Effectiveness of
Different Iron Supplementation Strategies on Hemoglobin
and Ferritin Levels Among Schoolchildren in Teresina, Piau
State, Brazil
Dos Santos MM, et al.
Cad Saude Publica, July 2007 ; 23(7) :1547-52.
This study evaluated the effectiveness of
supplementation with ferrous sulfate and iron bis-glycinate
chelate on
hemoglobin and serum ferritin levels among schoolchildren
(7-11 years) of both sexes. A randomized communitybased
trial including 138 anemic children (hemoglobin < 11.5 g/dL)
was conducted in Teresina, Piaui State, Brazil. Children
were assigned to two treatment groups on an individual
basis. One group (n = 71) received 40 mg iron as ferrous
sulfate once weekly and the other group (n = 67) received
3.8 mg of iron bisglycinate chelate-enriched
cookies, 3x/week, for 8 weeks. The interventions showed a
significant increase (p < 0.01) in hemoglobin levels (1.1
g/dL) for children who received ferrous sulfate and 0.9 g/dl
in those who received iron bisglycinate chelate, although
not significant in the inter-group comparison (p > 0.05). No
effect was observed on body iron for either intervention
(p > 0.05). Children with depleted iron stores <15 ng/mL) at
the beginning of interventions showed increased
serum ferritin concentrations after 8 weeks (p < 0.01),
although no difference between treatments (p > 0.05) was
observed. The results confirm the effectiveness of the iron
supplementation interventions and corroborate the use of
iron salts or ferrous bisglycinate chelate on a weekly basis
to overcome iron deficiency and anemia.
Copper Deficiency Causes
Reversible Myelodysplasia
Huff JD, et al.
Am J Hematol, July 2007; 82(7):625-30.
Copper deficiency is a recognized but often overlooked cause
of anemia and neutropenia. We began checking serum
copper levels on patients referred for evaluation for
unexplained anemia and neutropenia or myelodysplasia. Eight
patients were identified as copper deficient (serum copper
less than 70 microg/dL). The anemia was normochromic
and normocytic in seven patients. Neutropenia was present in
seven patients. Seven patients had been referred for
evaluation of myelodysplasia: Three were seen for
consideration for allogenic stem cell transplant. Five
patients had
concomitant peripheral neurological symptoms. Seven patients
were treated with oral copper gluconate. All treated
patients demonstrated a hematological response; seven had a
complete remission. The improvement in anemia and
neutropenia was rapid with normalization of blood counts
within three to four weeks. In one patient, normalization of
the underlying marrow dysplasia was demonstrated by bone
marrow histology eight months after copper
replacement. The cause of copper deficiency was felt to be
gastrointestinal malabsorption in five of our patients. We
conclude that copper deficiency should be considered in all
patients with unexplained anemia and neutropenia or
myelodysplasia.
Cardiac Nitric Oxide
Synthases Are Elevated in Dietary Copper Deficiency
Saari JT, et al.
J Nutr Biochem, July 2007; 18(7):443-8.
Dietary copper (Cu) deficiency leads to cardiac
morphological and functional defects suggestive of heart
failure.
However, simultaneous cytoprotective events also appear to
occur. The molecular mechanisms responsible for this
complex alteration of cardiac function by Cu deficiency have
not been elucidated. Because prior work has implicated
altered nitric oxide (NO) metabolism in this altered
function, we have examined this pathway in further detail.
Male
Sprague-Dawley rats were fed diets that were either Cu
adequate (6 mg Cu/kg diet) or Cu deficient <0.5 mg Cu/kg
diet) for 5 weeks. Endothelial NO synthase (NOS) and
inducible NOS (iNOS) protein expressions, as measured by
Western blot analysis, were 58% and 40% higher,
respectively, in Cu-deficient than in Cu-adequate rat
hearts.
Cardiac NOS activity, as measured by conversion of
(3)H-arginine to (3)H-citrulline, was 130% higher in
Cudeficient
than in Cu-adequate rats. NFkappaB is a known transcription
factor for iNOS. Activation of NFkappaB,
determined by an ELISA for the p65 subunit, was found to be
33% higher in Cu-deficient than in Cu-adequate rats.
Coupled with prior evidence of elevated cardiac
nitrate/nitrite production in Cu-deficient rats, these data
suggest
multiple pathways for enhanced NO production that may
contribute to altered cardiac function under dietary Cu
deficiency.
Stressor Exposure Increases Depressive
Mood in Iron Deficient Hispanic
American Women
Rahn M, et al.
The FASEB Journal, 2007;21:858.15.
The modifying effect of stressor exposure on the
relationship between depressive mood and iron deficiency
(ID) was investigated with 1375 premenopausal women of the
Hispanic Health and Nutrition Examination
survey (HHANES). Data were collected from 1982 to 1984;
participants were of Puerto Rican, Mexican,
Cuban or general Hispanic descent. Depression was assessed
with the Center of Epidemiologic studies -
depression scale (CESD, 20 statements). Removing 3
fatigue-related questions from the CESD-20 created
the variable CESD-17, which reflects depressive mood (range
0 to 51 points). Prevalence of depressive
mood was 7.9 %, with a cut-off score of 21 points (>90th
percentile). Fatigue was created as a summary
score from the 3 fatigue related statements (range 0 to 9
points). A total of 6.8% of the sample had iron
deficiency anemia, and 18.7% had iron deficiency without
anemia. ID was defined as low iron stores
according to the algorithm of Cook et al., (Blood,
1986;68:726[Abstract/Free Full Text]), which calculates
a continuous variable from individual values of hemoglobin,
ferritin, protoporphyrine, and transferrin
saturation. Logistic regression analysis adjusting for
survey design was performed, with depressive mood
greater than the 90th percentile of the CESD-17 as the
outcome. All models were controlled for fatigue,
socio-economic status (SES) and ethnic group. Stressors were
defined based on the reviewed literature and
available variables. ID women (iron stores < -200 mg) with
exposure to low SES, postpregnant status, or
low perceived control over their health had odds ratios of
depressive mood that were 1.66 to 5 times
greater compared to the reference group (no stressor
exposure, iron stores ≥ -200 mg). In conclusion,
exposure to stressors is an important modifier of the
relationship between depressive mood and ID.
Anti-atherosclerotic Properties of PP ARγ are
Dysfunctional During Zinc
Deficiency in LDL - R-/- Mice Treated with Rosiglitazone
Shen H, et al.
The FASEB Journal, 2007;21:697.5.
Low zinc concentrations may be associated with an
increased risk of cardiovascular diseases. We tested the
hypothesis that anti-atherogenic properties of PPARγ are
compromised during zinc-deficiency in
rosiglitazone (RSG)-treated LDL - R-/- mice. The mice
were maintained for four weeks on zinc deficient
(ZD) or adequate (ZA) diets. Half of the mice were
gavaged with the PPARγ agonist RSG. Subsequently,
selected inflammation and lipid parameters were studied.
RSG treatment deceased plasma insulin levels
only in ZA mice. iNOS gene expression in abdominal aorta
was down-regulated by RSG only in ZA mice.
MCP-l was induced by RSG only during ZD. RSG tended to
increase anti-inflammatory cytokine levels in
plasma of ZA but not ZD mice. Plasma IL-6 levels were
increased by RSG during ZD. RSG treatment
decreased plasma IL-12 levels in ZA mice, whereas
opposite effects were observed during ZD. RSG
treatment contributed to a proatherogenic
lipoprotein-cholesterol profile only in ZD mice. CD36
expression in abdominal aorta and plasma fatty acids
were increased by RSG only in ZD mice. In contrast,
RSG treatment increased LPL expression only in ZA mice.
These data suggest that in this atherosclerotic
mouse model PPARγ signaling was compromised during ZD
and that adequate dietary zinc is critical for
proper function of the anti-diabetic medicine
rosiglitazone.
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