British Journal ofHaematology, 1975,30, 419.

Utilization of Iron Dextran in Recurrent Iron Deficiency Anaemia LESLIE M. KERNOFF, JOHANNES DOMMISSE AND ERNETTE D.

DU

TOIT

Departments of Haematology and Obstetrics, Groote Schuur Hospital and University of Cape Town Medical School, and Cape Provincial Blood Grouping Laboratories, Medical School, Cape Town (Received 17 October 1974; accepted f o r publication 16]anuary 1975)

SUMMARY. Previously published studies have documented a reduction in the rate at which iron stores laid down by iron dextran therapy can be utilized for haemoglobiii syi~thesisafter the acute demands of haemorrhage and phlebotomy. In order to determine if a defect in the mobilization of these stores exists in the face of a chronic stimulus to red cell production, 93 patients who had previously received a total dose infusion of iron dextran were examined for a recurreiicc of iron dcficieiicy anaemia, and in those in whom anaemia had recurred, iron stores were assessed by marrow aspiration. Twenty of the 93 patients were found to have recurrent iron deficiency anaemia, and marrow aspiration in all failed to demonstrate stainable iron stores. Although the rate at which iron dextran can be mobilized fiom storage sites is reduced, the present study demonstrates that ultimately these stores are fully utilizable. Intravenously administered iron dextran has gained widespread acceptance as a safe and reliable method of correcting iron deficiency anaemia and replenishing body iron stores (Marchasin & Wallerstein, 1964; Bonnar, 1965 ; Will & Groden, 1968). Henderson & H i h i a n (1969) reported that the availability of a portion of these iron stores for erythropoiesis was reduced. As a result, the rate of erythropoiesis in rcsponsc to phlebotomy was less than predicted and iron deficiency anaemia developed in the prcscnce of stainablc reticulocndothelial (RE) stores, findings confirmed by Olsson & Wcinfeld (1972). By contrast, stainable RE iron was not demonstrable in a series of patients in whom iron deficiency anaemia recurred after previous successful treatment with intravenous iron dextran (Dommisse & du Toit, 1972). Because these conflicting results wcre obtained from a limited number of observations, it was decided to assess the marrow iron status of a larger series of patients in whom iron deficiency anaemia rccurred after prior successful treatment with iron dextran. This problciii was felt to merit reinvestigation since the existence of storage iron in the facc of iron deficiency anaemia would confirm that some of the artificially laid down RE iron was unavailable for haemoglobin synthesis. Consequently, the value of iron dcxtran in the treatment of iron deficiency anaemia would be diminished. Correspondence: Dr L. Kernoff, Dcpartmcnt of Haematology, Royal Postgraduatc Medical School, Du C a m Road, London Wrz oHS.

420

L. M. KernoJJ. Dommisse and E. D. dtt Toit MATERIALS AND METHODS

Ninety-three patients who had received a total-dose infusion (TDI) of iron dextran (Imferon: Fisons) during pregnancy were investigated after an interval ranging from 6 months to 6 years. Iron deficiency anaemia had been diagnosed during pregnancy on the basis of peripheral blood values (Dacie & Lewis, 1970) and morphology, serum iron concentration, unsaturated iron binding capacity (UIBC) and percentage saturation (Beale et uE, 1962). Intolerance or failure to take to oral iron preparations constituted the two indications for TDI. The dose of iron as iron dextran required to restore the circulating red cell mass and replenish body iron stores was calculated according to the manufacturers’ instructions and ranged from 1.5 to 3.5 g (mean 2.1 g). The therapeutic response to TDI was documented by haemoglobin estimations at further ante-natal visits but marrow aspiration to confirm the replenishment of iron stores was not performed. For the purpose of the present study, patients who had received oral iron medication or blood transfusion in the interval between TDI and the present investigation were excluded from consideration. Venous blood was obtained from all 93 patients investigated. Marrow aspiration was performed on all patients with haemoglobin values of less than 11 g/dl and at random amongst patients whose haemoglobin level was greater than 14 g/dl. Haemoglobin, PCV and erythrocyte indices were determined on a Coulter counter. Serum iron, UIBC and percentage saturation were measured according to Beale et al(1962). Results obtained by this method are in good agreement with a more recently introduced method (I.C.S.H. panel, 1971). Serum folate levels were determined by means of an L. cusei assay. Plasma urea and creatinine concentrations were determined by an automated technique employing a Technicon autoanalyser. Peripheral blood and bone marrow morphology were assessed on specimens stained with May-Griinwald-Giemsa, and marrow iron was stained with potassium ferrocyanide (Dacie & Lewis, 1970). RESULTS The haemoglobin levels of the 93 patients at follow-up are presented in Fig I, and are grouped in 6-month periods from 6 months to 6 years. Twenty of these patients had a haemoglobin concentration of less than I I g/dl. Details of these 20 patients are presented in Tables I and 11. Table I presents the criteria by which the diagnosis of iron deficiency anaemia was made initially at the time of TDI. Table I1 contains the information upon which the diagnosis of recurrent iron deficiency anaemia was made. At follow-up the mean serum iron concentration was 6.2 ,umol/l. (range 2.6-10.2). This differed significantly ( P < 0.001) from the mean serum concentration of 18.9pmol/1. of 24 patients in the series whose haernoglobin concentration was 14 g/dl or more (range 11.6-28.6). No patient whose haemoglobin concentration was less than 11 g/dl had a percentage saturation of greater than 16% (Bainton & Finch, 1964, whereas the lowest percentage saturation in those patients with a haemoglobin level greater than 14 g/dl was 18% (mean = 26, range 18-37). The MCH and MCV were markedly reduced (Table 11) , reflecting the hypochromasia and microcytosis of the erythrocytes on peripheral blood films. Bone marrow morphology showed the ragged and poorly haemoglobinized normoblast cytoplasm characteristic of iron

I I

I

I

I

I

2

3

4

5

I 6

Years

FIG I. Haemoglobin concentrations in 93 patients observed 6 months to 6 ycars after rcceiving total dose infusion of iron-dextran coniplcx.

TABLE I. Initial diagnosis of iron deficiency anaemia

PCV

Patierit

3

39 38 31

4

20

5 6 7 8 9

34 35 21

37 28

7.8 7.3 7.6 8.1 8.4 8.1 8.3 6.2 8.8

I0

20

8.0

I1

20

I2

43 42 42 37 39 35 24 33 26

I 2

I3

I4 IS 16 I7 18 I9 20

7.3 7.2 8.9 7.6 6.9 8.8 6.3 7.8 7. I 6.9

0.27 0.28 0.27 0.3 I 0.30 0.28 0.30 0.23

0.3 I 0.29

0.26 0.25

0.30 0.28 0.26 0.31 0.26 0.27

29 26 28 26 28 29 27 27 28 27 28 29 30 27 27 28

24 29

0.28

25

0.26

26

Serum iron

UlBC

(pnol//.)

(ptnfol/l.)

5.3 6.2 5.0 6.8 6.2 9.4 3.5 4.7 3.2

5.7 5.3 9.8 6.2

6.2 7.6 5.0 4.1 8.9 5.9 4.1

63.5 66.2 68.0 57.8 68.0 >71.6 71.2 69.2 70.7 55.8 64.9 >71.6 56.3 71.6 67.6 70.3 71.2 70. 5 >71.6 61.7

% Sat.

8 9 7 I2

9 < I3 5 7 5 I0

8 71.6 >71.6 71.0 70.7 51.3 >71.6 >71.6 >71.6 71.0 69.8 >71.6 >71.6 >71.6 50.4 >71.6 69.8 68.9 70,7 69.8

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Utilization of iron dextran in recurrent iron deficiency anaemia.

Previously published studies have documented a reduction in the rate at which iron stores laid down by iron dextran therapy can be utilized for haemog...
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