are seen in persons with iron overload. Each microgram of serum ferritin represents approximately 8 mg of stored iron. Serum ferritin is mainly secreted by reticuloendothelial cells and contains very little iron. When body iron stores are depleted, the resulting low serum ferritin concentration is usually associated with an increase in TIBC.
In a cohort study, Knekt et al. compared serum iron concentrations, TIBC capacity, and TS in 130 Finnish men who developed PC during a 14-year follow-up period with those of 21,085 men who did not. They observed no significant differences between both groups. Stevens et al. also did not observe significant differences in mean serum iron, TIBC, and TS between men with and those without PC who were included in the NHANES I survey. However, serum iron (hence, TS) is subject to wide daily and diurnal variations, and it is a poorer indicator of iron status than serum ferritin. In both cohort studies, data on serum ferritin were not reported.
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In the present study, we observed lower concentrations of serum ferritin and TS but higher TIBC in men with PC than in those without PC. This is in contrast to what has been reported for cancer of the liver and lung. The small differences persisted even after subjects were matched to controls by race and inflammatory status. TS and/or serum ferritin concentrations indicative of low body iron stores were observed more often in men with PC than those without PC. Conversely, TS and serum ferritin concentrations suggestive of elevated body iron stores were less often in men with PC than in those without PC. The median serum ferritin concentrations of African-American men without PC (223 Hg/L) that we observed are very close to the value (approximately 200 |xg/L) reported by Zacharski et al. for healthy African-American men (40-59 years of age) included in the NHANES IIP (see Figure 2 of the citation). The median of our overall study population (209 |ig/L) is also similar to the values of the 75th percentiles (182-209 |ig/L) of American men (inclusive of different races) 48-76 years of age. However, the median serum ferritin values of men with PC (115 |iig/L overall and 126 |ig/L for the African-American men) resemble those of the 50th percentile (111-128 ng/L) for men of the same age range. Since we observed the expected inverse relationship between the concentrations of serum ferritin and TIBC in PC patients, our data suggest sub-optimal body iron stores in men with PC.
Most studies on iron status and risk for cancer have focused on iron overload for two reasons. First, iron is a powerful catalyst of free-radical generation, and second, it is an essential growth nutrient. Although iron is not carcinogenic, it is known to induce hydroxyl radicals from the less reactive superoxide anion and hydroxyl peroxide via the Fenton reaction. The highly reactive free radicals are thought to induce DNA mutations, and therefore, to be the mechanisms by which iron may increase the risk of cancer. Indeed, administration of high amounts of iron to rodents has been shown to increase tumor burden induced by various chemicals, such as dimethylhydrazine. Iron administration was also shown to increase tumor burden in hepatocellular carcinoma xenography.
Many studies have shown increased risk of liver and lung cancer with increased body iron stores. Studies showing an inverse correlation between body iron stores and higher cancer risk have also been reported. Reduced levels of serum ferritin and/or serum iron were observed in persons with gastric cancer. These authors attributed the low serum ferritin levels to blood loss.
Our results suggest that there is a negative association between serum ferritin levels and the presence of PC, but a cause and effect are not directly implied. Our study has three limitations: small sample size, experimental design (cross-sectional but not prospective study), and lack of information on certain confounding variables, such as smoking, dietary iron intake, and blood loss in the urinary and gastrointestinal tracts. These factors are known to affect indicators of iron status, specifically serum ferritin Urinary blood loss in men with PC is not very common and, therefore, cannot explain the reduced serum ferritin levels and TS that were observed in this study. Reduced iron absorption due to inflammation and/or increased iron utilization by PC cells could be the mechanisms of reduced serum ferritin and TS in PC patients.
Indeed, inflammation was more common in men with than in those without PC. While 25 of the 34 cases (73.5%) had some degree of inflammation (at least one acute phase protein above normal), only 26 of the 84 controls (30.95%) did. In PC patients, 29.4% (10/34) compared with only 7.14% (6/84) had at least two acute-phase proteins above normal. pharmacy united kingdom
In summary, our results suggest that elevated body iron stores are less common in men with PC than in those without PC. In fact, they suggest that reduced body iron stores are more common in PC patients than in non-PC men. This is the first study correlating body iron stores with PC. A prospective study is required to determine whether reduced body iron stores are a consequence or cause of PC related to a third factor which is directly influencing both the iron status and carcinogenesis domains.