Treatment of H. pylori infection was associated with more rapid response to oral iron therapy as compared with the use of iron therapy alone. Such treatment also led to enhanced iron absorption even in those subjects who did not receive oral iron therapy.

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To investigate the influence of iron deficiency and iron supplementation on nitric oxide (NO) production, we measured serum iron markers, serum nitrate and nitrite (NOx) concentrations, reticulocyte maturity index (RMI), and serum transferrin receptor (sTfR) levels in 369 females aged 14-19 years. RMI was analyzed by flow cytometry, sTfR concentrations were measured by enzyme immunoassay, and serum NOx levels were tested by the Griess reaction. NOx concentrations of the subjects in iron depletion phase were significantly higher than those of healthy controls. NOx concentrations increased gradually as iron deficiency progressed and were threefold higher than for the healthy controls, when the subjects attained a frank iron deficiency anemia. In particular, the NOx concentrations were 7.5-fold higher in the patients with severe iron deficiency anemia (Hb<80 g/l) than for the subjects with high hemoglobin value (Hb>or=140 g/l). The increased NOx concentrations (132.6+/-42.1 microM) observed in the group with severe anemia decreased significantly (46.3+/-15.8 microM) after hemoglobin levels were normalized by iron supplementation ( P<0.01). NOx concentrations correlated inversely with hemoglobin levels ( r(2)=0.202, P<0.01), but correlated positively with the sTfR concentrations ( r(2)=0.322, P<0.01) and the RMI ( r(2)=0.369, P<0.01). In conclusion, iron deficiency anemia increases NO production, and elevated NOx concentrations in iron deficiency anemia return to normal with iron supplementation.

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The higher values of RMI and sTfR observed in male neonates indicate that erythropoietic activity is higher in this group. Iron transport to the foetus appears to be independent of maternal iron deficiency. However, iron transport and erythropoiesis in newborns seems to decline from the time that the mothers acquire frank iron deficiency anaemia.

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To investigate the influence of body iron status on reticulocyte subpopulations and reticulocyte maturity index (RMI), we measured serum iron markers, fluorescent intensity of reticulocytes, and serum transferrin receptor (sTfR) concentrations in 374 females aged 14-19 years. Reticulocyte subpopulations were analyzed by flow cytometry, and sTfR concentration was measured by enzyme immunoassay. There were no significant differences in the values of reticulocyte subpopulations and RMI between ferritin alonedepleted group and healthy controls. However, middle-and high-fluorescence reticulocytes and RMI were significantly higher in both the serum iron-and serum ferritindepleted groups than in the ferritin alone-depleted group. Middle-fluorescence reticulocytes and RMI increased gradually as the body iron store was depleted and were 3.4-and 3.6-fold higher, respectively, than normal controls, when the subjects attained a frank iron-deficiency anemia. There were no significant changes in the values of red blood cells or total reticulocyte counts during iron-depleted states. The mean value of sTfR (3.98 mg/l) in the subjects with RMI ≥ 1.5% was significantly higher than that (2.26 mg/l) in the subjects with RMI < 1.5% (P < 0.01). The sTfR concentration correlated significantly with RMI (r = 0.61, P < 0.01) and middle-fluorescence reticulocytes (r = 0.59, P < 0.01). In short, body iron depletion induces elevation of immature reticulocyte fractions and RMI. Am. J. Hematol. 67:130-135, 2001.

No abstract