![]()
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Iron status and risk-profiling for deficiency in New
Zealand blood donors
Krishna G Badami, Kate Taylor
Iron deficiency is a major health problem throughout the
world including New Zealand. Indeed, some evidence shows that deficiency, even
if insufficient to cause anaemia, may affect physical and mental performance and
health. An individual’s iron status is a balance between intake,
absorption, and loss.
Blood donation is a well-recognised risk factor for iron
deficiency. Iron deficiency is probably the most significant impact of blood
donation on donors. Current, ‘one size fits all’ protocols may be
insufficient to prevent iron deficiency in some blood donors.
Published information on the iron status of New Zealand
blood donors is limited.1 A study from the
United States suggested that up to 8 and 23% of male and female donors
respectively may be iron deficient.2
We report results from a two-site observational study on New
Zealand blood donors which aimed to determine:
MethodsThe study was undertaken between October and December
2006 at the Christchurch and Waikato New Zealand Blood Service (NZBS) sites
after approval by the multi-region ethics committee, Wellington.
Intending blood donors attending static and mobile
venues were given an information leaflet and asked if they wished to
participate. Inclusion in the study required:
Note:
Blood donors routinely undergo health assessment which includes a questionnaire,
an interview, pre-donation haemoglobin measurement and post-donation blood
tests.
Ferritin was measured using a validated enzyme
immunoassay (Abbot Axsym®). For the purposes of this study the iron status
of subjects, based on the ferritin level was classified as:
Subjects
with normal results were not informed but were given the opportunity to discuss
their results by telephone. Those with abnormal results were informed and
advised to see their own doctors.
Demographic data and blood test results were taken from
computer records and collated electronically. Data were analysed using the Epi
Info 2000 statistics package.
ResultsOf the 5046 participants approached, 5006 (99.2%)
participants were recruited: 3001 from Waikato and 2005 from Christchurch.
Figure 1 shows the study flow chart.
Characteristics of study subjects are shown in Table 1. They
were comparable with those for New Zealand blood donors as a whole and subjects
at the two sites were essentially comparable with each other.
Correlations between the three main variables (age, gender,
and donation history) for the 5006 subjects are shown in Figures 2–4.
Ferritin levels and the iron status of subjects are shown in Tables 2 and
3.
While the majority of subjects with a ‘low’ Hb
(as previously defined) had a low ferritin, a substantial minority of those with
acceptable Hb also had a low ferritin (Table 3); 99.0% of all subjects had an Hb
that was acceptable for blood donation (Table 3) as did 1694/1730 (97.9%) of
subjects with a low or borderline iron status.
Gender, age, and prior donation history influence the risk
of becoming iron deficient (Tables 2 and 3). Risk categorisation by cumulative
risk scores based on these variables is shown in Table 4 and the correlation
between risk category and ferritin level is shown in Table 5. Though this model
has not been validated and is incomplete (not having taken in to account other
determinants of iron status), it has biological
basis3 and our results suggest that there is a
good correlation.
In the scheme described above, cumulative risk scores 5 and
4 (together 6.1% of all subjects) might represent ‘high risk’, 3 and
2 (55.0%) ‘intermediate risk’, and 1 and 0 (38.7%) ‘low
risk’ for iron deficiency.
Figure 1. Study flow chart
![]() Note: Includes 48 ineligible to donate
on account of ‘low’ Hb but eligible for the study;
DA testing=donor accreditation testing (post-donation blood tests),
Hb=haemoglobin.
Table 1. Characteristics of subjects in the
study compared to New Zealand blood donors in 2006. All values are shown as n
(%)
Table 2. Serum ferritin levels (mcg/L) and
subject characteristics
Table 3. Iron status and subject
characteristics
Figure 2. Proportions (%) of males and females
in the 3 age groups
Figure 3. Gender and prior donation
history
![]() Figure 4. Age and prior donation
history
Table 4. Cumulative risk (risk categories)
based on gender, age, and prior donation history
Table 5. Ferritin levels (mcg/L) according to
cumulative risk (risk category) for iron deficiency)—all subjects
combined
*P value <0.0001 comparing the mean ferritin for
categories 3 and 5.
DiscussionThis is the first systematic assessment of iron status in a
broad range of New Zealand blood donors. Our results show that iron deficiency
is a significant problem in this group (Tables 2 and 3). Overall 14.1% and 20.4%
of subjects had low or borderline iron status respectively. Current standards
(see later), protect donors poorly in this regard. The vast majority (97.9%) of
subjects with a low or borderline iron status had an Hb that was adequate for
donation
The proportion of iron-deficient subjects in this study is
similar to those in previous reports on blood
donors1,2,4–6 but higher than those in
New Zealand population-based reports (with some
exceptions).7–10 Direct comparisons are
difficult because of inconsistencies in the use of terms such as
‘donor’ and ‘non-donor’ and in the ferritin levels
defining iron deficiency.
As expected, females, subjects aged under 20 years (y) and
those with more intense prior donation history had lower ferritin levels and
significantly worse iron status (Tables 2, 3). While the relationship between
gender and prior donation history is not clear-cut (Figure 3), it is unlikely
that prior donation history alone is sufficient to explain the worse iron status
of female subjects.
Factors not evaluated in the present study such as diet and
menstruation are likely to be more important. The relatively poor iron status of
<20 y subjects is possibly due to the combined effect of increased iron
requirements during growth and inadequate intake. Indeed, several studies have
confirmed the relatively poor iron intakes and iron status in
adolescents—especially,
girls.11–13
Intensity of blood donation during the previous 12 months
was inversely and significantly related to ferritin (Tables 2, 3).Those with the
highest two levels of prior donations, constituting 73.5% of all subjects (Table
1) accounted for 687/751 (91.4%) of those with low ferritin.
Red RBC (and hence iron) loss depends on the number and type
of donation. NZBS standards permit up to 4 whole blood donations or (at that
time) up to 15 L of plasma in a 12-month period with at least 90 days between
successive whole blood and 14 days between successive phereses donations subject
to satisfactory pre-donation health assessment as described under methods.
Loss of packed RBC is 175–330 ml with a whole blood
donation and, in our set-up, 10–15 ml with a pheresis donation. Additional
losses of blood occur—for routine blood tests in all donors and, for
instance, the initial blood draw into the diversion pouch (to reduce bacterial
contamination) in plateletpheresis donors.
The relationship between ABO/RhD group, ferritin levels, and
donation frequency has not previously been commented on. In this study, O
negative subjects had significantly lower ferritin levels (Tables 2 and 3)
perhaps because they donate blood more intensively than those of other groups.
54.2% and 26.5% of O-negative subjects donated 3–4 WB units and 1–2
WB / >15 ph units respectively during the previous 12 months compared to
48.5% and 15.4% respectively for those of other groups.
Waikato subjects had significantly higher ferritin levels
than Christchurch subjects, lower proportions of those with low and borderline
ferritin, and higher proportions of those with normal and high ferritin (Tables
2 and 3). The reasons are not clear. Christchurch had slightly more O negative
donors and subjects donating more intensively in the previous 12 months compared
to Waikato. Waikato though, had a slightly higher proportion of females and
<20 y subjects than Christchurch (results not shown) and possibly also a
higher proportion of Māori subjects.
In the last National Nutrition Survey (NNS
97),7 Māori (especially women) appeared to
have a worse iron status than that of their ‘European and Other’
counterparts. Factors not considered in the current study (such as ethnicity,
dietary iron intake and absorption, body-mass index, menstruation, oral
contraceptive vs intrauterine device use, and causes of ‘falsely’
elevated ferritin) may explain the difference between the two sites.
Individuals with latent iron deficiency (low ferritin but
‘normal’ Hb and red cell indices) may show increase in both Hb and
indices as iron status improves. Furthermore, latent iron deficiency may be
associated with a variety of significant, though sometimes subtle, health
problems such as fatigue,14 low physical
endurance,15,16 impaired
cognition,17,18 and the restless leg
syndrome.19
A small minority of subjects with borderline or normal
ferritin (6/1022 and 12/3249 respectively) but none with raised ferritin also
had ‘low’ Hb but they were not further investigated by us.
Explanations include:
While the
majority of subjects with a ‘low’ Hb had a low ferritin, a
substantial minority of those with acceptable Hb also had a low ferritin (Table
3) thus confirming again that anaemia develops late in iron deficiency. It is
sobering to note that 13.6% and 20.4% of the 4957 subjects who actually donated
blood had low or borderline iron status respectively on the day they donated
blood (Table 3).
Only 1% of all subjects (and 4.3% of those with a low
ferritin) had a ‘low’ Hb. Normally we would detect a higher
proportion of intending blood donors with a low Hb. The low numbers of ‘Hb
failures’ in this study may have resulted from the low enrollment of
subjects with low Hb. Nevertheless, our results suggest that the magnitude of
the problem of iron deficiency amongst New Zealand blood donors is perhaps no
less than stated.
In this connection it is interesting to consider ferritins
routinely checked in 1077 intending blood donors with a low Hb at the
Christchurch centre between July 2001 and February 2007 (not part of the current
study). This ranged from 1–464 mcg/L, the mean was14.9 mcg/L and the
median 6.0 mcg/L. Of these, 2 (0.18%), 148 (13.7%), 138 (13.7%), and 789
(78.3%), would have been classified as iron status high, normal, borderline and
low respectively according to the criteria used in this study.
Risks for iron deficiency are additive and a combination of
factors determines overall risk (Table 5). In this study, gender, age, and prior
donation history were evaluated. As expected, male donors, in general, are able
to maintain iron levels better than females. For example, the mean serum
ferritin in males aged >21 y donating 3–4 WB units during the previous
12 months was comparable (results not shown), not to that of females >51 y
with a similar donation history, but to >51 y female subjects with a past
history of 1–2 WB or pheresis equivalents.
Interestingly 27/5006 (0.5%) subjects had higher than normal
ferritin including 13/2758 (0.4%) of those who had donated 1–2 whole blood
units or >15 phereses units, 6/2611 (0.2%) of females and 1/415 (0.2%) of
those <20 y [Table 3].
In blood donors, raised or high-normal ferritin for reasons
other than genetic haemochromatosis (HC) are possible but unlikely. Indeed, some
subjects may have been patients with known HC (but accepted as blood donors) and
some who were previously undiagnosed have since had HC formally confirmed. While
the serum ferritin assay is not a good test for early HC, in blood donors it is
likely to uncover at least some cases of HC—an example of ‘value
addition’ to the donation process (from the perspective of the donor) that
has recently been mooted.20
Conclusions and RecommendationsA significant proportion of New Zealand blood donors have
poor iron status. As expected, female gender, lower age, and more intensive
blood donation history predict poor iron status. Current protocols protect blood
donors poorly from iron deficiency.
Iron deficiency affects donor health, donor retention, and
blood supply. The latter possibility been discussed in a previous
publication.21 Amongst New Zealand blood
donors, Hb failure is the prime single reason for deferral accounting for 20% of
all deferrals in 2006–2007 (internal NZBS data). Most of these are likely
to be due to iron deficiency.
This study has not considered all the risk factors for iron
deficiency and a further study is planned to consider factors such as diet,
menstruation, ethnicity, and BMI. However, even on the basis of the information
currently available, individually tailored protocols can be created that are
better able to preserve donor iron status.
Changes to donation protocols, if stratified by risk should
not prove too difficult to implement because only a minority of subjects (6.1%)
in our study were in a putative ‘high risk’ group requiring
particular attention while 55.0% and 38.7% respectively were in
‘intermediate’ and ‘low’ risk categories (Table 5).
Reducing donation frequency alone, in order to improve donor
iron status, may lead to unacceptable reduction in supply—at least in the
short-term. A stratified protocol taking into account risk, (but also Hb and
ferritin) and incorporating testing for deficiency, prophylaxis or, treatment
with iron supplements as appropriate and follow-up is the one most likely to
reconcile the conflicting demands of blood supply and donor well-being.
Competing interests: None known.
Author information: Krishna G Badami,
Transfusion Medicine Specialist, New Zealand Blood Service,
Christchurch; Kate Taylor, Medical Officer, New Zealand
Blood Service, Hamilton
Acknowledgements: We are grateful to the
following people and organisations for their assistance:
Correspondence: Dr
Krishna G Badami, Transfusion Medicine Specialist, New Zealand Blood
Service, 87 Riccarton Rd., Christchurch, New Zealand. Email: krishna.badami@nzblood.co.nz
References:
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Current
issue | Search journal |
Archived issues | Classifieds
| Hotline (free ads) Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals |