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Thyroid Function Among Children with Iron Deficiency Anaemia: Pre- and PostIron Replacement Therapy

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Abstract

Introduction: Metabolism of thyroid hormones and iron is quite interdependent. Data indicates that Iron Deficiency (ID) could impair thyroid metabolism. Aim: To investigate the possible occurrence of thyroid dysfunction among children with isolated Iron Deficiency Anaemia (IDA) of various severities, and test if the oral iron replacement therapy alone can reverse the associated thyroid function disturbances, if present or additional therapies are required. Materials and Methods: This prospective study was carried out on 60 children selected from the attendants to the outpatient paediatric clinics of Al-Azhar University, Assiut and Qena university hospitals, Egypt, in addition to 60 controls. Complete blood count, thyroid profile, ferritin, iron, Total Iron Binding Capacity (TIBC), Transferrin Saturation% (TFS%), unsaturated iron binding capacity and Urinary Iodine Excretion (UIE) were assessed in the studied groups at baseline, then haemoglobin level and thyroid profile repeated among the studied patients after three months of oral iron supplementation therapy. Thyroid profile and ferritin were measured using commercially available Enzyme Linked Immunosorbent Assay (ELISA) kits; while, iron, TIBC and UIE were measured using colorimetric methods. Results: Significant higher serum Thyroid Stimulating Hormone (TSH) levels with significant lower serum levels of Free Triiodothyronine (FT3) and Free Thyroxine (FT4) among patients versus controls (p
Journal of Clinical and Diagnostic Research. 2018 Jan, Vol-12(1): BC01-BC05 11
DOI: 10.7860/JCDR/2018/32762.11023 Original Article
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Thyroid Function among Children with
Iron Deficiency Anaemia: Pre and Post
Iron Replacement Therapy
INTRODUCTION
One of the worldwide concerns is ID and IDA, which commonly
occurs among children in the developing countries [1]. About 27%
of children in Egypt have IDA [2].
Depletion of the body’s iron stores leads to ID which manifests
early by elevated Red cell Distribution Width (RDW) and finally by
occurrence of IDA which is diagnosed by low haemoglobin level
(<11 gm/dL) and haematocrit value combined with low serum iron
and low transferrin saturation [3].
Data indicate that ID impairs thyroid metabolism [4,5], that has been
explained by the iron dependence of Thyroid Peroxidase (TPO),
which is a haem containing enzyme, responsible for iodide oxidation
into iodine, then its binding to tyrosine residue of thyroglobulin for
formation of Mono-Iodotyrosine (MIT) and Di-Iodotyrosine (DIT). Also,
this enzyme is important for oxidative coupling of two molecules of
DIT to form T4 or coupling of one MIT and one DIT to form T3 [6].
Limited studies investigating the interaction and display of ID and
thyroid hormones in humans are present [7,8]. We investigate the
possible occurrence of thyroid dysfunction among children with
isolated IDA and if the iron replacement therapy alone can reverse
the associated thyroid function disturbances or additional therapies
are required.
MATERIALS AND METHODS
Study Population
This prospective study was carried out on 60 children in the age
group from 2-16 years selected from the attendants to the outpatient
paediatric clinics of Al-Azhar University, Assiut and Qena University
Hospitals, upper Egypt, according to the inclusion criteria during the
study period from 1st March 2016 to 28th February 2017. This was
in addition to 60 apparently healthy age and sex matched children
selected as control group. This study was conducted according to
the guidelines laid down in the declaration of Helsinki [9], and all
procedures involving human patients were approved by the Ethics
Committee of both Faculty of Medicine, Al-Azhar University, Assiut
and Faculty of Medicine, South Valley University, Qena, Egypt. Also,
an informed consent was obtained from either parent of all included
children.
Patients were selected according to the following inclusion criteria:
any child aged 2-16 years old with clinical and laboratory diagnosis
of isolated IDA, serum albumin, cholesterol and UIE, all to be within
the normal range, his/her weight and height within normal range
for the corresponding age and sex with normal Body Mass Index
(BMI). Any child with the previous inclusion criteria, but with a
history of receiving iron, other haematinics or multivitamins in the
preceding three months, with acute or chronic illness, with chronic
or recent acute blood loss, on hormonal therapy, with family history
of hypothyroidism, with autoimmune thyroiditis, syndromic children,
malnourished children, disturbed cholesterol or albumin serum
levels, UIE less than 100 μg/L, C-reactive protein 0.6 mg/dL, were
excluded from the study.
Laboratory Workup
A morning urine sample was obtained from each child and
stored at -20°C until assay of urinary iodine by Sandell-Kolthoff
HOSNY MA EL-MASRY1, AMIRA MM HAMED2, MOHAMMED H HASSAN3, HANAN M FAYED4, MH ABDELZAHER5
Keywords: Iron therapy, Microcytic anaemia, Thyroid hormones
ABSTRACT
Introduction: Metabolism of thyroid hormones and iron is quite
interdependent. Data indicates that Iron Deficiency (ID) could
impair thyroid metabolism.
Aim: To investigate the possible occurrence of thyroid dysfunction
among children with isolated Iron Deficiency Anaemia (IDA) of
various severities, and test if the oral iron replacement therapy
alone can reverse the associated thyroid function disturbances,
if present or additional therapies are required.
Materials and Methods: This prospective study was carried
out on 60 children selected from the attendants to the outpatient
paediatric clinics of Al-Azhar University, Assiut and Qena
university hospitals, Egypt, in addition to 60 controls. Complete
blood count, thyroid profile, ferritin, iron, Total Iron Binding
Capacity (TIBC), Transferrin Saturation% (TFS%), unsaturated
iron binding capacity and Urinary Iodine Excretion (UIE) were
assessed in the studied groups at baseline, then haemoglobin
level and thyroid profile repeated among the studied patients
after three months of oral iron supplementation therapy. Thyroid
profile and ferritin were measured using commercially available
Enzyme Linked Immunosorbent Assay (ELISA) kits; while, iron,
TIBC and UIE were measured using colorimetric methods.
Results: Significant higher serum Thyroid Stimulating Hormone
(TSH) levels with significant lower serum levels of Free
Triiodothyronine (FT3) and Free Thyroxine (FT4) among patients
versus controls (p<0.001 for all). Significant positive correlation
between serum iron and FT3 (r=0.284, p<0.05) with significant
negative correlations between TSH versus both serum iron
(r=-0.635, p<0.001) and ferritin (r=-0.342, p<0.01). Significant
decrease in the serum levels of TSH, with significant increase
in the serum levels of FT3 and FT4 (p<0.001 for all) to euthyroid
status following oral iron replacement therapy.
Conclusion: Subclinical or primary hypothyroidism can occur
among children suffering from moderate to severe IDA, which is
reversible following oral iron replacement therapy only, without
need to add thyroid replacement therapy.
Hosny MA El-Masry et al., Thyroid Function among Children with Iron Deficiency Anaemia: Pre and Post Iron Replacement Therapy www.jcdr.net
Journal of Clinical and Diagnostic Research. 2018 Jan, Vol-12(1): BC01-BC05
22
Variables
Patients
(n=60)
Control
(n=60) *p-value
mean±SD mean±SD
Haemoglobin (gm/dL) 9.18±1.39 11.80±0.80 <0.001*
Haematocrit (%) 27.36±3.55 34.36±3.20 <0.001*
Red cell count (M/cmm) 3.58±0.39 4.29±0.39 <0.001*
Mean Corpuscular Volume (MCV) (fl) 62.32±4.87 79.53±6.61 <0.001*
Mean Corpuscular Haemoglobin
(MCH) (pg) 23.41±3.78 27.63±1.82 <0.001*
Red cell Distribution Width (RDW)
(%) 16.76±2.66 14.60±1.53 <0.001*
Ferritin (ng/mL) 12.01±5.39 46.80±7.57 <0.001*
Iron concentration (μg/dL) 20.82±4.08 91.05±9.72 <0.001*
Total Iron Binding Capacity (TIBC)
(μg/dL) 476.00±43.32 310.85±63.34 <0.001*
Transferrin Saturation percent
(TFS%) 4.40±1.10 30.55±7.66 <0.001*
Unsaturated Iron Binding Capacity
(UIBC) (μg/dL) 455.10±44.77 219.80±65.17 <0.001*
Urinary iodine (μg/L) 110.65±6.11 109.30±4.76 0.377
Cholesterol (mg/dL) 129.18±14.92 123.20±14.91 0.113
Albumin (gm/dL) 3.44±0.37 3.28±0.34 0.122
[Table/Fig-1]: Comparison of the mean±SD of blood indices, iron study
paramters, urinary iodine excretion, serum albumin and serum cholesterol among
patients versus controls.
* Statistically significant difference (p<0.05)
Thyroid profile parameters
Patients
(n=60)
Controls
(n=60) *p-value
mean±SD mean±SD
Thyroid stimulating hormone (μIU/mL) 4.03±1.41 0.79±0.46 <0.001*
Free T3 (pg/mL) 1.03±0.12 4.08±0.70 <0.001*
Free T4 (ng/dL) 0.96±0.37 1.33±0.21 <0.001*
[Table/Fig-2]: Comparison of the mean±SD of thyroid stimulating hormone, FT4
and FT3 among patients versus controls.
T3: Triiodothyronine, T4: Thyroxine
* Statistically significant difference (p<0.05)
RESULTS
We enrolled 60 children with isolated IDA (38 males and 22
females), mean age 5.82 years (±3.05) and 60 controls (34 males
and 26 females), mean age 6.28 years (±2.81). There were non
significant differences in the mean levels of UIE, serum cholesterol
and albumin among patients versus controls (p<0.05), which
were all within the normal range to confirm the inclusion criteria as
presented in [Table/Fig-1].
reaction, using conventional chloric acid digestion method in a
test tube; where, 250 μL from each urine sample or calibrators
(25,50,100,200,300 and 400 μg/L iodine standard solutions) was
added to 750 μL cholric acid solution, incubated for 60 minutes at
110°C, then 3.5 mL of arsenious acid was added to each test tube
after cooling. Then, 350 μL of ceric ammonium sulfate solution
added to each test tube and mixed properly. The absorbance
at 405 nm was measured, using spectrophotometer (CHEM-7,
Erba diagnostics Mannheim GmbH, Germany) [10]. Ten millilitres
fasting venous blood samples were drawn from an antecubital
vein of the included children, divided into two tubes, 2 mL on
Ethylenediaminetetraacetic Acid (EDTA) tube for measurement
of the complete blood count, using (Cell Dyn 1800-Abbott
diagnostics, Germany) and 8 mL on serum separator gel tubes,
were allowed to be clotted for 30 minutes then centrifuged for 15
minutes at 3000 rpm. Serum cholesterol and albumin of each
sample were assessed by colorimetric methods [11-13], using
Cobas C311 (Roche diagnostics, Germany) and the remaining
amount was transferred and divided into aliquots using 1 mL
cryotubes and stored at -20°C till time of biochemical analysis.
All samples were measured in a single assay to avoid repeated
freeze-thaw cycles. A commercially available ELISA kit was used
for biochemical analysis of serum FT3 and FT4 (using solid phase
competitive assay method), TSH and ferritin (using solid phase
sandwich assay method) [14,15], all were supplied by Calbiotech
Inc., 10461 Austin Dr, Spring Valley, CA, 91978. The catalog
numbers were: F3106T for FT3, F4107T for FT4, S227T for TSH
and R248T for ferritin. A commercially available colorimetric assay
kit was used for measurement of serum iron and TIBC (supplied
by Spectrum Diagnostics Co. Cairo, Egypt, Catalog No: 270001).
TFS% was determined by dividing the serum iron concentration by
the TIBC and multiplying by 100, unsaturated iron binding capacity
(μg/dL), obtained by subtracting serum iron concentration from the
TIBC [16,17].
Complete blood count, serum TSH, FT3, FT4, ferritin, iron, TIBC,
TFS% and unsaturated iron binding capacity were measured in the
studied groups at baseline, then haemoglobin level, serum ferritin,
TSH, FT3, FT4 repeated among the studied patients after three
months of oral iron supplementation therapy (6 mg/kg/day divided
into two doses). Value of the thyroid profile of the included subjects
to be judged as hypothyroidism should be less than the cut-off value
of the standard of the normal reference range provided by the used
kits, in children: in the present study, the normal reference ranges
for TSH=0.35-4.94 μIU/mL, for FT3=1.71-4.8 pg/mL and for FT4=
0.7-1.48 ng/dL.
Anaemia can be considered in children when the levels of
haemoglobin are less than 11 gm/dL and the severity of anaemia
based on the haemoglobin levels to be considered as mild anaemia
(10-10.9 gm/dL); moderate anaemia (7-9.9 gm/dL); severe anaemia
(<7 gm/dL) [18]. Subclinical hypothyroidism considered when there
is normal FT3 and FT4 levels with a slightly elevated TSH level [19],
while primary hypothyroidism in which the defect in the thyroid
gland itself, stated when there are decreased thyroid hormones
concentration with subsequent elevated TSH level [20].
STATISTICAL ANALYSIS
Date entry and data analysis were done using the Statistical Package
for the Social Sciences (SPSS) version 19.0. Data were presented as
number, percentage, mean and standard deviation. Chi-square test
was used to compare between qualitative variables. Mann-Whitney
U test was used to compare between two quantitative variables
in case of non parametric data. Wilcoxon signed rank test was
done to compare quantitative variables before and after treatment.
Spearman correlation was done to measure correlation between
quantitative variables. MedCalc program was used to calculate
sensitivity, specificity, positive and negative predictive values. The
p-values were considered statistically significant when p<0.05.
Comparison of the mean±SD of blood indices and iron study
parameters among patients versus controls is presented in [Table/
Fig-1], which confirms the presence of microcytic hypochromic
anaemia among the selected paediatric patients due to significant
lower haemoglobin, haematocrit %, Red Blood Cells count (RBCs),
Mean Corpuscular Volume (MCV), serum ferritin, iron and TFS% in
the patient group versus the controls (p<0.001 for all).
Comparison of the mean±SD of TSH, FT4 and FT3 among patients
versus controls is presented in [Table/Fig-2], which showed
significantly higher serum TSH levels with significantly lower serum
levels of FT3 and FT4 among patients versus controls (p<0.001 for
all). The frequency of euthyroid status among the included patients
(according to the supplied kit reference ranges for TSH, FT3 and
FT4) was 48% (79% had mild anaemia and 21% had moderate
anaemia) followed by subclinical hypothyroidism 28% (82% had
moderate anaemia and 18% had severe anaemia), while, primary
hypothyroidism has the lowest frequency 24% (all patients had
severe anaemia).
Comparison of the mean±SD of TSH, FT4 and FT3 levels in patients
in relation to the severity of anaemia was shown in [Table/Fig-3],
www.jcdr.net Hosny MA El-Masry et al., Thyroid Function among Children with Iron Deficiency Anaemia: Pre and Post Iron Replacement Therapy
Journal of Clinical and Diagnostic Research. 2018 Jan, Vol-12(1): BC01-BC05 33
with significant higher serum levels of TSH and significant lower FT3
in patients with severe IDA versus patients with moderate or mild
IDA (p<0.01 for all).
There was significant positive correlation between serum iron and
FT3 (r=0.284, p<0.05) with significant negative correlations between
TSH versus both serum iron (r=-0.635, p<0.001) and ferritin (r=-
0.342, p<0.01) as presented in [Table/Fig-4]. Correlations between
blood indices and thyroid profile among the included patients
are presented in [Table/Fig-5], which revealed significant positive
correlation between serum TSH levels and RDW (r=0.500, p<0.001)
and between FT3 and RBCs (r=0.359, p<0.01) with significant
negative correlations between serum TSH levels and MCV (r=-
0.333, p<0.01), haemoglobin (r=-0.714, p<0.001), haematocrit %
(r=-0.586, p<0.001) and RBCs (r=-0.298, p<0.05).
Cut-off values of some blood indices and serum iron study
parameters in predicting the occurrence of thyroid hypofunction
(high TSH with normal or low FT4) in patients with IDA are
presented in [Table/Fig-6], which showed that thyroid functions
started to be affected in IDA patients when haemoglobin levels
8.3 gm/dL, serum ferritin 15.2 ng/mL, serum iron 19.4 μg/dL
and TFS% 3.63.
Comparison of the mean haemoglobin levels and thyroid profile (TSH,
FT3 and FT4) among IDA patients pre and post iron replacement
therapy are presented in [Table/Fig-7] which revealed significant
decrease in the serum levels of TSH, with significant increase in the
serum levels of FT3 and FT4 (p<0.001 for all).
Variable Cut-off Sensitivity Specificity +PV* -PV* AUC*
Haemoglobin (gm/dL) 8.3 58.82 88.37 66.7 84.4 0.806
Mean Corpuscular
Volume (MCV) (fl) 58.5 52.94 90.70 69.2 83.0 0.720
Red cell Distribution
Width (RDW) (%) >17.5 58.82 90.70 71.4 84.8 0.722
Ferritin (ng/mL) 15.2 94.12 39.53 38.1 94.4 0.659
Serum iron (μg/dL) 19.4 76.47 76.74 56.5 89.2 0.778
Transferrin
saturation% 3.63 64.71 88.37 68.7 86.4 0.772
Unsaturated iron
binding capacity
(μg/dL)
>483 64.71 74.42 50.0 84.2 0.665
Total iron binding
capacity (μg/dL) >486 76.47 58.14 41.9 86.2 0.654
[Table/Fig-6]: Cut-off values of some blood indices and serum iron study
parameters in predicting the occurrence of thyroid hypofunction (high TSH with
normal or low FT4) in patients with iron deficiency anaemia.
* +PV= positive predictive value, -PV= negative predictive value, AUC= area under the curve
Thyroid
profile
param-
eters
Mild
anaemia
(n=23)
Moderate
anaemia
(n=20)
Severe
anaemia
(n=17)
**p-value
mean±SD mean±SD mean±SD p1 p2 p3
Thyroid
stimulating
hormone
(μIU/mL)
2.73±1.23 4.64±0.70 5.67±0.54 <0.001* <0.001* <0.001*
Free T3
(pg/mL) 1.05±0.08 1.04±0.15 0.93±0.03 0.829 <0.001* 0.006*
Free T4
(ng/dL) 0.89±0.39 1.02±0.35 0.88±0.36 0.269 0.902 0.560
[Table/Fig-3]: Comparison of the mean±SD of thyroid stimulating hormone, FT4
and FT3 levels in patients in relation to the severity of anaemia.
T3: Triiodothyronine, T4: Thyroxine
* Statistically significant difference (p<0.05)
** p1=mild anaemia versus moderate anaemia, p2=moderate anaemia versus severe anaemia,
p3=mild anaemia versus severe anaemia
Variables Thyroid stimulating
hormone (µIU/mL)
Free
T3 (pg/
mL)
Free T4
(ng/dL)
Red cell Distribution
Width (RDW) (%)
r-value 0.500 -0.221 -0.071
p-value 0.000* 0.089 0.590
Mean Corpuscular
Volume (MCV) (fl)
r-value -0.333 0.241 0.066
p-value 0.009* 0.063 0.619
Haemoglobin (Hb) (gm/
dL)
r-value -0.714 0.241 0.164
p-value 0.000* 0.063 0.210
Haematocrit (%)
r-value -0.586 0.237 0.195
p-value 0.000* 0.068 0.135
Red Blood Cell count
(RBCs) (M/cumm)
r-value -0.298 0.359 0.148
p-value 0.021* 0.005* 0.261
[Table/Fig-5]: Correlations between RDW, MCV, Hb, haematocrit, RBCs versus
TSH, FT3 and FT4 among the included patients.
T3: Triiodothyronine, T4: Thyroxine
* Statistically significant difference (p<0.05)
Variables Ferritin
(ng/mL)
Serum
Iron
Conc.
(µg/dL)
Thyroid
stimu-
lating
hormone
(µIU/mL)
Free T3
(pg/mL)
Free T4
(ng/dL)
Serum Iron
Conc. (μg/dL)
r-value 0.425
p-value 0.001*
Thyroid
Stimulating
Hormone
(TSH) (μIU/mL)
r-value -0.342 -0.635
p-value 0.008* <0.001*
Free T3 (pg/
mL)
r-value 0.029 0.284 -0.139
p-value 0.826 0.028* 0.288
Free T4 (ng/
dL)
r-value 0.023 0.060 -0.125 0.104
p-value 0.859 0.647 0.341 0.428
[Table/Fig-4]: Correlations between the serum levels of ferritin, iron, TSH, FT3 and
FT4.
T3: Triiodothyronine, T4: Thyroxine
* Statistically significant difference (p<0.05)
DISCUSSION
The findings of the present study revealed significantly higher serum
levels of TSH and significantly lower FT4 and FT3 among IDA
children and with increasing the severity of IDA in comparison to
the control group. In agreement with our findings, Kammal M and
Abdrabo AA reported significant increase in the serum TSH levels
among patients with IDA with non significant differences between
patients and controls with regard to free T3 and free T4 levels, which
means the presence of subclinical hypothyroidism in such patients
[4]. Gökdeniz E et al., reported the occurrence of subclinical and
primary hypothyroidism among IDA patients [21]. Also, a study
done by Akhter S et al., reported significantly higher TSH levels and
lower FT3 and FT4 among patients with low ferritin levels versus
the control group [6]. A study done by Metwalley KA et al., revealed
significantly higher TSH serum levels in children with IDA when
compared with the control with significantly lower levels of serum
FT3 and FT4 and significantly higher levels of serum TSH among
[Table/Fig-7]: Comparison of the mean haemoglobin levels and thyroid profile
(TSH, FT3 and FT4) among iron deficiency anaemia patients pre- and post-iron
replacement therapy.
TSH: Thyroid Stimulating Hormone, T3: Triiodothyronine, T4: Thyroxine
Hosny MA El-Masry et al., Thyroid Function among Children with Iron Deficiency Anaemia: Pre and Post Iron Replacement Therapy www.jcdr.net
Journal of Clinical and Diagnostic Research. 2018 Jan, Vol-12(1): BC01-BC05
44
children with severe IDA compared to those with mild to moderate
IDA [22]. In disagreement with the present findings, a study done
by Ipek I et al., reported no significant difference between the IDA
group and control group with regard to thyroid profile [7]. These
variations may be due to different geographic distribution, different
demographic characteristics, inclusion criteria and the severity of
anaemia of patients included in the study.
Thyroxine 5-deiodinase activity, which is responsible for peripheral
T4 to T3 conversion is impaired in ID [23]. In the present study,
there were significant increase in the TSH and significant lowering
in the FT3 levels as the severity of anaemia increases with presence
of significant positive correlation between serum iron levels and
FT3. This could explain that apathy, lack of concentration, cognitive
impairment, fatigue, lethargy, decreased physical activity and cold
intolerance among iron deficient paediatric patients especially severe
degree, could be attributed to the associated lower levels of thyroid
hormones (thyroid hypofunction). This indicates that peripheral
enzymatic conversion of T4 to T3 by thyroxine 5-deiodinase is iron
dependent. So, FT3 decreases with decreasing iron serum levels
and with increasing severity of anaemia; although, there was non
significant decrease in the levels of FT4 with the severity of the
anaemia. This indicates that IDA induced thyroid hypo function is
of mild severity.
The findings of the present study revealed the presence of a
significant negative correlation between TSH versus both ferritin
and iron, with non significant correlation between ferritin versus
either FT3 or FT4. In agreement with these findings, Kammal M
and Abdrabo AA, reported a significant inverse correlation between
serum TSH versus both iron and ferritin [4]. Bremner AP et al.,
reported inverse correlation between TSH and iron [24]. Other
studies also reported significant negative correlation between TSH
and ferritin. [16,22,25].
The findings of the present study also revealed significant positive
correlation between FT3 and RBCs count with significant negative
correlations of TSH and haemoglobin, haematocrit % and RBCs,
supporting the association between thyroid hormones and
erythropoiesis. In agreement with these findings, a study done
by Khatiwada S et al., reported the presence of hypothyroidism
among iron deficient children with negative correlation between
TSH and haemoglobin [26]. Another study by Bremner AP et
al., on relationships between thyroid hormones and erythrocyte
parameters, reported significant positive correlation between FT3
and RBC count and they reported significant inverse relationships
between TSH and each of haemoglobin, haematocrit and red cell
counts [24]. On the contrary, Akhter S et al., reported that in iron
deficient patients, haemoglobin levels and serum ferritin had no
significant negative correlation with serum TSH [6].
To the best of our knowledge, no previous studies can be traced in
the literature regarding the cut-off values of some blood indices and
serum iron study parameters in predicting the occurrence of thyroid
hypofunction (high TSH with normal or low FT4). The present study
revealed that thyroid hypofunction can be predicted among children
with IDA when haemoglobin levels 8.3 gm/dL, MCV 58.5 fl, RDW
>17.5%, ferritin 15.2 ng/mL, iron 19.4 μg/dL, TFS 3.63%,
unsaturated iron binding capacity >483 μg/dL and TIBC >486
μg/dL with the highest sensitivity was for ferritin and the highest
specificities were for MCV, RDW and TFS% respectively.
The dosage of elemental iron required to treat IDA in children is 3 mg/
kg/day, up to 60 mg/day for three months [27]. In the present study,
TSH, FT3 and FT4 return to the euthyroid status according to the
reference range, following three months of the oral iron replacement
therapy (6 mg/kg/day divided into two doses). In accordance,
Eftekhari MH et al., determined whether iron supplementation in iron
deficient patients would improve thyroid function and found that iron
supplementation improves thyroid function reporting a significant
increase in FT4 in iron deficient children and adolescents [16].
Gökdeniz E et al., reported subclinical and primary hypothyroidism
among patients with IDA with significant decrease in the TSH and
rising in the FT4 following iron supplementation [21]. The literature
also states that all patients with overt hypothyroidism and subclinical
hypothyroidism with TSH >10 mIU/L should be treated with
hormonal replacement therapy [20], while the mean level of serum
TSH among IDA in the present study was 4.03±1.41 μIU/mL which
did not indicate the need for thyroid hormone replacement therapy.
On the contrary, Tienboon P and Unachak K , found no difference
in FT4, FT3 and TSH levels in children with IDA before and after
iron treatment [28], these difference can be attributed to difference
in the number of cases enrolled, difference in the age and inclusion
criteria.
LIMITATION
The relatively small sample size of the present study, indicates the
need of future large scale studies to confirm the present finding.
Also, the other limitation was the non involvement of children with
other types of anaemia to evaluate the thyroid status, which require
future studies.
CONCLUSION
The findings of the present study revealed the presence of thyroid
hypofunction in the form of subclinical or primary hypothyroidism
according to the severity of anaemia among children suffering from
IDA, which is reversible once iron replacement therapy is started as
early as possible to such patients, without the need to add thyroid
hormone replacement therapy.
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www.jcdr.net Hosny MA El-Masry et al., Thyroid Function among Children with Iron Deficiency Anaemia: Pre and Post Iron Replacement Therapy
Journal of Clinical and Diagnostic Research. 2018 Jan, Vol-12(1): BC01-BC05 55
PARTICULARS OF CONTRIBUTORS:
1. Professor, Department of Paediatrics, Faculty of Medicine, Al Azhar University, Assiut, Egypt.
2. Assistant Professor, Department of Paediatrics, Faculty of Medicine, Al Azhar University, Assiut, Egypt.
3. Lecturer, Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, South Valley University, Qena, Egypt.
4. Assistant Professor, Department of Clinical and Chemical Pathology, Faculty of Medicine, South Valley University, Qena, Egypt.
5. Lecturer, Department of Medical Biochemistry, Faculty of Medicine, Al Azhar University, Assiut branch, Egypt and Faculty Of Medicine-Prince Sattam Bin Abdulaziz
University, Alkharg, Saudi Arabia.
NAME, ADDRESS, E-MAIL ID OF THE CORRESPONDING AUTHOR:
Dr. Mohammed H Hassan,
Lecturer, Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, South Valley University,
P.O. Box No. 83523, Qena, Egypt.
E-mail: mohammedhosnyhassaan@yahoo.com
FINANCIAL OR OTHER COMPETING INTERESTS: None.
Date of Submission: Sep 19, 2017
Date of Peer Review: Nov 16, 2017
Date of Acceptance: Dec 19, 2017
Date of Publishing: Jan 01, 2018
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functions. J Clin Exp Invest. 2010;1:156-60.
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school children with iron deficiency anaemia: relationship to intellectual function.
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metabolic activity. Journal of Restorative Medicine. 2014;3:30-52.
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thyroid function in Nepalese children. Thyroid Research. 2016;9(2):01-07.
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function. Asia Pac J Clin Nutr. 2003;12:198-202.
... In patients with IDA, thyroid function may be affected through several mechanisms; iron deficiency can impair thyroid metabolism [9] that can be attributed to the irondependent haem-containing thyroid peroxidase [TPO] enzyme [10] , which is accountable for the oxidation of iodide into iodine, and its organification into tyrosine residues of thyroglobulin to form Mono-Iodotyrosine [MIT] or Di-Iodotyrosine [DIT] [11] . Furthermore, TPO is a principal for the formation of T3 [by the coupling of one molecule of MIT and one molecule of DIT], and T4 [by the coupling of two DIT molecules] [12] . ...
... Several studies have investigated the association between thyroid function with iron status among school children, with conflicting results [12][13][14][15] . Although iodine nutrition continues to improve worldwide, thyroid dysfunction is still frequently reported in school-age children [13] . ...
... In the study by Khatiwada et al. [13] , 55.5 % of studied iron-deficient anemic primary school children were males and 44.5 % were females. Also, El-Masry et al. [12] reported that, among 60 children, 34 were males [57%] and 26 [43%] were females. The majority of studied children were rural residents [62%], which come to an agreement with Al Ghwass et al. [21] who reported that rural areas were significant risk factors [P = 0.026] for IDA in Egypt. ...
... Based on several investigations, IDA is interconnected with hypothyroidism which significantly increases serum thyroid-stimulating hormone (TSH) levels and decreases serum iron, serum ferritin, free T4 (FT4), transferrin, RBC count, and so on [14][15][16][17][18]. Ferritin is a universal protein that acts as an iron carrier, and serum ferritin level is negatively correlated with serum TSH levels [19,20]. In addition to iron and ferritin, values of total iron-binding capacity (TIBC), FT3, and FT4 have been reported as significantly lower in hypothyroid patients suffering from IDA [21,22]. This lower serum ferritin level is also associated with reducing sex hormones along with TSH, which exaggerates other endocrine dysfunctionalities [23]. ...
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Anemia and thyroid disorders are global health issues that affect all ages but are more apparent in women. In this case, some serological components responsible for iron deficiency anemia (IDA) and thyroid-stimulating hormone (TSH) downregulation in women have been found actively regulated through a complex vitamin D3 mediated mechanism. This research has been investigated the correlation between activated vitamin D3 and the serological components responsible for IDA and dysregulation of TSH in childbearing and non-child-bearing women of different health conditions. Experimental sampling from 482 women suffering from both IDA and TSH dysregulation was taken, aged between 0 and 70 years. Serological parameters, such as iron, total iron�binding capacity, and ferritin, were assessed for IDA profiling, whereas thyroid-stimulating hormone and free thyroxin were for TSH profiling based on the individual’s serum vitamin D3 concentration. The resulting serological data were interpreted using sophisticated computer programming language and algorithms for quantitative biochemical analysis. The study resulted in a significant correlation between FT4 and vitamin D3 (p < 0.0001) for all age groups. TSH also showed strong interactions with the fluctuation of vitamin D3 levels (p < 0.0001), except for the children aged below 10 years (p < 0.063). The iron, TIBC, TSH, and FT4 showed phenomenal regulation with the steroidal-vitamin D3 concentration for congenital patients. Unlike the others, ferritin has a substantial connection with activated Vitamin D3 (p < 0.0064) fluctuation in the serum. To ratify, the concentrations of TSH, FT4, iron, TIBC, and ferritin were found to be significantly interconnected in terms of serum vitamin D3 concentration in women suffering from IDA and TSH downregulation simultaneously. In addition, the BMI condition of the patients can be a major factor in terms of correlating vitamin D3 with the regulatory factors of IDA and thyroid TSH as resulted in this research. To understand the accuracy and efficacy of the serum vitamin D3 in IDA and TSH downregulation, some other inflammatory markers and parathyroid hormone analysis of many samples can be conducted in continuation of this study.
... Based on several investigations, both ID and Anemia are interconnected with hypothyroidism which significantly increases serum TSH levels and decreases serum iron, serum ferritin, Free T4, transferrin, RBC count, and so on [14][15][16][17][18]. Ferritin is a universal protein that acts as an iron carrier, and serum ferritin level is negatively correlated with serum TSH levels [19,20]. In addition to iron and ferritin, Values of TIBC, FT3, and FT4 were significantly lower in hypothyroid patients suffering from IDA [21,22]. This lower serum ferritin level is also associated with reducing sex hormones along with TSH, which exaggerates another endocrine dysfunction [23]. ...
Preprint
Anemia and thyroid disorders are global health issues that affect all ages but are more apparent in women. In this case, some serological components responsible for IDA and TSH disorders in women have been found actively regulated through a complex steroidal-calcitriol mediated pathway. This research has been investigated the correlation between Calcitriol and the serological components responsible for IDA and TSH disorders in childbearing and non-child-bearing women of different health conditions. Experimental sampling from 452 women suffering from both IDA and TSH disorders were taken, aged between 0 and 70 years. Serological parameters, such as iron, total iron-binding capacity and ferritin, were assessed for IDA profiling, whereas thyroid-stimulating hormone and free thyroxin were for TSH profiling based on the individual’s serum calcitriol status. The resulted serological data were interpreted using sophisticated computer programming language and algorithms for quantitative biochemical analysis. The study resulted in a significant correlation between FT4 and Calcitriol (P<0.0001) for all age groups. TSH also showed strong interactions with the fluctuation of calcitriol level (P<0.0001), except for the children aged below 10 years (P<0.063). The iron, TIBC, TSH, and FT4 showed phenomenal regulation with the steroidal-calcitriol concentration for congenital patients. Unlike the others, ferritin has a substantial connection with Calcitriol (P<0.0064) fluctuation in the serum. To ratify, the concentrations of TSH, FT4, iron, TIBC, and ferritin were found to be significantly interconnected in terms of serum calcitriol level in women suffering from IDA and TSH disorders simultaneously. To understand the accuracy and efficacy of the Calcitriol in IDA and TSH disorders, some other inflammatory markers and parathyroid hormone analysis are need in future studies, besides a large number of samples.
Objectives: This study aims to develop coenzyme Q10 nanostructured lipid carriers (NLCs) using tristearin and stearyl alcohol as well as isopropyl palmitate (IPP) as solid and liquid lipid respectively for the dermal delivery system. Methods: The coenzyme Q10 NLCs were optimized using tristearin, and stearyl alcohol in different concentrations and further characterized by dynamic light scattering (DLS) for particle size, polydispersity index (PDI), zeta potential, differential scanning calorimetry (DSC) and X-ray diffractometry for crystallinity behavior, Fourier transform infrared spectroscopy (FT-IR) for drug-lipid interaction, scanning electron microscopy (SEM) for particle shape, viscometer for viscosity, and pH meter for pH value. Furthermore, entrapment efficiency (EE), drug loading (DL), and skin penetration in vivo were also evaluated while molecular docking was conducted to examine the interaction between coenzyme Q10 and the lipids. Results: The coenzyme Q10 NLCs with tristearin-IPP and stearyl alcohol-IPP as lipid matrix had <1,000 nm particle size, <0.3 PDI, less negative than -30 mV zeta potential, about 41% crystallinity index, and about six as the pH value. Moreover, the EE, DL, viscosity, and in vivo skin penetration of the NLCs using tristearin were higher compared to stearyl alcohol, however, the skin penetration depths for both NLCs were not significantly different. Furthermore, the in silico binding energy of coenzyme Q10-tristearin was lower compared to coenzyme Q10-stearyl alcohol. Both of them showed hydrophobic and van der Waals interaction. Conclusions: The NLCs of coenzyme Q10 were formulated successfully using tristearin-IPP and stearyl alcohol-IPP for dermal delivery.
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Objectives National Baseline Health Research 2013 showed that there were 706,757 (0.4%) hyperthyroid patients in Indonesia. Hyperthyroidism is characterized by abnormal thyroid stimulating immunoglobulin (TSI) which causes low TSH and high FT4 levels. Hyperthyroid patients have a decrease of serum iron levels due to acute phase reactions of hyperthyroidism. This study aimed to analyze the correlation between dietary iron intake and serum iron with TSH and FT4 levels in adult hyperthyroid patients. Methods This study was conducted in February–July 2020 at the Clinic of Magelang Health Research and Development Center. Sampling of this cross sectional study was based on inclusion criteria in order to obtain 50 adult hyperthyroid patients. Dietary iron intake was collected with 2 × 24 h dietary recall, serum iron was measured with colorimetric analysis, the levels of TSH and FT4 were measured by ELISA. The collected data were analyzed using Spearman correlation and multivariate linear regression with 95% confidence level. Results Deficiencies of dietary iron intake was found in 20 hyperthyroid patients (40%). Low serum iron levels were found in 10 hyperthyroid patients (20%). Spearman correlation analysis showed that dietary iron intake had a negative correlation with TSH (r=−0.294; p<0.05) but did not correlate with FT4 (r=−0.142; p>0.05), while serum iron didn’t associated with both TSH (r=0.110; p>0.05) and FT4 (r=0.142; p>0.05). Furthermore, regression analysis showed that dietary iron intake, serum iron, phytate, and thyrozol intake correlate with TSH levels (R square=0.193; p<0.05) and FT4 levels (R square=0.341; p<0.05), but there were no independent association between dietary iron intake and serum iron with TSH and FT4 levels (p>0.05). Conclusions Intake and serum of iron didn’t correlate with TSH and FT4 levels in adult hyperthyroid patients.
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Background and Aim Thyroid diseases are among the most common endocrine disorders. Animal and human experiences indicate that iron deficiency disrupts thyroid metabolism. On the other hand, iron therapy can improve thyroid function and even decrease the dose of levothyroxine. Methods and Materials In this randomized clinical trial, we selected 94 women with hypothyroidism by simple random sampling method and divided them into two equal groups by simple block sampling. At the beginning of the study, we measured and recorded T4, TSH, T3, and iron profiles (Serum iron, total iron-binding capacity, ferritin, Hemoglobin) in all patients. Then, the patients in the intervention group were treated with levothyroxine plus 100 mg oral iron daily for 8 weeks, and the patients in the control group were treated with levothyroxine only. After two months, we measured their T4, TSH, T3 levels and iron profiles in both groups again. Ethical Considerations The Research Ethics Committee of Arak University of Medical Sciences approved this study (Research Ethics Code: 1396154). Also, the study has been registered at the Iranian Registry of Clinical Trials (Code: IRCT 20151114025031). Results After 2 months, the TSH Mean±SD serum levels were found as 2.2±1.0 mIU/L and 2.9±1.1 mIU/L for the intervention and control group, respectively (P=0.04). Also, the serum Mean±SD level of T4 and T3 were found as 9.3±1.48 mcg/dL vs. 8.2±0.9 mcg/dL (P=0.01), and 1.6±0.3 ng/mL vs. 1.1±0.3 ng/mL (P=0.01), for two different groups, respectively. Conclusion Concurrent administration of iron supplementation with the usual dose of levothyroxine in patients with hypothyroidism decreases THS level and improves laboratory parameters and response to treatment.
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The thyroid produces and secretes adequate amounts of hormones that regulate various physiological processes, including growth, development, metabolism, and reproductive function. The production and metabolism of thyroid hormones are dependent on micronutrients such as iodine, selenium, zinc and iron. Iodine is essential for the proper synthesis of thyroid hormones. The risk of iodine deficiency is high in places where the food consumed comes from iodine-deficient sources. To avoid complications, various government strategies have been developed to enrich food with this element. Selenium is incorporated in the deiodinases, which are enzymes that also play an essential role in the metabolism of thyroid hormones, in addition to contributing to the antioxidant defense in the thyroid. Zinc participates in the process of deiodination, in addition to being necessary for the T3 receptor to adopt its biologically active confirmation. Iron is found in hemeproteins, including thyroid peroxidase (TPO), which participates in the first two stages of thyroid hormone biosynthesis. Deficiencies of these elements can impair thyroid function. In general, the influence of micronutrients on thyroid function reveals the need for more research to increase scientific knowledge so that preventive and therapeutic measures can be taken regarding thyroid dysfunctions, to maintain a healthy thyroid.
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Background Deficiencies of iodine and iron may have adverse effect on thyroid function. This study was undertaken to investigate the association between iron status and thyroid function in Nepalese children living in hilly regions. Methods A cross-sectional study was conducted among 227 school children aged 6–12 years living in hilly regions of eastern Nepal. Urine and blood samples were analyzed for urinary iodine concentration, free thyroxine, free triiodothyronine, thyroid stimulating hormone, hemoglobin, serum iron and total iron binding capacity, and percentage transferrin saturation was calculated. Results The cohort comprised euthyroid (80.6 %, n = 183), overt hypothyroid (1.3 %, n = 3), subclinical hypothyroid (16.3 %, n = 37) and subclinical hyperthyroid (1.8 %, n = 4) children respectively. About 35.2 % (n = 80) children were anemic, 43.6 % (n = 99) were iron deficient and 19.8 % (n = 45) had urinary iodine excretion < 100 μg/L. Hypothyroidism (overt and subclinical) was common in anemic and iron deficient children. The relative risk of having hypothyroidism (overt and subclinical) in anemic and iron deficient children was 5.513 (95 % CI: 2.844−10.685, p < 0.001) and 1.939 (95 % CI: 1.091-3.449, p = 0.023) respectively as compared to non-anemic and iron sufficient children. Thyroid stimulating hormone had significant negative correlation with hemoglobin (r = −0.337, p < 0.001) and transferrin saturation (r = −0.204, p = 0.002). Conclusions Thyroid dysfunction, iron deficiency and anemia are common among Nepalese children. In this cohort, anemic and iron deficient children had poor thyroid function.
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Iron deficiency is the most common nutritional disorder worldwide and accounts for approximately one-half of anemia cases. The diagnosis of iron deficiency anemia is confirmed by the findings of low iron stores and a hemoglobin level two standard deviations below normal. Women should be screened during pregnancy, and children screened at one year of age. Supplemental iron may be given initially, followed by further workup if the patient is not responsive to therapy. Men and postmenopausal women should not be screened, but should be evaluated with gastrointestinal endoscopy if diagnosed with iron deficiency anemia. The underlying cause should be treated, and oral iron therapy can be initiated to replenish iron stores. Parenteral therapy may be used in patients who cannot tolerate or absorb oral preparations.
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