1

Dissertation on

“PROFILE AND OUTCOME OF NUTRITIONAL

ANEMIA IN CHILDREN ATTENDING THE
PEDIATRIC DEPARTMENT OF A TERTIARY
CARE HOSPITAL IN CHENNAI”

Submitted to
THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY
in partial fulfillment of the requirement
for the award of degree of

M.D., BRANCH – VII

PEDIATRIC MEDICINE

ESIC MEDICAL COLLEGE & PGIMSR

K. K. NAGAR
CHENNAI

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

CHENNAI, TAMILNADU

APRIL 2015
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CERTIFICATE

Certified that this dissertation entitled “PROFILE AND

OUTCOME OF NUTRITIONAL ANEMIA IN CHILDREN

ATTENDING THE PEDIATRIC DEPARTMENT OF A

TERTIARY CARE HOSPITAL IN CHENNAI” is a bonafide work

done by Dr.A.T.INDHUMATHI, Post graduate, ESIC Medical College

& PGIMSR, K.K. Nagar, Chennai, during the academic year 2013-2015

Prof. Dr. Sowmya Sampath, M.D, DNB Prof. Dr. Sowmya Sampath, M.D, DNB
Professor and Head, Professor and Head, Guide
Department of Pediatrics, Department of Pediatrics,
ESIC Medical College & PGIMSR,
ESIC Medical College & PGIMSR,
K. K. Nagar,
Chennai K. K. Nagar,
Chennai

Prof. Dr. Srikumari Damodaram, MS, MCh

The Dean,
ESIC Medical College & PGIMSR
K. K. Nagar,
Chennai
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DECLARATION

I solemnly declare that the dissertation entitled “PROFILE AND

OUTCOME OF NUTRITIONAL ANEMIA IN CHILDREN

ATTENDING THE PEDIATRIC DEPARTMENT OF A

TERTIARY CARE HOSPITAL IN CHENNAI” is done by me at

ESIC Medical College & PGIMSR, Chennai – 78 during 2013 to 2015

under the guidance and supervision of Prof.Dr.SOWMYA SAMPATH,

M.D., DNB., to be submitted to The Tamilnadu Dr.M.G.R. Medical

University towards the partial fulfillment of requirements for the award

of M.D. DEGREE IN PEDIATRIC MEDICINE –BRANCH VII.

Place: Chennai
Date: (Dr. INDHUMATHI.A.T.)
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ACKNOWLEDGEMENT

I wish to thank, first and foremost, the Lord Almighty for helping
me to complete the dissertation successfully. I would like to thank all the
children and their parents who willingly participated in this study and
sincerely came for follow up when called. This study would have been
impossible without them.

I would like to thank, Prof. Dr. Srikumari Damodaram, our

Dean, for her support to post graduates for allowing us to conduct the
study in an uninterrupted manner in our hospital.

I am indebted to Prof. Dr. R. Kulandai Kasthuri, our former

Head of Department and guide for her motherly support and guidance.

It gives me great pleasure in acknowledging the support and help

of my Professor and guide Prof. Dr. Sowmya Sampath. Thank you
madam, for the long hours spent correcting this dissertation, amidst your
aches and pains. I sincerely thank you madam for all the support we have
received.

I would like to thank,

Prof. Dr. S. Shobhana, Associate professor, for her extra ordinary
support in writing this dissertation in a fluent and coherent manner.

Prof. Dr. T. L. Ratna Kumari, Associate professor, for her advice

and positive inputs related to this study.
 5

Prof. Dr. V. Rajalakshmi , Prof. Dr. Thuthi Mohanan, for

helping me when I approached them for the acquisition of investigations
and reports, in an uninterrupted manner.

Dr. Aruna Bholenath Patil, statistician, for her excellent and

crystal clear statistical results. Thank you madam for enlightening me on
the beauty of statistics.

Dr. Sridharan (The Iron Man), Dr. Suresh David (support),

Dr.Kumar (Journal selection and proof reading), Dr. Sathish (brotherly
moral support), Dr. Sunitha (friend and philosopher), Dr. Mohan
Kumar (clues for the mystery unknown), Dr. Shantha Kumari and
Dr.Prasantha Kumar (encouragement).

I share the credit of my work with my fellow post graduates and

the staff nurses, who helped in sampling. I owe my deepest gratitude to
Prof. Dr. Nedunchezhian, who has been an inspiring teacher from my
DCH days, for his continuing support and guidance academically.

Behind every successful woman is a man. This thesis would have

remained a dream had it not been for my husband Dr.S.Sridhar for his
unending companionship in all my endeavors. I also thank my family for
the love and support.
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CONTENTS

SL.NO. TITLE PAGE NO.

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 40

3. STUDY JUSTIFICATION 52

4. AIMS AND OBJECTIVES 53

5. MATERIAL AND METHODS 54

6. STATISITICAL ANALYSIS 59

7. RESULTS 60

8. DISCUSSION 96

9. CONCLUSION 103

REFERENCES

ANNEXURES
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ABBREVIATIONS

ANOVA Analysis of variance

BMI Body mass index

CRP C-reactive protein

DALY Disability Adjusted Life Years

DMT-1 Divalent metal transporter-1

DNA Deoxy Ribonucleic acid

ESR Erythrocyte sedimentation rate

EDTA Ethyelene diamine tetra acetic acid

ESI Employees state insurance

Hb Hemoglobin

Hct Hematocrit

IDA Iron deficiency anemia

I-PMC Iron poly maltose complex

LBW Low birth weight

MCV Mean corpuscular volume

MCH Mean corpuscular hemoglobin

MCHC Mean corpuscular hemoglobin concentration

MHA Microcytic hypochromic anemia

NFHS National Family Health Survey

NHA Normocytic hypochromic anemia

NNA Normocytic normochromic anemia

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N Number

PCV Packed cell volume

RBC Red blood corpuscle

RE Reticulo-endothelial system

RDW Red cell distribution width

SF Serum ferritin

SD Standard deviation

TIBC Total iron binding capacity

UIBC Unsaturated iron binding capacity

WHO World Health Organization

WBC White blood corpuscle

M Male

F Female
 ABSTRACT

AIM: To study the profileof nutritional anemia in children and to determine the

treatment outcome of iron deficiency anemia

METHODS: A total of 150 children with confirmed anemia were enrolled in this

study. After a targeted history and clinical examination, hematological

investigations were done. Children with microcytic hypochromic anemia were

treated with oral iron and followed up after 1 and 3 months for improvement.

RESULTS: In the study population, 55 children were found to have microcytic

hypochromic, 15 children had normocytic hypochromic and 80 children had

normocytic normochromic anemia. Among the microcytic hypochromic group, the

mean hemoglobin was found to be 8.22 ± 1.27 g/dL. Symptom analysis revealed

54.5% of children with iron deficiency anemia had lethargy and 34% had

irritability. Pica was seen in 47.3% of children with microcytic hypochromic

anemia. Hemoglobin levels correlated well with red cell indices, but it was found

that 52.7% of children had normal serum ferritin levels. After treatment, it was

found that the mean hemoglobin increased from 8.25 ± 1.30g/dLto 9.17 ±

1.36g/dLafter one month and after three months, there was a further increase z

10.39 ± 1.36g/dL.
CONCLUSION: In children with iron deficiency anemia, normal or high ferritin

level should not distract the physician away from the diagnosis as co-existing

infection and inflammation may confound the picture. In cases of normocytic,

normochromic anemia, S. ferritin levels can mask a latent iron deficiency.Hence, a

therapeutic trial of oral iron is more cost effective.

KEYWORDS: Children, Iron deficiency anemia, Red cell indices, Iron profile,

Treatment outcome.
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INTRODUCTION

1.1. History of iron deficiency:

Iron deficiency, described in various texts since ancient times, is

‘probably the most frequent nutritional deficiency in the world’. Globally

about 1.62 billion individuals are said to be suffering from iron deficiency

anemia.1 Around 1500 B.C, Papyrus Ebers, which is considered to be the

oldest manual of therapeutics, has described a similar disease condition

characterized by pallor, dyspnea, and edema.2

In 1713, Lemery and Geoffroy, and in 1747, Menghini found

residual particles which were attracted to lodestone after burning blood to

ash and thus presumed those particle to be made up of iron. The German

biochemist Felix Hoppe-Seyler (1825–1895), using absorption

spectrometry showed that hemoglobin is made up of a complex of

haematin and protein. Stokes (1819–1903), a professor of mathematics at

the University of Cambridge, showed that hemoglobin exists as two

forms and demonstrated the changes between them in response to oxygen

administration.

Bunge (1902, Basle) was the first to suggest the fact that iron

deficiency caused hypochromic anemia. He also showed that iron was

found in higher concentrations in the liver and kidneys of newborn

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infants than older infants, children or adults. He also stated that iron

content in human milk was very low and the iron derived from

hemoglobin in meat was poorly absorbed. This fact was very much in

contrast to today’s evidence which suggests that haem iron is rapidly

absorbed from the gastrointestinal tract. He was the first to recognize that

a high concentration of iron was present in egg yolk, spinach, apples,

lentils and beef. Koilonychia, a specific feature of iron deficiency also

represented in the ancient literature as ‘Lydney hand’ was described in

the twentieth-century by Kaznelson (1931).

In the middle of the 16th century, European physicians had treated

a disease condition known as chlorosis or "green sickness". This

condition had been treated with iron salts and other remedies (including,

oddly enough, phlebotomy) in France, by the middle of the 17th century.

Not long thereafter, Sydenham had also recommended iron as a specific

remedy for chlorosis.3

In 1832, pills containing 1.39 g of ferrous sulphate and 0.1 g of

potassium carbonate were widely recommended for chlorosis and other

conditions. These pills were introduced by Blaud. The original pills

contained 64 mg of iron. Later on, arsenic was often included to these

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pills as many physicians thought iron combined with arsenic was more

effective. This trend continued even into the 1930s.

Finally, the study of blood cell morphology was made possible by

the pioneering work of Paul Ehrlich (1854–1915) who developed aniline

dyes to stain blood films and lead to the birth of modern hematology.

Only after the 1932 studies by Heath, Strauss, and Castle that it was

shown that the response of anemia to iron was stoichometrically related

to the amount of iron given and that chlorosis was, indeed, iron

deficiency.

1.2. Prevalence:

Iron deficiency is the most widespread nutritional disorder in the

world. Anemia is the most common problem among micronutrients

deficiency. Anemia affects health, education, economy and thereby,

productivity of the entire nation. Thus, anemia constitutes a public health

epidemic. The numbers are staggering. Over 30% of the world's

population is anemic, mainly due to iron deficiency. This figure is

frequently exacerbated by malaria and worm infections in developing

countries.
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Impact of anemia in South East Asia:

South East Asia has the largest number of anemic persons,

including children contributing to 12,500,000 Disability Adjusted Life-

Years (DALYs) and 324,000 deaths in this region, which is the highest in

the world. More than 66% of the children in this region are anemic. In

children aged less than two years, the prevalence of anemia may exceed

90%.4

Magnitude of Anemia in Indian Children:

Fig.1 Comparison of anemia among 6 – 35 months children–NFHS 2

and NFHS 3
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Anemia has been a big public health problem in India. The

prevalence of anemia among children less than five years of age has been

shown to be around 70% as per the data collected by National Family

Health Survey (NFHS) III, with Bihar topping the list. The prevalence of

anemia increases to 79% among children aged less than three years, with

the highest prevalence among six to twenty-three months age group. This

value, when compared to NFHS II survey done six years prior to the

NFHS III survey, was five percent more. However, the prevalence of

severe anemia had slightly reduced in the same period.5

Iron deficiency affects the activity of numerous enzymes adversely.

Infants, whose organs are still developing, including the brain, are

affected significantly by anemia resulting in growth retardation and

impairment of intellectual development. In these modern times where we

strive for millennium development Goal 4, this silent morbidity is

completely unacceptable as children are denied of their right to full

mental and emotional development, even before they reach a classroom.

At the same time, iron deficiency anemia can usually be prevented

easily at a very low cost. The cost-benefit ratio of implementing

preventive programs for iron deficiency is recognized as one of the

highest in the realm of public health.

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1.3. Nutritional anemia in children:

The term ‘nutritional anemia’ includes all pathological conditions

characterized by low blood hemoglobin concentration, which may be due

to a deficiency in one or several nutrients. Iron, folic acid and vitamin B12

are the main nutrients required for the synthesis of hemoglobin. By far,

the first cause of nutritional anemia worldwide is iron deficiency. Folic

acid deficiency is less common. Rarer among the main nutrient

deficiencies is Vitamin B12 deficiency. Also folic acid deficiency is often

observed with iron deficiency.4

1.4. Iron deficiency:

Iron deficiency is defined as a condition characterized by signs of

compromise in supply of iron to tissues including the erythrocyte, as there

are no mobilizable iron stores. Iron deficiency is usually the result of

inadequate bioavailable dietary iron, increased iron requirement during

rapid growth, and increased blood loss for any reason.6

Iron deficiency anemia:

Anemia, when caused by severe iron deficiency is termed as iron

deficiency anemia (IDA) and represents a very late stage of iron

deficiency. Iron deficiency anemia is commonly associated with

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decreased physical capacity, reduced immunity and cognitive

impairment. Severe iron deficiency anemia also affects the capacity to

maintain body temperature and is also life-threatening.

Diag. 1 Stages of depletion and status of compartments of iron3

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Hemoglobin levels:

World Health Organization defined criteria, using hemoglobin

levels for anemia classification7

Hemoglobin ( g/dL)

Age Groups No anemia Mild moderate severe

6 -59 months of 11 10 – 10.9 7 – 9.9 <7

age

5 – 11 years of age 11.5 11 – 11.4 8 – 10.9 <8

12-14 years of age 12 11 – 11.9 8 – 10.9 <8

Table - 1 : Hemoglobin values

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Causes of iron deficiency anemia:

Decreased intake or 1. Insufficient dietary iron

absorption
2. Too early introduction or delayed
introduction of complementary feeding
without supplementation of iron

3. Poor bioavailability due to increased

absorption inhibitors and decreased
absorption enhancers

Increased requirement Rapid growth phase in infancy and early

childhood

Increased blood loss 1. Infections (hookworm,trichuris trichura,

plasmodium, helicobacter pylori)

2. Gastrointestinal blood loss (Meckels

diverticulum, peptic ulcer, esophageal
varices, hemorrhoids, hereditary
telangiectasia, ulcerative colitis,
diverticulosis, angiodysplasia)

3. Other causes (Hemoglobinuria,

Widespread bleeding disorders)

4. Malabsorption (Gluten-induced
enteropathy, gastrectomy, atrophic
gastritis, chronic inflammation )

5. Bovine milk allergy

Table 2 Causes of iron deficiency anemia8

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Pathophysiology of anemia in children:

At birth, hemoglobin concentrations are normally higher than at

any other time of life. This occurs as a result of the adaptation of the fetus

to the hypoxic environment of the uterus. The neonatal reserves of

storage iron are also relatively generous.

From two months of age, the hemoglobin concentration starts

declining from a mean of 17.0 g/dL at birth and reaches a low level of

11.0 g/dL. This occurs due to breakdown of hemoglobin in order to meet

the iron needs. This decrease in hemoglobin concentration is known as

‘early anemia of infancy’. This condition is usually unresponsive to iron

treatment and hence, distinguished from the ‘late anemia of infancy’.

Thus, in a term infant, the total body iron between birth and four months

of age is almost not changed and there is only a modest need for

exogenous iron during this period.

After about four months of age, the period of continued rapid

growth begins and a gradual shift to marginal iron reserves occurs.

Between four and twelve months, blood volume is rapidly expanding and

a large amount of iron is needed in order to maintain a near constant

mean hemoglobin concentration of 12.5 g/dL. The children are highly

vulnerable to iron deficiency during this period.

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By four to six months of age, dietary iron absorption becomes

important as iron stores are usually depleted. Low birth weight babies

have less iron stores and hence, they need extra iron as well as iron at an

early age from the diet source.

During the first 15 years of life, an average of 0.8 mg of iron needs

to be absorbed each day. In addition, a small amount is also needed to

balance normal losses of iron caused by shedding of cells. Therefore,

approximately 1 mg of iron is needed daily in order to maintain positive

iron balance in childhood. This can be achieved by ensuring a dietary

intake of 8-10 mg of iron daily, since only 10% of dietary iron usually is

absorbed.

When growth is most rapid, approximately 1 mg/L of iron in

bovine and breast milk makes it difficult to maintain the body iron.

Breast-fed infants have an advantage because they absorb iron 2-3 times

more efficiently than infants fed with bovine milk.

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Dietary iron absorption:

Iron status

Haem iron in the diet

Fish, meat, poultry.

Constitutes less than 10% of the total

Haem iron absorption
intake in developing countries.

However, bioavailability is high.

Calcium content in meal (e.g. milk,

cheese)

Method of food preparation

(temperature, time)

o Iron status

o Dietary non haem iron

Cereals , pulses, vegetables, tubers

Non-haem iron
absorption
Bioavailability is low

o Contamination iron

Soil, dust, water, iron pots

Table 3 Dietary iron absorption

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Enhancers and inhibitors of iron absorption:

Ascorbic acid present in fruits, fruit juices,

Enhancing vegetables
factors
Fish, meat, chicken

Phytates and other inositol phosphates

- rice (unpolished ), oats

- breakfast cereals,

- bread

Calcium (e.g. milk, cheese)

Inhibiting factors Iron binding phenolic compounds

- tea, coffee, cocoa, certain spices,

- certain vegetables

- most red wines

Nuts, peas, soybeans

Table 4 Enhancing and inhibiting factors9

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Diag. 2 Adverse effects of anemia

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Sequence of events in iron deficiency anemia

Depletion of iron stores:

This is the first event which occurs in a state of negative iron

balance. Iron stores are depleted in order to enhance hemoglobin

production. As a result, iron absorption is increased even when serum

iron level is still normal and even before anemia develops. During this

stage, the serum ferritin would have already fallen.

Iron-deficient erythropoiesis:

When the serum ferritin drops below 15ng/L, the serum transferrin

saturation starts to fall to less than 15%. This occurs due to a fall in serum

iron and a rise in transferrin concentration. At this stage, iron-deficient

erythropoiesis occurs characterized by increasing concentrations of red

cell protoporphyrin and serum transferrin receptors. But, the hemoglobin,

mean corpuscular volume (MCV) and mean corpuscular hemoglobin

(MCH) may still remain within the reference range, although the values

may rise significantly after iron therapy is given.

Iron deficiency anemia:

Frank iron deficiency anemia develops when the negative balance

continues. The red cells at this stage become obviously microcytic,

hypochromic and poikilocytosis becomes more marked. The MCV and

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MCH are also reduced. Target cells may be present in the peripheral

smear. The reticulocyte count is also low for the degree of anemia. The

serum iron falls and serum TIBC rises. As a result, the percentage

saturation of the TIBC is usually less than 10%. This may be

accompanied frequently by increase in platelet numbers.

Iron metabolism:

Iron is present in most living organisms and is critical for normal

functioning by being part of electron transport in cytochromes and

cytochrome oxygenase. Krebs cycle, in which heme containing iron acts

as a coenzyme, is the active site of electron transport. Heme is also the

site of oxygen uptake by myoglobin and hemoglobin. Circulating red

cells in the human body has the highest concentration of iron, containing

about 1 mg of iron per ml of packed cells. The storage form of iron is

either ferritin or hemosiderin.3

At the same time, antioxidant mechanisms are needed by the body

to protect against the damage by free iron in chemical reactions that

generate free radicals such as singlet O2 or OH.

In a person with normal iron status, approximately 1 mg to 2 mg of

iron (10% of the iron in a normal diet) is absorbed each day from the

duodenal lumen into the intestinal mucosal cell (enterocyte), usually in

the ferrous (Fe2+) state. After iron is absorbed from the diet, it is either
 28

transported by ferroportin into plasma or retained in the enterocytes as

ferritin and shed later.

The main regulating mechanism of iron content in the body is iron

absorption. The transport of iron from enterocyte to the plasma is tightly

regulated by a peptide known as hepcidin. Hepcidin is produced in the

liver and up regulated in states of inflammation. It is this process of

intestinal iron absorption that serves as the primary mechanism of iron

homeostasis.

When iron deficiency is present, hepcidin is decreased, thus

fostering enhanced absorption of iron. In contrast, during states of iron

excess or inflammation, hepcidin levels are usually increased, thereby

blocking ferroportin and limiting its ability to mobilize iron into the

plasma from enterocytes and storage sites.

Iron circulates in the plasma bound to transferrin, the iron transport

protein until it interacts with specific transferrin receptors present on the

surface of marrow erythroid cells. The iron-transferrin complex is

internalized after the interaction via clathrin-coated pits. Once

internalized, the complex is then transported to an acidic endosome,

where low pH causes the iron to be released and made available for heme

synthesis.
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Diag.3 Iron absorption in the intestine

1. Iron is absorbed in the ferrous sate from the duodenal lumen into

the enterocyte via divalent metal transporter 1 (DMT 1)

2. Iron is retained as ferritin and subsequently sloughed

3. Iron is transported across the basolateral membrane into the plasma

via ferroportin

4. Iron is bound to transferrin and transported to marrow iron stores

5. During states of iron excess or inflammation, hepcidin increase and

block ferroportin limiting the ability to mobilize iron into plasma

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Iron is then incorporated into hemoglobin within the erythroid cell

and subsequently enters the circulation. This form of iron will not become

available for reutilization until the red cell dies. At the same time, excess

iron is bound to a storage protein, apoferritin and forms ferritin.

Hemosiderin is a protein aggregate formed within in the RE system when

excess ferritin accumulates. Iron present in the hemosiderin is less readily

available.

An average red cell life span is 120 days in a normal individual,

which means about 0.8 to 1% red cells turnover each day. Once the red

cell reaches the end of its life span, it undergoes phagocytosis after being

recognized as senescent by reticulo-endothelial cells. Once the

hemoglobin from the ingested red cell is broken down, the iron is shuttled

back to the surface of the RE cell and presented to circulating transferrin.

1.5. Megaloblastic anemia:

Megaloblastic anemia is the most common manifestation of

deficiency of vitamin B12 and folic acid. Vitamin B12 and folic acid

deficiency primarily results in decreased capacity of DNA synthesis and

manifests as reduction in number as well as enlargement of all rapidly

proliferating cells of the body, including marrow cells. The commonest

age is 3 to 8 months with maximum number of cases in 9 to 12 months.10

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Animal products such as eggs, meat, milk and other dairy products

are the main source of cobalamins. Intrinsic factor, a protein present in

the gastric juice, is required for absorption. Once bound to intrinsic

factor, the cobalamins are subsequently absorbed in the ileum and are

taken up from circulation and stored in the liver. They are then released

into circulation as and when needed. Vitamin B12 acts as a coenzyme in

two important metabolic functions which are vital to DNA synthesis and

normal cell growth. The two vital chemical reactions are concerned with

methionine synthesis and formation of succinyl CoA from methylmalonyl

CoA.

The most common cause of vitamin B12 deficiency is defective

secretion of intrinsic factor which results in inadequate vitamin B12

absorption. This condition is known as pernicious anemia and is most

common among people aged over 50 years. Other causes are

malabsorption due to surgical resections, gastrectomy and bacterial or

inflammatory diseases affecting the small intestine. There has been no

known incidence of clinical problems caused by elevation in vitamin B12

levels.

Folic acid is present in foods such as dark leafy vegetables, milk,

egg, yeast, beans and citrus fruits. It is also absorbed in the small intestine

and stored in the liver. Folate deficiency can be caused by decreased

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dietary intake, malabsorption or excessive utilization as in pregnancy,

liver-damaging diseases. Folate deficiency is characterized by

megaloblastic anemia and ultimately, severe neurological problems14.

Some peculiar features to Megaloblastic anemia include

hyperpigmentation of knuckles, terminal phalanges and mild enlargement

of liver and spleen. Other less common manifestations include

neurodevelopmental effects and abnormal movements.

1.6. Clinical features:

Iron deficiency anemia is asymptomatic in most cases. Pallor is the

most common manifestation and is identified in children over palmar

creases, palms, nail beds or conjunctivae. Pallor is associated with fall in

hemoglobin levels to 7 to 8 g/dL. When the hemoglobin decreases

further, child displays mild irritability.8

When hemoglobin decreases further to 5 g/dL, the children

complain of headache, fatigue, dizziness, shortness of breath, palpitation,

chest pain and manifest irritability, lethargy and anorexia. Hemic

murmurs may be heard on auscultation. This stage is associated with

significant physical, psychological and social consequences. Tachycardia

and high output cardiac failure occurs, when hemoglobin continues to

fall. .
 33

Other features include pica, pagophagia (the desire to eat ice cubes)

and plumbism, poor school performance, leg cramps, reduced resistance

to infections. Children who are iron deficient suffer from growth

impairment and tend to be shorter than non-iron deficient children. In

early iron deficiency, even before iron deficiency anemia develops, the

most important non hematological side effect is intellectual impairment,

cognitive function and motor function.11These changes are not reversible

with iron therapy and hence prevention is better than cure. Physical

examination may reveal pallor, spoon shaped nails (koilonychia),

leuconychia, platynychia, splenomegaly in severe and persistent untreated

anemia.

1.7. Investigations

Investigations for iron deficiency anemia includes complete blood

count, iron profile, peripheral smear and stool for occult blood and serum

B12 and folic acid to look for other nutritional anemias.

Complete blood count:

Most clinical laboratories now employ automated machines to

perform complete blood count to estimate hemoglobin, hematocrit

(packed cell volume), and red blood cell count. MCV, MCH and MCHC

are calculated values from hemoglobin, hematocrit, and red blood cell

count.
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Red cell indices are used in the morphologic classification of

anemias based on the size of the red blood cell as being normocytic

(normal MCV), macrocytic (increased MCV), or microcytic (decreased

MCV). . Red cell indices were first introduced by Wintrobe in 1929.

MCV = Volume of packed cells / 1000 mL of blood fL or m3

Red blood cell count (millions / mL)

MCH = Hemoglobin in g / 1000 mL of blood pg/cell

RBC count (millions /mL )

MCHC = Hemoglobin in g / 100 mL of blood X 100 g/dL or %

Volume of packed cells /100 mL of blood

MCV defines the size of the red blood cells and is expressed as
15
femtoliters (10 ; fL) or as cubic microns ( m3). MCH quantifies the

amount of hemoglobin per red blood cell. MCHC indicates the amount of

hemoglobin per unit volume. In contrast to MCH, MCHC correlates the

hemoglobin content with the volume of the cell. It is expressed as g/dl of

red blood cells or as a percentage value.

Microcytic anemias were also often described as being

hypochromic based on peripheral smear examination and MCHC when

this value was determined manually.

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Red cell distribution width (RDW), otherwise known as red cell

morphology index represents the coefficient of variation in the volume

distribution (size) of the red blood cell and is expressed as a percentage,

thereby quantifies the variation in the size of red cells (anisocytosis).

Spurious results associated with Automated Cell Counters.

In the case of red cell agglutination, larger clumps are not counted

as red blood cells at all and doublet erythrocytes are counted as

one. This leads to a "decrease" in red cell count and a falsely

elevated MCV. Pre-warming the sample eliminates these spurious

values.

In hyperglycemic conditions, red cells are swollen as they are

transiently hypertonic in relation to the isotonic diluting fluid

resulting in elevated MCV. Providing some time to allow for

equilibration after dilution can avoid this spurious result.

Conditions such as hyperlipidemia, hyperbilirubinemia, a very high

white blood cell count and high serum protein can interfere with

absorption characteristics of hemoglobin. Since hemoglobin is

quantified based on its absorption characteristics, this can result in

falsely elevated hemoglobin values.

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Since MCH and MCHC are calculated and are not directly

measured, these indices also become abnormal when the values of

hemoglobin, red cell count, and MCV are affected.

The reference values of red cell indices and iron profile are given

in Table 2 shown below:8

Parameters Reference range

6m to 2 years: 3.7 to 5.3 million/cu.mm

RBC count 2 to 6 years: 4.9 to 5.3 million/cu.mm

6 to 12 years: 4 to 5.2 million/cu.mm

1 to 23 months: 32 -42 %

PCV 2 to 9 years : 33 -43%

10 to 17 years : 36 -45%

1 to 23 months: 72 to 88 fL

MCV 2 to 9 years : 76 to 90 fL

10 to 17 years : 78 to 95 fL

1 to 23 months: 24 – 30 pg

MCH 2 to 9 years : 25 – 31 pg

10 to 17 years : 26 – 32 pg

MCHC 32.0 – 36.0 %

RDW 10.0 – 15.0 %

Platelet count 154000 – 400000 cells/cu.mm

Reticulocyte count <1%

 37

Serum Iron 50.00 – 120.00 µg/dL

TIBC 250.00 – 400 µmol/L

Transferrin
15 - 55%
saturation

Serum Transferrin 208 – 400 mg/dL

Serum Ferritin 6.0 – 67.0 µg/L

Serum B12 140.00 – 700.00 pg/mL

Serum Folic acid 1.8-9.0 ng/mL

ESR 5-15 mm/Hr

CRP 0.01-2.80mg/L

Table 5 Red cell indices and iron profile

Erythrocyte sedimentation rate

The rate at which red blood cells sediment in a period of one hour

is called erythrocyte sedimentation rate. ESR is a non-specific indicator

of inflammation. The high proportion of fibrinogen present during an

inflammatory process results in red blood cells sticking to each other.

This results in rouleaux formation and red blood cells settle faster.
 38

Peripheral smear examination:

A blood smear is used to categorize the type of anemia based on

the size, shape and color of RBC (indicators of hemoglobin content). It

also helps in identifying conditions that affect one or more type of blood

cells. Examples include anemia, myeloproliferative disorders, leukemia,

and parasitic infections. If the result from an automated cell count or a

differential count indicates the presence of abnormal WBC, RBC and/or

platelets, it has to be verified and confirmed by a good peripheral smear

examination, making it the most important investigation of hematology.

The reticulocyte count is calculated manually and it is corrected for

appropriate hemoglobin levels.

Diagnostic methods for investigating iron metabolism12

Serum iron and iron binding capacity:

The serum iron level indicates the amount of circulating iron bound

to transferrin. The iron supply to the tissues is measured by serum iron

and the saturation of the total iron-binding capacity of transferrin (TIBC).

The serum iron shows a diurnal rhythm in normal subjects, the values

being lower in the morning than in the evening. The TIBC is an indirect

measure of the circulating transferrin. Serum transferrin is determined by

adding Serum iron with TIBC. Transferrin saturation levels below 20%
 39

are associated iron deficiency states. Transferrin saturation is obtained by

the following formula:

Serum iron x 100

Serum transferrin

Serum Ferritin:

Serum ferritin is a non-invasive measure of iron stores and the

most convenient laboratory test to estimate iron stores as the levels

correlate with total body iron stores. In neonates, over the first 2 months

of life, the fetal hemoglobin is broken down and cord blood concentration

(median approximately 100µg/L) rises further. Thereafter, throughout

childhood and adolescence, serum ferritin levels fall to low levels

(median 20–30 µg/L). Until the onset of puberty, there is no gender

difference in ferritin values. Once puberty is attained, serum ferritin

levels rise in males. The normal serum ferritin value varies according to

the age and gender of the individual. In children less than 5 years, serum

ferritin levels less than 12 µg/L and in children more than 5 years, levels

less than 15µg/L is considered as depleted iron stores.13

Serum ferritin values falls to <15 µg/L as iron stores are depleted.

Serum ferritin values below 15µg/L are virtually specific for storage iron

depletion. However, normal values do not exclude storage iron depletion

and values above 300µg/L do not necessarily indicate iron overload.

 40

Confounding factors influencing Serum ferritin:

Serum ferritin is an acute-phase reactant and is increased in

conditions like infection, inflammation or malignancy. Serum ferritin is

released from the tissues when iron-rich organs are damaged as in hepatic

necrosis, chronic liver disease and bone marrow or splenic infarction in

sickle cell disease.

Serum transferrin receptors:

Serum transferrin receptor concentration reflects both iron supply

to the bone marrow and the number of erythroid precursors. It is an

important and invaluable indicator of iron deficiency in anemia of chronic

disease.

Serum folic acid levels:

Folate status is assessed by measuring folate levels in both serum

and red blood cells. Red blood cell (RBC) folate is the best indicator of

long term folate stores whereas serum folate level is an indicator of recent

folate intake. Prolonged folate deficiency is indicated by low RBC folate

values. Folate uptake into red blood cells is also affected vitamin B12

deficiency, leading to low RBC folate values even after adequate folate

intake.14
 41

Serum vitamin B12 levels:

A deficiency of either vitamin B12 or folic acid disrupts the

synthesis of methionine as both are linked to the reaction pathway. This

leads to the same symptoms and medical problems. Therefore, in a

clinical workup, measurement of both vitamins is often necessary and

treatment varies depending on which vitamin is deficient.

C-reactive protein:

C-reactive protein is an acute phase reactant and is increased in

processes such as infections, inflammatory diseases and malignant

neoplasms. Clinical symptoms, including fever, are frequently preceded

by the CRP response. Normal CRP values in healthy individuals have a

range up to 5 mg/an L. Serum CRP value rise rapidly and extensively

after onset of an acute phase response and are detectable within 6 to 8

hours and reaches the peak within 24 to 48 hours. CRP activates the

classical complement pathway. CRP is an ideal tool for clinical

monitoring as it has a half-life of only a few hours. Whenever high serum

CRP concentration persists in a clinical condition, it generally indicates

the presence of an uncontrolled infection.

 42

1.8. Treatment of iron deficiency anemia

The objectives of therapy in IDA are

i) To restore the hemoglobin to normal

ii) Replenish the depleted iron stores

iii) Treat etiological factors and prevent their recurrence.

Severe iron deficiency anemia can be rapidly treated with the help

of iron supplements in all sex and age groups. Whether iron

supplementation can be given daily or twice or once per week without

compromising the efficacy of supplementation is an ongoing debate and

numerous studies have been conducted. However, daily supplementation

for young children remains the current recommendation.

Oral iron supplements should be started as soon as a diagnosis of

IDA is established. The standard dose is 3 mg/kg of elemental iron per

day up to a maximum of 180 mg/day. Higher doses (6mg/kg body

weight) were previously used; but were associated with more frequent

gastrointestinal side effects. Single daily doses are effective, but 2-3

divided doses are better tolerated by children. Ideally, oral iron should be

given at least half an hour before a meal to ensure maximal absorption. It

can also be given 1-2 hours after meals.1,15,16,17

 43

Oral iron therapy must continue for a period of at least three

months to replenish depleted iron stores, if an adequate response to

therapy is seen. Stoppage of iron, once anemia is corrected, is the most

frequent cause for recurrence of IDA.

In 12 to 24 hours of starting therapy, there is replacement of

intracellular iron enzymes leading to dramatic improvement in sense of

wellbeing, decreased irritability and increased appetite. In 36 to 48 hours,

the bone marrow responds by way of erythroid hyperplasia. An increase

in reticulocyte count is observed in 48-72 hours and peaks in 5-7 days.

The hemoglobin level rises at an average rate of 0.15 g/dL per day,

usually commencing about one week after the institution of therapy.

Repletion of iron stores occurs by 1 to 3 months.

Choice of iron preparations:

Various salts have been used. Ferrous sulphate is used most

frequently, is least expensive and causes few side effects, if administered

in appropriate doses. Ferrous sulphate tablets are available as pediatric

iron tablets of 66 mg with an elemental iron content of 20 mg. Ferric

hydroxide polymaltose complex was recently introduced salt in the

market and has fewer gastrointestinal side effects. The non-ionic iron

polymaltose, has been shown to have no oxidative potency on

 44

lipoproteins in healthy subjects. Hence, a better compliance is expected

than with ferrous sulphate. But, the data on efficacy are lacking.18,19

Activated hydroxyl radicals are released when ferrous compounds

are oxidized in the lumen of the gut or within the gut mucosa. These

molecules attack the gut wall resulting in a range of gastrointestinal

symptoms and discomfort. In an attempt to avoid these problems, enteric

coated ferrous formulations designed to minimize iron release in the

stomach are available. But, this may compromise the absorption of iron.

Therefore, enteric-coated tablets should not be used as maximum

absorption of iron occurs in the duodenum and proximal jejunum.

Nausea, vomiting, abdominal discomfort, diarrhea and constipation

occur in some patients. These side effects are dose related and can be

minimized by adhering to standard doses, gradual hiking up of dose and

administration of iron with or after meals.

 45

Oral iron preparations:

Iron preparation Percentage of elemental iron

Ferrous sulfate 20

Exsiccated ferrous sulfate 30

Ferrous fumarate 33

Ferrous succinate 23

Ferric ammonium citrate 18

Table 6 oral iron preparations20

 46

Commercial iron preparation:

Elemental iron
Iron preparation
(per tab/cap or per 5 ml)

Fersolate Tab 66 mg

Tonoferon pediatric syrup

80 mg

Vitcofol syrup, Hemsi syrup,

33 mg
Fesovit syrup

Mumfer, Trifer 50 mg

Table 7 commercial oral iron preparations

Helminthic control:

Albendazole is given as a single dose (400 mg) in children more

than 2 years and as a single dose of 200 mg in children less than 2 years.

Other drugs used are single dose of Mebendazole (500 mg), single dose

of Levamisole (2.5 mg/kg) or single dose of Pyrantel (10 mg/kg).

 47

1.9. Prevention

Diag.4. Methods of prevention and correction of iron deficiency and

IDA
 48

Food-based Interventions:

Dietary diversification1

Improvement of nutritional status can be achieved by educating

households on methods of food preparation, including minimizing the

amount of inhibitors of iron absorption in the diet and recommending

minimal cooking in small amount of water of vegetables rich in vitamin

C, folate and other water soluble vitamins. Also, the bioavailability of

iron is improved by adding a small portion of haem iron containing diets

like meat or fish, since iron content is low in cereals and tuber based

diets.

Food fortification

Food fortification is being done in many countries as a part of

prevention of anemia. The best method is to fortify a staple food of the

local population, since it will be consumed in significant quantities.

Successful implementation of iron fortification of wheat flour has been

achieved in several countries in the North America, Great Britain, South

America, and Caribbean.15

Another method is to fortify a widely consumed condiment such as

salt and sugar which have all been successfully fortified with iron. Both

dried and liquid milk and dairy products such as yogurt have been

fortified with iron in South America.

 49

In the control of iron deficiency anemia in children receiving

complementary foods, fortified infant foods are an especially important

component. This method has been shown to be effective in preventing

infant iron deficiency anemia in Latin America and United States.

In our country, this can be made possible by taking advantage of

existing technology and health care network.

National health programs:

IFA supplementation for children has been recommended by the

Ministry of health and family welfare. As part of this program, 20 mg

elemental iron and 100µg folic acid per mL of liquid formulation for

children aged 0 to 5 years and 30 mg elemental iron and 250 µg per day

in children aged 6 to 10 years, both for a period 100 days with age

appropriate deworming is recommended.

In the year 2013, a policy decision to develop the National Iron+

Initiative was taken by the Ministry of Health and Family Welfare.

Existing national programs were brought together under this initiative and

new age groups were introduced as given below.1

Preschool children aged 6 months to 5 years are given iron

supplementation of 20 mg elemental iron and 100 µg folic acid bi-

weekly.
 50

Children from 1st to 5th grade (5 to 10 years of age) in Govt. &

Govt. Aided schools are given weekly iron supplements containing

45 mg of elemental iron and 400 µg of folic acid by school

teachers. Out of school children are given iron supplements at

Anganwadi Centers.

In the case of adolescents (10–19 years), weekly iron

supplementation is given containing 100 mg elemental iron and

500 µg of folic acid through school teachers.

 51

Review of

Literature
 52

REVIEW OF LITERATURE

2.1. Articles related to prevalence:

In the year 2011, Sudhagandhi et al. conducted a study among

school children aged 8 to 16 years of Kattankulathur, Tamil Nadu to

know the prevalence of anemia. A total of 900 children were included in

this study and it was found that 52.88% were anemic and the prevalence

of anemia among girls (67.77%) was significantly higher when compared

to the boys (35.55%) and anemic children were underweight.21

Rayn et al., conducted a cross-sectional study in two rural districts

of Karnataka, in the year 2010 among children aged 12 to 23 months. Out

of the 401 children included in the study, anemia was detected in 75.3%

children. It was also found that low ferritin levels, maternal anemia and

food insecurity were associated with anemia. In this study, correlation

statistics revealed a direct association between children's ferritin levels

and their iron intake, CRP levels and the maternal hemoglobin levels. An

inverse association was also demonstrated between children’s ferritin

levels and history of continued breastfeeding and the child's energy

intake.22

A prevalence study was conducted by Sabitha basu among school

going adolescents girls of Chandigarh who were apparently healthy.

Results of the study revealed that anemia is more common among rural
 53

adolescents (25.4%) when compared to urban (14.2%) adolescents. Also,

81.7% and 41.6% of the adolescent girls and boys respectively had

deficiency in Serum ferritin levels reflecting reduced iron stores.23

In the year 2010, a nationwide survey was done by Chellan et al.,

to find the prevalence of anemia and to assess the influences of

socioeconomic and demographic factors on the degree of anemia. The

prevalence of anemia was high not only in the low socioeconomic group,

but also in the higher strata. But the percentage of severely anemic

children declined with mother’s educational level and standard of

living.24

Gomber et al., in Indian Journal of Medicine in October 2003

conducted a study in corporation schools among children of age 5 to 11

years from an urban slum and it was found that prevalence of anemia as

per WHO recommended cut-off values of hemoglobin was 41.8 per cent.

The commonest type of anemia noted was pure or mixed iron deficiency

anemia in 68.42% children followed by pure or mixed B12 deficiency

noticed in 28.42% children. Iron deficiency was the commonest cause

among the pure variety occurring in 41.05 % (39 of 95) children.25

Duque et al. conducted a study among Mexican children aged less

than 2 years in rural as well as in urban areas to determine the prevalence

of anemia as well as deficiencies of iron, folic acid and zinc. In this study,

anemia was found in 20% of children. About 27.8% rural children and
 54

32.6% urban children in the study had iron deficiency. Low serum zinc

was noted in 28% urban and 13% rural children included in the study.

Similarly, folic acid deficiency was noted in 10% children in the urban

areas, and 8% children in rural areas. Thus, the principal micronutrient

deficiencies noted among Mexican children in the age group of less than

2 years was iron and zinc deficiencies. More important was the fact that

low ferritin concentrations were not seen in more than 50% of anemia.26

In January 2011, a study was done to determine the prevalence of

iron deficiency anemia by Al-Sayes et al. among apparently healthy

young female university students in Saudi and it was found that 50.2% of

students were normal and 25.9% of students had deficient iron store and

23.9% of students had iron deficiency anemia. There was a significant

correlation between iron deficiency and iron deficiency anemia with

inadequate meat intake and impaired exercise capacity.27

2.2. Articles related to clinical profile:

The study by Jain et al. among school girls of age 8 to 11 years in

2012 regarding correlation between hematological and cognitive profile

in anemia showed that among 111 children in the sample, 77% were

anemic with low iron studies ,lower IQ, intellectual capacity and

educational achievement than those of their non-anemic counterparts.

These three parameters had significant correlation (p<0.05) with Hb and

serum iron.28
 55

Lukowski et al. found that frontostriatal-mediated executive

functions like inhibitory control, set-shifting and planning were

performed less well by infants with chronic, severe iron deficiency. The

hippocampus-based recognition memory task was also impaired. These

deficits suggest that early iron deficiency in the long-term may affect the

hippocampus, dopamine system as well as their interaction.29

Peirano et al. conducted a study which showed affective

differences among infants with iron deficiency anemia. Also, infants with

iron deficiency anemia tested lower in mental and motor developmental

assessments. It was found that even after iron therapy, they had persistent

sleep disturbances and neurofunctional affects which lead to reduced

behavioral and cognitive outcomes indicating that iron may have key role

in the normal development and progression of several neurofunctional

systems.30

Fretham et al. published an article regarding the role of iron in at

least 3 major neurobehavioral domains in learning and memory, including

learning, speed of processing and affect. Learning and memory, being

particularly prominent, were affected by early life iron deficiency and

were found to persist despite iron repletion. In the case of adults,

interactions between direct and indirect effects of iron deficiency

contributing to abnormal hippocampal structure and plasticity is the likely

cause of learning deficits.31

 56

In the year 2014, the relationship between pagophagia (ice pica)

and iron deficiency anemia was studied by Uchida et al. Out of 81

patients with iron deficiency anemia, pagophagia was present in 13

patients (16.0%), and it was found that oral iron therapy can cure the

pagophagia earlier than hemoglobin recovery and repair of tissue iron

deficiency.32

2.3. Articles related to investigations:

Sazawal et al. conducted a study among 2091 children in the age

group of 1–3 years from an urban low socio-economic population of

Delhi to determine the role of RDW in discriminating IDA and published

an article in the year 2014. The study found that in children with

hemoglobin values 10.0 g/dL, RDW values greater than >15% identifies

iron deficient anemia without the need for iron status.33

In the year 2009, Aulakh et al. of Christian medical college,

Ludhiana conducted a study among 151 children aged 6 months-12 years

with microcytic (MCV<75 fL) anemia to determine the usefulness of Red

Cell Distribution Width (RDW) for the diagnosis of iron deficiency. On

the basis of serum ferritin and total iron binding capacity (TIBC),

Children with microcytic hypochromic anemia were classified into iron

deficient and non-iron deficient anemia. It was concluded that the RDW

had sensitivity and specificity of 81.0% and 53.4% respectively, in the

 57

diagnosis of IDA. Similarly, the positive and negative predictive value of

RDW in the diagnosis of IDA was 63.0% and 72.2% respectively.34

Lee et al., in 2001 investigated hematologic profiles of anemic

children aged 5 to 36 months (198 patients) comparing them with the

control group. The children were mainly brought to the clinic for

infectious or inflammatory illness. Only 13.1% children with iron

deficiency anemia had come directly for evaluation of pallor. Among the

children with IDA, the correlation between hemoglobin and MCV was

much more than the control group (P 0.001). It was concluded in the

study that the accuracy of diagnosis of IDA can be increased by

combining hemoglobin, MCV, RDW as well as iron profile in screening

for iron deficiency.35

In the year 2014, the HELENA study conducted among adolescent

girls in 10 European cities to evaluate the usefulness of iron profile

confirmed that serum ferritin and serum transferrin receptors can be used

in assessing the iron status of adolescents and it was also found that

adolescent girls are at high risk of iron deficiency.36

2.4. Articles related to various iron therapies:

Aggarwal et al., in 2004 conducted a study among predominantly

breast fed term low birth weight (LBW) infants aged 50–80 days to

evaluate the hematological effects of iron supplementation. Total 73

 58

infants enrolled were randomized into two groups. One group received

iron (3 mg/kg/day) and the other group received placebo drops. Baseline

anthropometry and hematological parameters were measured. These

measurements were repeated after four and eight weeks and no significant

differences were found in serum ferritin and anthropometry. However,

there was a significant positive change in hemoglobin levels in the iron

supplementation group.37

In 2004, a review article published in Indian Pediatrics regarding

iron supplementation recommended oral iron for treating iron deficiency

anemia. According to the article, the type of iron salt to be used has to be

based on the bioavailability of the iron salt, side effects and cost

effectiveness.38

Ferrous salts, specifically ferrous sulfate, are preferred for

treatment of IDA, since all iron needs to be reduced to ferrous form for

absorption. As ferrous sulfate is not stable in liquid form, other ferrous

salts are used in liquid formulations. One important side effect of ferrous

sulfate is gastrointestinal intolerance. Various measures have been

suggested to overcome this side effect. These measures include

administration after meals and at bed time, since decreased intestinal

motility during sleep may help improve absorption.

 59

In the case of ferric salts, ferric ammonium citrate is used. The

important drawback of these salts is the low bioavailability which is

considered to be 3-4 times less than ferrous salts.

Better bioavailability is claimed with iron-amino acid chelators,

which are other group of iron preparations, because absorption of this salt

is said to be not interfered by phytates in the diet. However, when

compared to ferrous sulfate in clinical studies in young children and

infants, equal rise in hemoglobin has been reported.

Iron polymaltose complex (I-PMC) and carbonyl iron are two more

types of iron preparations that deserve mention. The bioavailability of

iron polymaltose complex (I-PMC) has been demonstrated to be similar

to ferrous sulfate. Also, both ferrous sulfate and I-PMC in equivalent

doses were found to have similar efficacy in a recent meta-analysis on

iron polymaltose complex use in adults with IDA.

In the case of carbonyl iron, the main advantages are the small

particle size of the molecule contributing to increased bioavailability as

well as the considerably higher doses of administration. However, this

fact needs further research as the result of two Indian studies are

conflicting, one stating that the bioavailability to be higher and another

study finding the bioavailability to be similar. Carbonyl iron has been

mainly used in food fortification industry.

 60

Conventionally, a dose of 4-6 mg/kg/day of elemental iron were

recommended for treatment of IDA in children. However, it was found

that smaller doses were also equally effective as well as better tolerated.

Hence, currently a dose of 3 mg/kg/day of elemental iron is

recommended. It is to be noted that approximately 25 mg of elemental

iron saturates the absorptive capacity of iron in the duodenum. Therefore,

absorption of iron will not be increased at higher doses.

Low et al. in a meta-analysis of randomized controlled trials on the

effects of daily iron supplementation in 5-12 years old primary school

children identified 16501 studies in which a total of 7089 children were

evaluated. A total of 31 studies had been conducted in low or middle

income settings. The review concluded that there was improvement in

intelligence quotient (p = 0.04), global cognitive scores (p = 0.01) as well

as measures of attention and concentration among anemic children on

iron supplementation.39

An improvement in age-adjusted height and weight among anemic

children on iron supplementation was also noted. According to this

review, the risk of iron deficiency and iron deficiency anemia were 50%

and 79% respectively by iron supplementation.

Desai et al. conducted a study in Western Kenya among children

less than 2 years living in a malaria-endemic area, comparing the efficacy

of supervised as well as unsupervised, daily and twice weekly iron

 61

supplementation over a period of 6 weeks in the treatment of mild and

moderate anemia after administering a single dose of sulfadoxine-

pyrimethamine at enrollment. Daily supervised or unsupervised iron

supplementation was given in the dose of 3–6 mg/kg/day and twice

weekly supervised or unsupervised iron supplementation was given in the

dose of 6–12 mg/kg/wk.40

Results from the study revealed that hemoglobin concentration in

the daily supervised iron supplementation group was significantly higher

than twice weekly supervised iron supplementation group. In case of

unsupervised iron supplementation groups, hemoglobin concentrations

were significantly higher at 12 weeks. But, the hemoglobin

concentrations were not different at 6 weeks of iron supplementation.

It was concluded that, in the treatment of anemia in preschool

children, regardless of compliance to therapy, hematological responses

can be expected after 6 weeks of daily iron supplementation rather than

twice weekly iron supplementation.

2.5. Articles related to treatment and improvement in hemoglobin:

Maheswari et al. conducted a study among a total of hundred

anemic school children from three government schools of Raipur city.

They were subjected to anthropometry, iron status and clinical

examination before they underwent iron therapy and the response to iron
 62

was assessed by estimation of hemoglobin after one month following iron

therapy. In all the 100 children, clinical pallor was the most common

finding (100%), followed by fatigue (54%), weakness (38%), anorexia

(18%) and icterus (5%). The commonest blood picture was that of

microcytic hypochromic.41

Age dependent MCV, MCH, MCHC and RDW showed that the

maximum number of cases had below normal MCV, MCH and MCHC

values. RDW values were increased in 74% cases. 82% cases had serum

iron values below normal (<50 g/dl) and 91% cases had TIBC values

above the normal range. The serum ferritin levels in 35% children was

<15ng/ml (in 18% boys and in 17% girls). The mean and SD of Hb

before therapy was 8.60 ± 2.05 and after therapy, it was 9.55±1.88

respectively. A significant increase in the hemoglobin (p<0.009) level

was observed in both boys and girls after 30 days of iron

supplementation.

A systematic review of randomized controlled trials in 2007

showed the effect of iron supplementation on hemoglobin response in

children by Gera et al. He found that there is significant, but modest

increase hemoglobin levels after iron supplementation. The review also

concluded that children who were anemic at the beginning of the trial

showed a greater increase in hemoglobin, whereas improvement in

 63

hemoglobin was much lower in those children living in malarial hyper-

endemic areas and in those consuming iron-fortified food.42

In the year 2010, Huang et al. in Taiwan conducted a study to

determine the various causes of iron deficiency anemia and the treatment

outcomes. It was found that the most common cause in children less than

2 years was inadequate intake and blood loss was common in children

aged 2 to 10 years. Treatment with iron supplementation for 3 months

resulted in improvement of hemoglobin levels in 78.9% of IDA

patients.43

Paracha et al. conducted a study to determine the effects of iron

supplementation on iron status in selected pre-adolescent school girls

aged 8 to 11 years in North West Frontier Province, Pakistan by dividing

them into treatment and control groups. The treatment group received 76

mg elemental iron per day over a period of 11 weeks. At the same time,

both the groups received multivitamin tablets daily. It found that the 35%

of the pre-adolescent schoolgirls had IDA. The improvement in

hemoglobin (15g/dL), Hct (3%) and serum ferritin (20ng/mL) was

significant (P<0.05) in the anemic treatment group when compared to the

control group.44
 64

STUDY JUSTIFICATION

3.1. Study justification:

Iron deficiency anemia is most prevalent among nutritional anemia

and it constitutes more than 70%. Though there are many studies on

prevalence in rural and in varied populations and in schools, the present

study is done to assess the prevalence and profile of iron deficiency

anemia among the children of working group mothers. Though children

attending the ESI HOSPITAL belong to parents who are educated and are

aware of nutritional importance of minerals, most of them are not able to

take care of their children because of the work and hence my study is

done to assess the clinical profile in this particular population, and also to

test the correlation of various red cell indices with iron studies. Though

there are lot of studies on iron therapies and comparison of various

formulations there are not many studies on improvement in hemoglobin

or follow up studies after oral iron supplementation. Hence, this study is

intended to follow up children with iron deficiency anemia to know the

improvement in hemoglobin.
 65

Aim and

Objectives
 66

AIMS AND OBJECTIVES

4.0. Aim of the study:

The aim is to study the profile of nutritional anemia in children and

to determine the treatment outcome of iron deficiency anemia.

4.1. Objectives:

To assess the proportion of various types of anemia like microcytic

hypochromic, normocytic hypochromic, normocytic normochromic or

megaloblastic anemia.

To analyze the various presenting symptoms in relation to anemia

To assess the correlation of Red cell indices and peripheral smear

with iron profile, folic acid and vitamin B12.

4.2. Secondary objective:

To determine the treatment outcome of iron deficiency anemia in

children after oral iron supplementation for 12 weeks.

 67

Material and

Methods
 68

MATERIAL AND METHODS

5. Material and methods:

Study design:

Cross-sectional study and interventional study

Place of study:

ESIC Medical College & PGIMSR, KK Nagar, Chennai

Period of study:

9 months

Sample size:

150 children

5.1. Inclusion criteria:

Children in the age group of 1 to 10 years with hemoglobin levels

less than the cut-off values for the age, as per WHO guidelines, were

included in the study. Out of the 150 children, those with iron deficiency

anemia were followed up for treatment outcome after iron therapy.

 69

5.2. Exclusion criteria:

Chronic diarrhea

Children with renal disease

Children with cyanotic heart disease

Children with endocrine diseases

5.3. Methods:

150 children in the age group of 1 to 10 years with pallor were

confirmed to have anemia by hemoglobin estimation.45, 46 The criteria for

diagnosing anemia was hemoglobin values less than 11 g/dL in children

aged 12 months to 59 months, less than 11.5 g/dL in children aged 5 years

to 11 years. Children who fulfilled the criteria were included in the study

after obtaining informed written consent from their parents.

Fig. 2 IMNCI guidelines for assessment of pallor45

 70

The history and examination was documented on a pre-designed

proforma. A social demographic profile including parents’ education,

family structure and diet consumed (vegetarian, non-vegetarian) was

noted. A detailed general physical examination was done to look for

pallor, icterus, edema, lymphadenopathy, and signs of vitamin deficiency.

The anthropometric measurements (weight, height) were made by a

single observer and finally, a thorough systemic examination was also

done.

The following investigations were done in all cases – complete

blood count, red cell indices, peripheral smear study, reticulocyte count,

RDW, ESR, CRP, stool for occult blood, serum ferritin, iron indices,

vitamin B12 and folic acid assay.

Children with iron deficiency anemia were given oral iron syrup

(iron polymaltose complex) in the dose of 3 mg/kg/day once daily, for 3

months and hemoglobin levels were checked at 1 and 3 months after

starting iron supplementation. Reticulocyte count was also checked after

one month of therapy.

 71

Blood sampling:

Blood samples were collected under strict aseptic precautions.

About 2 mL of blood was collected in EDTA tube for complete blood

count and peripheral smear examination. Around 3 mL of blood was

collected in 2 separate serum containers. One container was used for

spectrophotometric assay of serum iron and TIBC and the other container

for assessment of serum Ferritin, Vitamin B12 and folic acid by chemi

luminescent assay

Stool sampling:

Patient was instructed to eat a well-balanced diet including fiber

such as bran, cereal, fruits and vegetables. Red meat and excess of

vitamin C and iron supplements in excess of 250mg per day was avoided

3 days before collection of sample.

5.4. Laboratory techniques:

Complete blood count was done using five part automated cell

counter from Beckman Coulter with tri level Quality control from Bio-

Rad for measuring the following values such as hemoglobin, red cell

count, white cell count, PCV, MCV, MCH, MCHC and platelet count. A

peripheral blood smear was prepared, stained using Leishman stain and

examined under the microscope. Reticulocyte count was calculated

manually after supravital staining.

 72

The ferritin assay was done by using the technique of

chemiluminescent immunoassay on Access 2 equipment from Beckman

Coulter in human serum using monoclonal anti ferritin antibodies.

Serum iron and serum unsaturated iron binding capacities (UIBC)

were quantitatively determined on Roche/Hitachi cobas c 311 systems

using spectrophotometric immunoturbidimetric assay. TIBC was derived

from the sum of serum iron and UIBC. Serum transferrin and serum

transferrin saturation are derived values from serum iron and TIBC.

Vitamin B12 and serum folate were also determined using

chemiluminescent immunoassay.

Erythrocyte sedimentation rate was estimated by automated infra-

red based machines using Westergrens method. The C-reactive protein

was determined in human serum done by immunoturbidimetric assay on

Roche/Hitachi cobas c 311 systems.

Stool samples were tested for occult blood by hemospot test.

 73

STATISTICAL ANALYSIS

6. STATISTICAL ANALYSIS

In the above study, the statistical methods used for quantitative

data were descriptive statistics presented by N, Mean, Standard Deviation

and Range. For qualitative data, frequency count, N and percentage were

put in tabular columns.

To analyze the data, appropriate statistical tests were applied. To

compare the difference between variances in the subjects, one way

ANOVA was used. To find the correlation between hemoglobin, red cell

indices & iron profile, Pearson’s correlation coefficient was used.

All the statistical analysis had been done by using statistical

software SPSS (version 16.0). Other data are displayed by various tables

and charts by using Microsoft excel (windows 7).

* Significant at p < 0.05

** Very significant p <0.01

*** Highly significant p < 0.001

 74

Results
 75

RESULTS

7. RESULTS

A total of 150 children were enrolled as study population and

statistical analysis revealed the following observations.

Demographic profile:

Fig. 7.1 Age distribution of children

Among the 150 children, 66.7% (n= 100) were between 1 to 5

years of age and 37.3% ( n=50 ) were between 5 to 10 years of age. The

mean age of children with microcytic hypochromic anemia (MHA),

normocytic hypochromic (NHA), and normocytic normochromic anemia

(NNA) was 3.39 years ± 2.75, 5.2 years ± 3.67 and 5.05 years ± 3.22

respectively.
 76

Fig. 7.2 : Age distribution among various types of anemia

 77

Fig. 7.3 : Mean age among various types of anemia

In children with MHA, 80% (n=44) were in the age group of 1 to 5

years and 20% (n=11) were in the age group of 5 to 10 years. In children

with NHA and NNA, 53.30% (n=7) and 58.80% (n=48) were between 1

to 5 years of age respectively. Among 5 to 10 years age group, the

children with NHA were 46.70% (n=8) and the children with NNA were

40% (n=32).
 78

Fig. 7.4: Sex distribution of children

 79

Fig. 7.5: Sex distribution among various types of anemia

 80

Table 7.1. Sex distribution among various types of anemia

MHA NHA NNA

Gender
N % N % N %

Female 22 40.00% 4 26.70% 33 41.20%

Male 33 60.00% 11 73.30% 47 58.80%

Among the study population, 60.7% (n=91) were male and 39.3%

(n=59) were female. In the study group with MHA, 60% (n=33) children

were males and 40% ( n=22) were females. In children with NHA,

73.30% ( n=11) were male and 26.70% ( n=4) were female. In children

with NNA, 58.80% (n=47) were male and 41.20% (n=33) were female.
 81

Fig. 7.6: Socioeconomic status of the families

 82

FIG. 7.7: Prevalence of anemia in various socioeconomic classes

 83

The socio-economic status of the children was assessed by

modified Kuppuswamy’s scale47 and it was found that majority of the

families belonged to class II [ 68.7% (n=103) ] followed by class III [

28.7% (n=43) ] and class IV [ 2% (n=3) ] and class I [ 0.7% (n=1) ]

On analysing the socioeconomic class in children with MHA, it

was found that 78.20% (n=43) belonged to class II socioeconomic status

and 21.80% (n=12) belonged to class III.

 84

Fig. 7.8: Dietary habits of families

Majority of the families consumed non-vegetarian diet [82.7%

(n=124)] and only 16.7% (n=26) consumed vegetarian diet.

 85

Fig. 7.9: Gestational age at birth

Out of the 150 children included in the study, 11.3% children were

born preterm (n= 17) and the rest were born at term gestation.
 86

Fig. 7.10: Duration of exclusive breastfeeding

It was found that 53% (n=79) of the children were exclusively

breast fed up to 6 months. In 26% (n=39) of children exclusive breast

feeding was practiced only up to 4 months. In 12% (n=18) of cases,

exclusive breastfeeding was given for more than 6 months. In 8.7%

(n=13) of children exclusive breastfeeds were received only up to one

month.
 87

Fig. 7.11: Time of introduction of artificial feeding

Early cow’s milk/formula feeds were started in 26% (n= 32) of

children between 1 to 4 months and 29% (n=36) between 4 to 6 months

and 34% (n= 42) between 6 to 12 months. In 4.9% of children, artificial

feed was introduced in the first month of life.

 88

Fig. 7.12: Time of introduction of complementary feeding

Majority of the children (58.6 %) received early complementary

feeding by 4 to 6 months and in 26.6% , the children received

complementary feeding between 6 to 10 months.

 89

Fig. 7.13: History related to anemia

History of worm infestation was present in 42.7% (n=64) of

children, pica in 35.3% (n=53), pagophagia in 12.5% (n=19), past

infections in 28.7% (n=43), Gastrointestinal bleed in 4% (n=6), family

history of hemolytic anemia in 2% (n=3) and drug intake in 0.7% (n=1)

of children.
 90

Fig. 7.14: Proportion of anemic children having pica

Pica was found to be more in children with MHA constituting

47.30% (n=26).
 91

Fig. 7.15: Symptoms of anemia

Symptom analysis revealed that majority of children had lethargy

which was found in about 47.3% (n=71 ) followed by easy fatigability in

41.3% (n=62), irritability in 25.3% (n=38), poor school performance in

20.7% (n=31), breathlessness in 7.3% (n=11), headache and dizziness in

2.7% (n=4) and 2% (n=3) respectively with palpitation and chest pain

accounting for the least number in about 1.3% (n=2).

 92

Fig. 7.16 Symptom analysis among various groups of anemia

 93

Table 7.2 Symptom analysis among various groups of anemia

Types of anemia MHA NHA NNA

Symptom N Mean N Mean N Mean

Irritability 19 34.50% 4 26.70% 15 18.80%

Lethargy 30 54.50% 6 40.00% 35 43.80%

Poor school
7 12.70% 2 13.30% 22 27.50%
perfomance

Easy fatigability 23 41.80% 5 33.30% 34 42.50%

Among the 150 children with various types of anemia, irritability [

34.50 % (n=19)] and lethargy [ 54.50% (n=30)] was more in children

with MHA.
 94

Fig. 7.17: Signs of anemia

Among the 150 children examined, leuconychia was present in

33.3% (n=50), koilonychia in 32% (n=48), generalized lymphadenopathy

in 23.3% (n=35). Cheilitis, glossitis, hepatosplenomegaly was found in

14% (n=21), 12% (n=18) and 10% (n=15) respectively.

 95

Fig. 7.18: Proportion of various types of anemia

It was noted from our observation that among the 150 children,

36.7% (n=55) had microcytic hypochromic anemia, 10% (n=15) had

normocytic hypochromic anemia and 53.3% (n=80) had normocytic

normochromic anemia.
 96

Fig. 7.19: Descriptive statististics of CBC profile

 97

Table 7.3 Mean values of red cell indices

Types of anemia MHA NHA NNA

Hb 8.22 1.27 9.58 0.91 9.925 0.91

PCV 28 9.22 31.43 3.58 32.33 3.58

MCV 59.1 12.30 70.29 7.06 73.98 10.44

MCH 19.33 5.96 21.39 1.94 23.53 2.95

MCHC 35.08 36.18 34.1 13.5 31.31 2.50

Statistical analysis of complete blood count reveals the mean Hb is

8.22 1.27 in children with MHA and in children with NHA and NNA,

the mean Hb is 9.58 0.91 and 9.925 0.91 respectively. The mean

values of PCV, MCV, MCH, are less in MHA when compared to NHA

and in NNA.
 98

Fig. 7.20: Scatter plot diagram showing correlation between

hemoglobin and RDW

The mean RDW in children with MHA was 16.75 3.96, 14.61

2.44 in NHA and 14.50 2.93 in NNA. The scatter plot diagram shows

that, in our study, the red cell distribution width increases as hemoglobin

values decrease.
 99

Fig. 7.21: Descriptive statistics of iron profile

 100

Table 7.4 Mean values of iron profile

Types of anemia MHA NHA NNA

S. Iron ( g/Dl) 31.62 23.90 46.22 23.40 51.64 22.52

TIBC ( mol/L) 392.82 103.7 359.96 79.11 315.8 81.36

S. Transferrin
424.44 90.45 406.17 83.63 367.44 77.38
(mg/dL)

Transferrin
8.76 11.25 11.45 5.71 14.68 7.63
saturation (%)

S. Ferritin (ng/mL) 38.84 49.75 69.97 138.01 91.93 203.90

 101

The descriptive statistics of iron profile revealed that the mean

serum iron levels were 31.62 23.90 g/dL in children with MHA,

46.22 23.40 g/dL in children with NHA and 51.64 22.52 g/dL in

children with NHA. The mean TIBC was increased in children with

MHA with a mean of 392.82 103.7 mol/L, and in children with NHA,

the mean TIBC is 359.96 79.11 mol/L, and in NNA , the mean is

315.8 81.36 mol/L. Serum transferrin was high in children with MHA

and in children with NHA, the mean transferrin levels were low when

compared to MHA. The mean serum ferritin levels were 38.84 49.75

ng/dL in children with MHA and in children with NHA the mean levels

were 69.97 138.01 ng/dL, and 91.93 203.90 ng/dL respectively.

 102

Table 7.5 Pearson’s correlation statistics between hemoglobin, red

cell indices and iron profile

Pearson S. S. S.
MC MC MCH RD TIB Transf Reticuloc
Correlati PCV Iro Transfer Ferrit
V H C W C er. Sat yte count
on n rin in

- -
Hemoglo .366 .316 .308 0.25
0.225 .287 0.22 0.188 -0.193 0.125 -0.072
bin ** * * 9
* 8

0.00 0.01 0.02 0.03 0.05 0.09

P value 0.099 0.169 0.158 0.362 0.603
6 9 2 4 7 4

On analyzing the data of MHA with Pearson correlation statistics

of hemoglobin and red cell indices, it was found that hemoglobin had

weak positive correlation with PCV, MCV, MCH and weak negative

correlation with RDW. The correlation is at p<0.05 level significance.

Hemoglobin has weak correlation with iron studies and it is not

statistically significant.
 103

Table 7.6 Comparison of mean differences between 3 groups of

anemia

ANOVA test

MHA NHA Sig

Types of
NNA
anemia

Parameters Mean SD Mean SD Mean SD p value

Hemoglobin 8.23 1.27 9.58 0.76 9.93 0.91 0.0001***

PCV 28.00 9.23 31.43 3.59 32.33 3.90 0.0001***

MCV 59.10 12.30 70.29 7.07 73.98 10.44 0.0001***

MCH 19.33 5.97 21.39 1.94 23.53 2.95 0.0001***

MCHC 35.09 36.18 34.10 13.52 31.32 2.50 0.617

RDW 16.75 3.96 14.61 2.44 14.50 2.93 0.001**

Reticulocyte 1.08 1.19 0.55 0.26 0.84 0.36 0.045*

count

S. Iron 31.62 23.90 46.22 23.40 51.65 22.52 0.0001***

TIBC 392.82 103.70 359.96 79.11 315.80 81.36 0.0001***

Transferrin 8.76 11.25 11.46 5.71 14.68 7.63 0.001**

saturation

S. 424.44 90.45 406.18 83.63 367.45 77.38 0.001**

Transferrin

S. Ferritin 38.84 49.75 69.98 138.01 91.93 203.90 0.164

 104

One way ANOVA test was used to compare the differences in

mean of various indices among the children with MHA, NHA and NNA.

The mean difference between groups with respect to hemoglobin, PCV,

MCV, MCH and RDW was statistically highly significant (p=0.0001).

The reticulocyte count also was compared and the difference was

statistically significant (p = 0.045). It is seen from the table above that the

mean difference in serum ferritin levels (p=0.164) and MCHC (p=0.617)

was not statistically significant between the groups.

 105

Table 7.7 Comparison of serum ferritin, ESR and CRP between the

groups

Types
of S. Ferritin ESR CRP
anemia

<10 >10
< 15 >15 < 20 >20
Values
ng/mL ng/mL mm/Hr mm/Hr
mg/L mg/L

26 29 29 26 35 20
MHA
(47.27%) (52.72%) (52.72%) (47.27%) (63.63%) (36.36%)

4 11 8 7 8 7
NHA
(26.6%) (73.33%) (53.33%) (46.67%) (53.33%) (46.67%)

17 63 37 43 43 37
NNA
(21.25%) (78.75%) (46.25%) (53.75%) (53.75%) 46.25(%)
 106

Table 7.8 Proportion of cases with elevated ESR/ CRP and normal

serum ferritin levels

Types of anemia ESR CRP

MHA 15 (51.7%) 10 (34.48%)

NHA 5 (45.45%) 3 (27.27%)

NNA 38 (60.3%) 31 (49.20%)

From the previous observations, it was obvious that serum ferritin

was not reduced in all children with anemia. Hence, the correlation with

ESR and CRP was done and it revealed that out of 29 children with

MHA, 15 had elevated ESR and 10 children had elevated CRP. In NHA,

5 out of 11 children and in NNA, 38 out of 63 children had increase in

ESR. In NHA, 3 out of 11 and 31 out 63 had increased CRP levels.

A total of 7 out of 29 children with MHA had elevations in both

ESR and CRP and 3 out 11 children with NNA and 24 out of 63 children

also had elevations in both ESR and CRP.

 107

Treatment outcome (n=50):

Out of the 150 children, a total of 55 children had MHA. These

children were given oral iron supplementation and were followed-up. 5

children were lost to follow-up. The results of the follow-up are shown

below.

Fig. 7.22: Improvement in hemoglobin after iron therapy

The follow-up study after oral iron supplementation had shown that

the mean hemoglobin increased from the baseline value of 8.25 1.302

mg/dL to 9.17 1.365 mg/dL after one month and it increased to 10.38

1.368 mg/dL after 3 months.

 108

Table 7.9 Follow-up hemoglobin and its significance

Paired Samples Test

Paired Differences 95% Confidence interval of the Difference

Parameters Std.
Std. t test
Mean Error Lower Upper df p value
Deviation value
Mean

Hb level -
Baseline and
follow-up -0.916 1.100 0.156 -1.229 -0.603 -5.888 49 0.0001***
after 1
month

Hb level -
Baseline and
follow-up -2.126 1.277 0.181 -2.489 -1.763 -11.771 49 0.0001***
after 3
months

Hb level
after 1
month and 3 -1.210 0.651 0.092 -1.395 -1.025 -13.137 49 0.0001***
months
follow-up

Reticulocyte
count -
Baseline and 0.125
-0.272 1.232 0.174 -0.622 0.077 -1.56 49
follow-up (NS)
after 1
month

*** Highly Significant, NS-Not Significant

The mean increase in hemoglobin at 1 month from baseline month

and then at 3 months was statistically significant (p=0.0001).

 109

Table 7.10 Improvement in reticulocyte count after one month

Corrected

reticulocyte Mean Std. deviation Std. error

count

Baseline 0.729 0.610 0.086

Follow-up after 1
1.001 0.968 0.137
month
 110

Fig 7.23 Mean increase in reticulocyte count after treatment

It is seen from the observation that the corrected reticulocyte count

has increased from the baseline of 0.7 to 1.0.Though there is an increase

in reticulocyte count it has not shown any statistical significance

(p=0.125).
 111

Discussion
 112

DISCUSSION

This study was primarily designed to determine the clinical and

laboratory profile of nutritional anemia among children attending the

Pediatric outpatient Department of a tertiary care hospital.

A total of 150 children were recruited, following confirmation of

anemia with hemoglobin estimation. After a targeted history and detailed

clinical examination, they were subjected to red cell indices and iron

studies besides RDW, reticulocyte count and peripheral smear. Serum

vitamin B12 and folic acid levels were estimated in all cases. An attempt

was also made to look for laboratory evidence of inflammation by

estimating ESR and CRP in all cases.

Based on the above investigations, anemia was grouped into

microcytic hypochromic anemia (MHA, 55cases), normocytic

hypochromic anemia (NHA, 15 cases) and normocytic normochromic

anemia (NNA, 80 cases). There were no cases of macrocytic anemia on

peripheral smear examination and serum B12 and folic acid levels were

normal in all cases.

On analyzing the group characteristics of MHA, it was found that

80% of the children belonged to a younger age group (1-5 years). A

similar observation was also noted in a study by Rayn et al. wherein 75%
 113

of children with IDA were in the 1-2 years age group. However, there

was no statistically significant difference in gender distribution.

On the socio economic front, most of the cases belonged to a

relatively higher class (78% in Class II Kuppuswamy Scale). The

presence of anemia, in this socioeconomic group, is explained by the fact

that most of the mothers were working and hence the diet of the child

probably remained unsupervised. Chellan et al. also observed a greater

prevalence of anemia in higher socioeconomic strata.24

Worm infestation, which may have been a predominant contributor

to IDA, was seen in up to 44% of cases and pica was seen in 47.3% of

children with microcytic hypochromic anemia. Subjective symptoms

(lethargy, easy fatigability, irritability) were seen in 55% of cases

whereas objective symptoms like breathlessness and palpitations were

seen in very few. The absence of objective symptoms in our series is

presumably because of the lesser severity of anemia as evidenced by

mean hemoglobin of 8 g/dL. Maheshwari et al. had observed fatigue in

54% and weakness in 38% of their cases.41

Among the 55 cases with MHA, though MCV and MCH values

were suggestive of iron deficiency, serum ferritin values were normal in

53% of cases. This was similar to the observation made by Duque et al.26

where >50% children in the age group of 1-2 years had no correlation

between iron deficiency and serum ferritin levels. It was also seen that in
 114

the study conducted by Maheshwari et al. only 35% had low ferritin

levels.41

Ferritin is an acute phase protein that rises in response to

inflammation. The presence of normal ferritin in cases of IDA can be

explained by the fact that in a hospital based study like ours, subclinical

infection or latent inflammation could well be the cause for such an

elevation, thus masking the true size of the iron store.13 This association

with inflammation is also suggested by the elevated CRP in 36.36% of

cases and elevated ESR in 47.3%.When such confounders are

encountered; the estimation of RDW may help in identifying true IDA.

RDW is a quantitative measure of all the variation in the width of

the RBCs. It is of great value in discriminating IDA from other causes of

microcytic hypochromic anemia, but studies in children are few. Elevated

RDW (>15%) was seen in 67% of our MHA cases. RDW was found to

have a strong correlation with IDA in the present study. In studies by

Sazawal et al and Aulakh et al. the sensitivity of RDW was found to be

81% in diagnosing IDA.33,34

A small proportion of patients (n=15) with NHA are probably

patients with evolving iron deficiency as the average MCH value in this

group was low at 21.9%. With time, these children would have evolved

into frank hypochromic, microcytic anemia. In a resource poor setting,

there is an urgent need to identify IDA in its earliest stage and replenish
 115

stores to prevent cognitive impairment and growth failure. Probably, this

group of children too will benefit from oral iron therapy.28

Among the 150 recruited cases, we were surprised to find that more

than half the children (80 cases) belonged to the category of normocytic

normochromic anemia, which is classically associated with chronic

disease, even though we did not include any cases with overt systemic

illness or inflammation in the study.13 Symptomatology of these cases

mimicked iron deficiency and the finding of pica and koilonychia in one-

third of the cases also prompted us to study the parameters in greater

detail. The ferritin levels were normal in the majority of this group (79%)

and low in only one-fifth of the cases.

Inflammatory disorders cause elevation of circulating hepcidin,

which causes a blocking effect on enterocytes and reticulo-endothelial

system leading to iron deficient erythropoiesis. Since hepcidin levels

cannot be assessed easily, an alternate and cheaper modality would be

needed.

A widely used and easily available marker of inflammation is the

CRP with values above 10 - 30mg/L being significant. On analysis of

cases of NNA with normal ferritin, it was found that 39% had elevated

CRP while 47% had increased ESR, again indicating transient infection

or inflammation being the triggering agents. Thus, in anemic children

with elevated CRP, concurrent iron deficiency must be considered despite

 116

high ferritin levels. In such situations increased RDW has been seen to be

a strong pointer towards iron deficiency.

In our study, RDW had a strong correlation with anemia in only

35% of children with normocytic normochromic anemia. It is unlikely

that such a significant number of children would actually be suffering

from anemia of chronic disease. It is likely that such children too may

have latent iron deficiency anemia and it is this group that in a busy OPD,

may get overlooked. It is important to note that they too may benefit from

oral iron therapy and that further studies are needed to establish the same.

In terms of correlation of the hemoglobin with the red cell indices,

we found a positive correlation between hemoglobin and MCV and MCH

which was statistically significant and a statistically significant negative

correlation with the RDW. This has been borne out amply in many

studies wherein a high RDW has been found to be a sensitive marker of

iron deficiency.

Treatment and follow up:

All cases with MHA were treated with iron supplements in

therapeutic doses and hemoglobin and reticulocyte count were repeated at

1 month followed by hemoglobin alone at 3 months after starting

treatment.
 117

There was an increase in reticulocyte count as well as hemoglobin

at 1 month follow up but the rise in the reticulocyte count was much

lower than the expected i.e. from a mean count of 0.7% to 1 %. The mean

increase in hemoglobin was only 2 g% over three months while the

expected rise is about 1 – 2 g% per month8. This was attributed to issues

related to compliance, GI intolerance and also to frequent inter current

infections necessitating temporary iron withdrawal. The studies done by

Maheshwari et al.41 and Huang et al.43 showed that only 78.9% cases

improved with iron indicating that supplementation of a deficient nutrient

may not result in 100% improvement due to multiple confounders.

In summary, in our study we found a major percentage of children

with normocytic normochromic anemia rather than microcytic

hypochromic anemia. These cases, as discussed earlier, are presumably

cases with latent iron deficiency and will probably benefit with oral iron

therapy followed by a meticulous follow up to detect other disorders.

Though, in the formulation of the study design we had treated only

established cases of MHA with iron supplements, the finding of such a

large number of children with NNA, makes us postulate that it would be

ideal to give a trial of oral iron to this group also and then estimate the

response rather than go in for expensive investigations to definitely

establish other causes.

 118

Since the ferritin values were inconclusive in the diagnosis of

anemia, it may not always be useful as a single parameter to either

diagnose or exclude IDA. Probably RDW could have a better diagnostic

value in IDA. Larger studies comparing RDW with anemia are needed in

the future.

LIMITATIONS

1. Sample size should have been larger

2. The group with NNA and NHA could have been given a

therapeutic trial of iron in order to validate our postulate

 119

Conclusion
 120

CONCLUSION

1. In children with IDA, normal or high ferritin level should not

distract the physician away from the diagnosis as co-existing

infection and inflammation may confound the picture.

2. In cases of normocytic, normochromic anemia, S. ferritin levels

can mask a latent iron deficiency. In doubtful cases a therapeutic

trial of oral iron is more cost effective. If red cell and iron indices

do not improve with an adequate trial of iron, it may be worthwhile

to go ahead with more sophisticated and expensive investigations

to find alternate causes.

 121

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 122

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 term_ dur_ timeintrof time_ Fami_
Socst preter breast breastf eed intrcfee V_N worm pagop Giblee Heanem irritab letharg poorsc easyfat breath palpit chest dizzy heada Drugi Ht_ GL Ede Koilon Leuco glossit cheili hepat MC MC RD Plt_co Retic_ TIB Trans Stransf SFerri SB1 SFolica FUHB Ret_
S. N Name age agegr sex ats m fed eed _cm d V infe pica hagia pastinfec d ia ility y perf ig LN ation pain ness che ntake Ht m Wt BMI pallor icterus A ma ychia nychia is tis osp Hb WBC RBC PCV V MCH HC W unt count sIron C feSat errin tin 2 cid ESR CRP PS FOBT 1 ct FUHb2

1 Nithish 1.5 1--5 M 2 T Y 6 1.5 7 NV N N N Vfever N N N N N N N N N N N N 80 0.8 9.3 14.53 Y N N N N N N N N 9.5 9--11 12900 4.36 29.2 67 21.7 32 16.2 2.74 0.5 28.4 414 6.42 442.09 3.9 196 80.31 10 0.69 NNA N

2 Srikanth 7 5--10 M 2 T Y 6 0 6 NV N N N N N N N N N N N N N N N N 108 1.08 17.8 15.26 Y N N N N N N N N 10 9--11 11700 4.42 33.2 75 22.7 30 16.1 2.2 0.8 34.36 310 9.98 344.16 31.9 315 4.67 31 13.08 NNA N

3 Mohammed Firadaus 5 1--5 M 2 T Y 6 17 6 NV Y N N N N N N Y N N N N N N N N 100 1 15 15.00 Y N N N N N N N N 9 7--9 6000 5.24 29.4 56.2 17.7 32 15.6 4.06 0.5 115.6 152 43.25 267.19 131.9 651 15.92 59 1.04 MHA N 10.0 1.0 11.2

4 Sivasakthi 5 1--5 M 2 T Y 1 2 6 NV N N N N N N N N N N N N N N N N 109 1.09 15.2 12.79 Y N N N N N Y Y N 6.6 >=7 7900 3.68 20.2 54.9 17.9 33 21.8 3.61 0.5 7.97 279 2.77 287.46 83.7 347 4.85 12 25.92 MHA N 7.1 0.3 8.8

5 Vaishali 2.5 1--5 F 2 T Y 5 12 5 NV Y Y N N N N N N N N N N N N N N 80 0.8 10 15.63 Y N N N N N N N N 9.6 9--11 6600 4.57 31.1 68 21 31 15.7 3 0.6 53.97 350 13.37 403.56 7.1 325 11.13 9 3.37 NNA N

6 Logesh 1.5 1--5 M 3 T Y 10 12 10 NV N N N N N N Y N N N N N N N N N 80 0.8 10 15.63 Y N N N N N N N N 10 9--11 11001 4032 32.7 75.7 24.9 33 14 3.63 1 87.65 327 21.13 414.88 23.6 937 25.2 31 3.11 NNA N

7 Tharani 2 1--5 F 3 T Y 5 5 9 NV N Y N Walri N N Y N N N N N N N N N 78 0.78 8.3 13.64 Y N N N N N N N N 8 7--9 9000 4.31 25 57.9 18.6 32 19.6 2.79 1 21.75 424 4.88 445.79 25 200 180 43 6.27 MHA N 9.0 1.0 9.5

8 Mohan kumar 5.5 5--10 M 2 T Y 6 8 6 NV N Y N N N N Y Y N N N N N N N N 106 1.06 16.3 14.51 Y N Y N N N Y N N 7.1 7--9 5600 4.63 23.4 50.5 15.4 30 20.1 3.2 2 13.68 443 3.00 456.26 2.7 617 13.74 20 0.5 MHA N 8.8 0.7 10.5

Atypicalfe
9 Dhanshika 2 1--5 F 3 PT Y 6 0 6 NV N N N brileillness N N N N N N N N N N N N 86.5 0.87 10.3 13.77 Y N Y N N N N N N 10.4 9--11 13600 4.74 31.3 66 22 33 18.2 3.6 1 29.31 394 6.92 423.4 37.4 270 11.97 41 6.31 NNA N

10 jayachandiran 2 1--5 M 3 T Y 6 7 6 NV N N N Vfever N N Y N N Y N N N N N N 85 0.85 9.93 13.74 Y N Y N N N N N N 9.8 9--11 9300 4.33 29.7 68.6 22.7 33 14.2 2.79 0.3 92.64 342 21.32 434.42 17.3 274 8.82 15 1.25 NHA P

11 vidharth 2 1--5 M 2 T Y 6 12 6 NV Y N N N N N N N N N N N N N N N 91 0.91 13.6 16.42 Y N N N N N N N N 10 9--11 14400 5.76 38.5 66.8 20.4 31 15.1 2.72 0.1 79.62 410 16.25 490.02 13.7 194 14.78 13 0.24 NHA N

12 varnika 3 1--5 F 2 T Y 6 7 6 NV Y Y N N N N N N N N N N N N N N 90 0.9 13 16.05 Y N N N N N N N N 8.1 7--9 8700 4.77 28.1 59 16.9 29 19.9 2.94 0.6 29.78 387 7.15 416.68 18.4 261 11.32 40 0.73 MHA N 9.1 0.8 9.7

13 Hariharan 2 1--5 M 2 T Y 6 7 7 NV Y N N loosestool N N N N N N N N N N N N 70 0.7 10 20.41 Y N N N N N N N N 10 9--11 27000 4.83 29.2 60.4 20.8 35 16.9 3.13 0.6 49.7 292 14.54 341.9 12 386 11.25 50 10.36 MHA N 9.6 1.4 10.6

14 Sangeetha 8 5--10 F 3 T Y 9 9 9 NV N N N Vfever N N N N N Y N N N N N N 180 1.8 17.8 5.49 Y N Y N N N N N N 9.8 9--11 11300 3.67 28.1 77.4 26.6 34 12 1.69 0.9 78.26 214 26.80 292.06 47 185 17.92 84 14.07 NNA N

15 Masthan 1.5 1--5 M 2 T Y 6 7 7 NV N N N loosestool N N N N N N N N N N N N 78 0.78 8.7 14.30 Y N N N N N N N N 10.2 9--11 15800 5.33 35.2 66 19.1 29 22.7 3.96 0.5 49.44 375 11.64 424.63 10.9 635 10.96 1 0.75 NNA N

16 Santhosh Raj 2 1--5 M 3 T Y 8 9 9 NV Y Y N loosestool N N Y N N N N N N N N N 75 0.75 9.2 16.36 Y N N N N N N N N 7.6 7--9 18600 4.87 25.4 52.2 55.6 30 19.6 4.8 2 20.94 435 4.59 455.81 2.2 269 5.38 10 6.53 MHA N 7.9 1.0 8.5

17 Mohammed haroon 1.4 1--5 M 2 T Y 3 7 3 NV N N N N N N N N Y N N N N N N N 83 0.83 11.5 16.69 Y N N N N N N N N 9.8 9--11 32900 3.63 28.3 77.8 26.9 35 12.5 2.57 1.5 63.81 242 20.90 305.35 20.12 562 12.15 12 27.34 NNA N

18 Keerthirajan 3 1--5 M 2 T Y 5 12 6 NV N N N N N N N N Y N N N N N N N 97 0.97 16.1 17.13 Y N Y N Y N N N N 9.9 9--11 5700 4.13 30.6 74 22.1 30 12.9 2.47 0.8 24.64 306 7.45 330.93 62.8 325 17.24 62 9.88 NNA N

19 Rithikagowda 2.9 1--5 F 2 T Y 1 2 6 NV Y N N N N N N N N N N N N N N N 92 0.92 11.4 13.47 Y N Y N N N N N N 10.8 9--11 23600 4.59 32.1 70 23.5 34 15.3 2.65 1 16.93 299 5.36 315.73 76.1 315 17.04 28 77.19 NNA N

20 jonathan samuel 1 1--5 M 2 T Y 6 0 7 NV N N N UTI N N N Y N N N N N N N N 75 0.75 8.48 15.08 Y N N N N N N N N 9 7--9 13800 4.22 21.3 64.6 21.3 33 14 6.8 0.6 20.38 429 4.53 449.76 16.9 211 22.43 68 57.03 NNA N

21 Gokulnath 2 1--5 M 2 T Y 3 4 6 NV N N N N N N N N N N N N N N N N 87 0.87 11.1 14.67 Y N Y N N N N N N 8.8 7--9 11800 4.29 26.5 61.8 20.5 33 17.6 2.75 0.4 20.99 301 6.52 321.99 65 325 17.82 25 224.47 NHA N

22 Chandreleka 2 1--5 F 3 T Y 8 9 10 NV N N N N N N N N N N N N N N N N 84 0.84 9.7 13.75 Y N Y N N N N N N 10 9--11 14500 4.64 31.2 67.1 22.9 34 19.4 5.82 1 47.94 440 9.83 487.89 48 173 13.68 8 0.27 NNA N

23 Goutam 9 5--10 M 2 T Y 4 8 4 NV Y N N N N N N N Y Y N N N N N N 120 1.2 25.8 17.92 Y N N N N N N N N 9.6 9--11 13400 4.46 29.3 65.7 21.6 33 12.1 4.86 0.6 14.77 433 3.30 447.77 3.7 483 5.27 21 1.25 NHA N

24 Harini 1.6 1--5 F 2 T Y 6 6 7 NV N Y N N N N N Y N N N N N N N N 71 0.71 7.12 14.12 Y N N N N Y N N N 8.1 7--9 12900 4.71 28.2 59.9 17.3 29 15.3 5.5 1 22.07 526 4.03 548.07 2.12 275 9.75 12 3 MHA N 9.2 0.8 10.0

25 Roshan 1 1--5 M 3 T Y 6 0 6 NV N N N N N N N N N N N N N N N N 70 0.7 8.6 17.55 Y N N N N N N N N 8.9 7--9 11100 3.67 26.7 72.8 24.3 33 12.9 3.5 5 54.38 386 12.34 440.57 2.19 492 17.82 11 0.44 MHA N 10.6 1.0 11.9

26 Govardha harini 2.5 1--5 F 2 T Y 0.1 5 6 NV Y Y N N N N Y N N Y N N N N N N 94 0.94 12.7 14.37 Y N N N N N N N N 8.6 7--9 13300 4.81 27.6 57.3 18.7 33 15.5 3.6 1 34.47 543 5.97 577.73 75 512 14.04 28 0.13 MHA N 10.8 0.8 11.9

27 Yuvashree 4 1--5 F 2 T Y 6 8 6 NV Y N N Vfever N N Y Y Y N N N N N N N 93 0.93 10.7 12.37 Y N Y N Y N N N N 9 7--9 11400 4.96 27.9 56.3 18.3 32 22.4 4.05 1 28.84 406 6.63 434.83 52 522 15.5 25 3.45 MHA N 10.5 0.6 11.8

28 Varshini 6 5--10 F 2 PT Y 2 2 6 NV Y N N Vfever N N Y Y Y N N N N N N N 102 1.02 14.4 13.84 Y N Y N N Y Y Y N 8.7 7--9 6500 3.91 26.9 68.9 22.4 32 27.5 2.2 0.5 155.4 46.5 76.96 201.96 220.1 317 5.16 100 15.84 MHA N 9.0 0.6 9.4

29 Elavarasan 3 1--5 M 3 PT Y 0.6 0.6 5 NV N N N N N N Y Y N Y N N N N N N 95 0.95 12.3 13.63 Y N N N N N Y Y N 7.3 7--9 16500 5.09 24.4 47.9 14.3 30 20.1 3.43 1 31.3 454 6.45 485.6 4.5 915 12 20 10 NNA N

30 Yokesh 2 1--5 M 2 T Y 4 7 4.5 NV Y Y N N N N N Y N Y N N N N N N 78 0.78 11.5 18.90 Y N N N N Y N N N 10.9 9--11 7400 5.8 33.3 57.3 18.7 33 21.6 2.22 0.9 51.48 263 16.40 313.98 200.5 431 25.2 13 5.5 NNA N

31 maharaj 10 5--10 M 2 T Y 6 0 7 NV Y N N N N N N Y N Y Y N N N N N 127 1.27 30 18.60 Y N N N Y Y N N N 7.8 7--9 6300 4.44 27.5 62 20.1 32 27.3 5.5 1.6 41.64 415 9.12 456.44 21.1 559 25.2 25 6 NNA N

32 Thrishika 1.5 1--5 F 2 T Y 3 4 5 v Y N N N N N Y Y N N N N N N N N 81 0.81 9 13.72 Y N N N Y Y N N N 6.7 >=7 9500 4.5 22.3 49.3 14.7 30 22.1 3.12 0.4 26.5 516 4.88 542.9 103 586 7.91 10 0.34 MHA N N N N

33 Suriya varman 1 1--5 M 2 T Y 6 0 7 V N N N Vfever N N N N N N N N N N N N 68 0.68 7.45 16.11 Y N N N N N Y Y N 9.1 9--11 7300 3.87 27.8 72 23.6 33 16 2.22 0.8 33.75 308 9.89 341.25 199.3 463 13.42 35 1.38 NNA N

34 Divesh 1 1--5 M 2 T Y 1.5 1.5 7 NV N Y N Dysentery N N N N N N N N N N N N 77 0.77 8.65 14.59 Y N N N N N N N N 7.8 7--9 12600 4.01 26.5 66 19.4 29 17.5 3.16 1 22 269 7.56 291.1 37.8 786 13.06 4 26.27 MHA N 9.4 1.0 11.5

35 Pramila 6 5--10 F 3 T Y 2.5 0 3 V Y N N Vfever N N Y N N N N N N N N N 100 1 16 16.00 Y N N N N N N N N 10.2 9--11 11800 4.03 31.2 77 25.2 33 11 2 0.4 25.12 248 9.20 273.02 52 425 4.25 37 63.71 NNA N

36 Jayashree 10 5--10 F 3 T Y 6 6 6 NV Y Y Y N N N N N Y Y N N N N N N 131 1.31 27 15.73 Y N N N N N N N N 10.6 9--11 10500 4.06 32 79 26.2 33 12 3.02 1 83.56 269 23.68 352.86 59.3 343 5.58 28 1.38 NNA N

37 Swetha 9 5--10 F 2 T Y 3.5 0 5 NV N N N N N N N Y Y Y Y N N Y Y N 138 1.38 33.2 17.43 Y N N N Y N N N N 10.7 9--11 7300 3.89 33.1 85 27.6 32 10.2 2.18 0.4 100.8 242 29.37 343.2 22 629 11.54 6 0.21 NNA N

Hypocalce
38 Deenaprasandan 1 1--5 M 2 PT Y 5 7 5 NV N N N micseizures N N N N N N N N N N N N 72 0.72 7.5 14.47 Y N N N N N N N N 8.4 7--9 20000 4.51 28.6 63 18.7 30 12 4.68 0.8 34.79 328 9.60 362.49 115.2 540 20.31 76 320.3 MHA N 9.6 0.6 11.5

39 Praveen 8 5--10 M 3 T Y 6 6 6 NV N N N N N N N N N Y N N N N N N 122 1.22 19.3 12.97 Y N N N N N N N N 10.6 9--11 11600 4.46 30.8 69.1 23.7 34 12.8 6.51 0.8 49.74 302 14.13 352.04 69.4 941 3.23 12 10 NNA N

bronchopne
40 Sairam 3 1--5 M 2 T Y 6 6 6 V N Y N umonia N N N Y N Y N N N N N N 90 0.9 10 12.35 Y N N N Y N N N N 10.3 9--11 8300 3.61 29.1 80.5 28.4 35 13.1 2.72 0.8 102.2 195 34.35 297.62 25 242 12.8 13 10 NNA N

41 Nilson 9 5--10 M 3 PT Y 3 4 5 NV Y N Y N N N N N N N N N N N N N 121 1.21 18.7 12.77 Y N Y N N N N N N 9.6 9--11 7200 4.11 29.1 70.8 23.3 33 16 4.09 0.8 36.53 266 12.08 302.43 45.7 965 3.24 94 32.88 NNA N

42 Jaitheeasri 1.5 1--5 F 2 T Y 3 4 5 NV N N N UTI N N N Y N Y N N N N N N 80 0.8 10 15.63 Y N N N N Y N N N 5.9 >=7 10500 3.19 18.4 58 18.5 32 11 6.88 0.4 47.76 365 11.57 412.96 11.6 451 9.53 74 10.87 MHA N 8.3 0.3 9.0

Atypicalfeb
43 kamesh 1 1--5 M 2 T Y 6 0 7 NV N N N rileillness N N N N N N N N N N N N 79 0.79 10.4 16.66 Y N Y N N N Y N N 8.4 7--9 7300 4.5 28 62 18.6 30 18.2 1.13 0.1 17.47 441 3.81 458.07 6.1 296 6.24 19 19.71 MHA N 8.9 0.5 10.2

44 Monish 4 1--5 M 3 T Y 5 7 5.5 V Y N N N N N N N N N N N N N N N 93 0.93 11.5 13.26 Y N N N N N N N N 10.8 9--11 12200 4.15 31.8 76.6 26.1 34 14.2 3.25 2.2 50.64 343 12.85 393.94 18.2 524 17.55 17 1.44 NNA N
Bronchiolit
45 Gracy 6 5--10 F 2 T Y 6 6 7 NV Y N N s N N N N N N N N N N N N 100 1 11.7 11.70 Y N N N N N N N N 9.6 9--11 13800 4.05 30.8 76 23.8 31 11 3.47 0.4 16.78 267 5.91 283.98 113.4 482 14.55 39 11 NHA N

46 Tamilselvan 10 5--10 M 3 T Y 6 12 6 NV Y Y N N N N N N N N N N N N N N 121 1.21 18.6 12.70 Y N N N N N N N N 8.1 7--9 7900 4.78 26.7 55.8 17 30 18.9 3.45 0.8 46.73 417 10.08 463.42 1.6 ### 8.46 24 0.43 NHA N

47 Naveen 5 1--5 M 2 T Y 5 12 5.5 V Y Y N Walri N N Y Y Y N N N N N N N 108 1.08 16.9 14.63 Y N N N N N N N N 10.3 9--11 11800 4.38 35.4 80.9 28 35 13 3.25 1.6 33.12 363 8.37 395.72 42 392 12.5 49 11.57 NNA N

48 Nikilesh 3 1--5 M 2 T Y 5 6 5 NV Y Y N N N N N N N Y N N N N N N 94 0.94 13 14.71 Y N Y N N N N N N 8 7--9 4000 4.26 24.1 56.6 18 32 11 1.55 0.7 13.02 430 2.94 443.12 10.1 366 17.14 7 5 MHA N 9.1 0.8 10.1

49 Kalaiselvi 2 1--5 F 2 T Y 9 0 9 NV N N N N N N Y Y N Y N N N N N N 78 0.78 7.2 11.83 Y N N N Y Y N Y Y 8.4 7--9 11200 4.31 26.6 61.7 19.5 32 18.4 3.05 0.8 14.77 435 3.28 449.77 194 ### 6.35 23 90 MHA P 9.5 1.0 11.2

Atypicalfeb
50 Jayan 2 1--5 M 2 T Y 1 2 5 NV N N N rileillness N N N N N N N N N N N N 79.5 0.8 9 14.24 Y N N N N N N N N 10.5 9--11 7300 5.13 31.8 62 20.4 33 17.2 4.59 1 15.49 361 4.12 376.19 50 512 10.42 20 1.84 NNA N

51 Saran 10 5--10 M 2 PT Y 6 10 6 V N N N N N N N N N N N N N N N N 70 0.7 6.87 14.02 Y N N N N N N N N 9.2 9--11 22700 4.57 32.6 71.4 24.2 34 14.3 6.75 1.5 55.85 423 11.67 478.63 10.1 130 17.34 11 0.31 NNA P

bronchopne
52 Dharun 2 1--5 M 2 PT Y 7 0 7 V Y N N umonia N N N N N N N N N N N N 82 0.82 8.3 12.34 Y N N N N N N N N 7.3 7--9 4500 3.2 24.1 75 22.7 30 19.1 14 0.2 14.42 240 5.67 254.12 11.1 575 12.21 80 27.59 NNA N

53 Rukesh 4 1--5 M 2 T Y 7 12 7 NV N Y N N N N N Y N Y N N N N N N 98.8 0.99 14 14.34 Y N Y N N Y N N N 10.1 9--11 12600 4.45 32.3 73 22.6 31 11.2 1.76 0.4 66.27 401 14.18 467.47 15.8 594 12.61 112 0.18 NNA N

54 Yuvaraj 9 5--10 M 2 T Y 6 0 6 NV N N N N N N N N N N N N N N N N 118 1.18 18.1 13.00 Y N N N N N N N N 9.8 9--11 5900 4.14 31.4 76 26.4 35 12.7 21.3 0.8 36.22 270 11.84 305.92 56 587 8.96 23 14.7 NNA N

55 Anisha 1 1--5 F 2 T Y 5 5.5 5 V Y N N N N N N Y N Y N N N N N N 78 0.78 8.6 14.14 Y N N N N N N N N 10 9--11 12300 4.26 30.6 71.8 23.4 33 10.8 3.4 0.7 42.93 354 10.83 396.53 8.12 350 15.26 9 5.5 MHA N 10.5 0.2 11.8
56 Saranya 10 5--10 F 4 T Y 6 0 9 NV Y N N Vfever Y N N N N N N N Y N N N 146 1.46 30 14.07 Y N N N N Y N N N 10.8 9--11 8400 4 31.3 78.2 26.9 34 14 2.91 0.9 96.39 301 24.26 397.39 42 482 15.15 11 5 NNA N

57 Yokeshwari 9 5--10 F 2 T Y 5 5 5 NV Y N N N N N N Y N Y Y Y Y Y Y Y 126 1.26 24 15.12 Y N Y N Y Y N N N 7.8 7--9 4800 2.88 22.7 79 27.3 35 18.9 4.44 0.4 44.81 194 18.75 239.01 25 161 16.5 4 5.3 MHA N 9.1 1.0 9.8

58 Krish sudharsan 6 5--10 M 2 T Y 6 0 6 NV Y N N N N N N Y N Y N N N N N N 107 1.07 14 12.14 Y N N N N N N N N 9.8 9--11 27200 3.62 29.6 81.9 26.9 33 13.7 2.46 0.8 52.16 251 17.20 303.26 32 738 17.82 31 14.8 NNA N

59 Johnjonathan 5 1--5 M 2 T Y 6 7 6 NV N Y Y N N N Y Y N Y N N N N N N 101 1.01 14.5 14.21 Y N Y N Y N N N Y 10.3 9--11 9300 4.36 33.9 78 23.7 31 12.2 3.07 0.6 62.23 292 17.55 354.49 139 760 6.1 29 12 NNA N

60 Prince Bhavya 5 1--5 F 1 T Y 1 2 6 V N N N N N N N Y N N N N N N N N 90 0.9 24 29.63 Y N N N N N N N N 10 9--11 5900 4.9 34.2 70 20.4 29 16.8 2.52 0.8 67.08 370 15.36 436.78 35.1 523 4.42 10 5.3 NNA N
Denguefeve
61 Kamaleshwaran 1.5 1--5 M 2 T Y 2 3 4 NV N N N r N N N N N N Y N N N N N 79 0.79 11 17.63 Y N N N N N N Y N 10.1 9--11 9700 4.37 33.4 76 23.2 30 11.4 1.25 1.6 34 287 10.61 320.6 12 452 12.32 22 40.7 NNA N

62 Ritesh 1 1--5 M 2 T Y 5 7 5 NV N N N N N N N N N N N N N N N N 73 0.73 8.5 15.95 Y N N N N Y N Y N 10.5 9--11 10600 4.74 31.7 67 22.7 34 16.1 5.1 0.5 52.76 534 9.00 586.47 86.9 217 12.37 27 2.21 NHA N

63 Yona 5 1--5 F 2 T Y 4 4 6 NV N N N N N N N N Y Y N N N N N N 110 1.1 15 12.40 Y N Y N Y Y N N N 10.5 9--11 6900 4.43 33.4 75.4 24 32 16.2 4.33 0.6 32.99 284 10.39 317.39 29.4 188 18.53 43 12 NNA N

64 Mithra 1 1--5 F 2 T Y 4 4 4 NV N Y N N N N N N N N N N N N N N 67 0.67 7.2 16.04 Y N N N Y Y N N N 10 9--11 17000 3.8 30.9 81.3 26.6 33 13.5 63.02 1.1 52.7 169 23.74 222 32 234 17.82 11 26.3 NNA N

65 Kabilesh 4 1--5 M 2 T Y 5 5 6 V N Y N N N N N N N N N N N N N N 94 0.94 12 13.58 Y N N N Y Y N N N 10.4 9--11 9200 4.84 32.1 66.2 21.5 32 17.6 3.26 0.4 37.74 353 9.66 390.54 9.5 455 18.92 21 12 MHA N 10.8 0.5 12.0

Developme
66 Mahalakshmi 10 5--10 F 2 T Y 5 6 5 V Y N N ntal delay N N Y N Y N N N N N N N 127 1.27 21 13.02 Y N N N Y Y N N N 6.4 >=7 5100 2.52 21.1 84 25.4 30 13.2 2.82 0.81 65.1 289 18.37 354.4 35.12 396 8.63 33 5.5 NNA N

67 Prabhu 10 5--10 M 2 T Y 3 0 3 NV N Y Y N N N N Y Y N N N N N N N 138 1.38 20 10.50 Y N N N N N N Y N 9.7 9--11 4200 4.66 33.7 72.4 20.8 29 14.2 1.43 0.9 53.11 235 18.45 287.81 554 352 7.19 67 75.8 NHA N

68 Haroon raship 3 1--5 M 2 T Y 6 6 6 NV Y N N Malaria N N N Y N Y N N N N N N 89 0.89 10.4 13.13 Y N N N N Y N N N 9.2 9--11 7800 5.73 35 60.1 16 27 12.2 2.92 0.5 24.18 395 5.77 419.18 98 572 7.5 18 12.9 MHA N 9.0 2.0 10.2

69 Hariharan 1 1--5 M 3 T Y 1 3 8 V N N N N N N Y Y N N N N N N N N 78 0.78 8.5 13.97 Y N N N N N N N N 8.3 7--9 7300 4.25 27.6 65 19.5 30 15.3 1.91 0.5 27.78 405 6.42 432.58 12.95 356 19.5 31 5.8 MHA N 8.9 2.0 9.7

70 Karthik 10 5--10 M 3 T Y 5 7 5 NV N N N N N N N N N N N N N N N N 135 1.35 30 16.46 Y N N N N N N N N 10.8 9--11 7300 4.54 38.4 84.5 24 28 11.7 3.36 0.8 74.53 246 23.27 320.23 18.2 452 13.15 27 5 NNA N

simplefebril
71 Harish kumar 3 1--5 M 2 T Y 3 3 7 NV Y Y N eseizures N N N N N N N N N N N N 86.5 0.87 10.5 14.03 Y N Y N N Y N N N 8.5 7--9 15800 4.73 28 61 17.9 29 10.2 2.5 0.89 35.37 453 7.24 488.67 9.1 473 11.66 63 9.6 MHA N N N N
Appendicec
72 Bharathkumar 9 5--10 M 2 T Y 6 6 6 NV Y N N tomy N N N N Y N N N N N N N 135 1.35 30 16.46 Y N N N N N N N N 10.3 9--11 6000 4.33 34.2 78.9 23.7 30 12.2 2.87 0.9 69.81 262 21.02 332.11 66.3 253 4.72 55 9.9 NNA N

73 Deepak 10 5--10 M 2 T Y 3 4 6 NV N N N N N N N Y N Y N N N N N N 127 1.27 25.3 15.67 Y N N N N N N N N 10.7 9--11 13100 4.88 37.8 77.5 22 82 13.4 2.52 0.5 53.92 371 12.69 425.02 15.9 453 983 9 6.6 NHA N

74 Dharshini 8 5--10 F 3 PT Y 5 11 5 NV N N Y Vfever N N N N N N N N N N N N 115 1.15 19 14.37 Y N N N N Y N N N 10 9--11 6000 4.84 35.4 73.2 20.7 28 13.9 2.24 0.5 70.64 320 18.07 390.94 55.5 711 6.68 21 30.8 NNA N

75 Joaatha leoma 3 1--5 F 2 T Y 4 5 3 NV Y N N N N N N Y N N N N N N N N 85 0.85 8.4 11.63 Y N Y N Y N N N N 9.2 9--11 9800 4.32 32.4 75 21.4 28 14 2.5 1.2 36.62 233 13.56 270.02 1010 724 25.2 50 43.2 NNA N

76 Sandhya 6 5--10 F 2 T Y 6 8 6 NV Y N N N N N N N Y Y Y N N N N N 123 1.23 39.3 25.89 Y N N N N N N N N 10.3 9--11 1300 5.16 40.8 79 23.9 30 12.2 4 1.1 68.71 341 16.75 410.11 25.1 343 7.72 18 8.4 NNA N

77 Emancy 2 1--5 F 2 T Y 5 10 5.5 NV Y N N N N N Y Y N Y N N N N N N 80.7 0.81 9.6 14.74 Y N N N Y N N N Y 9.4 9--11 12200 4.39 32.5 73.9 21.4 29 13.4 6.19 0.8 39.35 308 11.34 346.85 25.2 285 11.45 61 20.7 MHA N 10.6 0.8 11.2

78 Bharathkumar 2 1--5 M 2 T Y 6 24 6 NV N N N N N N N Y N Y N N N N N N 79 0.79 8.5 13.62 Y N N N Y Y N N N 9.8 9--11 12900 4.5 32.2 68.1 20.8 31 17.4 4.16 0.6 33.47 292 10.28 325.67 58 505 12.5 44 90 MHA N 10.2 1.0 11.5

79 Priyanka 10 5--10 F 2 T N 0.5 1 3 NV Y Y N Vfever N N N N Y Y N N N N N N 136 1.36 24 12.98 Y N N N N N N N N 10.5 9--11 9800 4.04 35 8.7 25.9 30 12.1 1.95 0.7 56.99 337 14.46 393.99 28.2 227 12.5 5 5 NNA N

80 Sai sugeesh 1 1--5 M 2 T Y 6 6 6 NV N Y N N N N N N N N N N N N N N 67 0.67 8.3 18.49 Y N N N Y N N N N 9 7--9 8300 4.39 28.9 65.7 20.5 31 14.8 6.43 0.5 34.17 390 8.07 423.67 52 422 12.5 22 9.8 MHA N 10.8 0.2 11.6

81 Thrisha 1 1--5 F 2 T Y 5 0 5 NV N Y N N N N N N N N N N N N N N 75 0.75 7 12.44 Y N N N Y Y N N N 10.7 9--11 10800 4.42 35 79 24.1 31 14.4 2.9 0.6 52.95 221 19.30 274.35 65 425 12.5 25 14 NNA N

82 Litheeswaran 4.5 1--5 M 2 T Y 4 4 4 NV N Y Y N N N Y Y Y N N N N N N N 108 1.08 17.5 15.00 Y N Y N Y Y N N N 10.4 9--11 12800 4.53 34.5 76 23 30 13.9 4.5 0.8 20.14 335 5.67 355.14 45.8 222 12.89 63 18 NNA N

83 B/O Kalavathy 1 1--5 M 2 T Y 3 3 6 NV Y N N N N N N N N N N N N N N N 75 0.75 9.5 16.89 Y N N N N N N N N 7.7 7--9 9800 3.9 23.5 63.7 19.7 31 12.8 6.03 1.75 31.92 320 9.07 351.95 31.9 293 22 12 2.1 MHA N 8.2 2.0 8.6

84 Bharathy 2 1--5 M 2 T Y 7 8 7 NV Y N N N Y N Y Y N Y N N N N N N 93 0.93 11.4 13.18 Y N Y N N N N N N 10 9--11 10500 4.25 34.2 80.6 23.9 30 13.9 4.26 0.8 68.67 275 19.96 343.97 32.5 572 18.25 30 10.3 NNA N

85 Abishek 1 1--5 M 3 PT Y 6 7 6 V N N N N N N N N N N N N N N N N 67 0.67 6 13.37 Y N N N N N N N Y 9.3 9--11 6800 4.97 32.4 65 18.7 29 16.5 2.68 0.5 25.97 591 4.21 616.97 7.86 756 20.24 35 22 MHA N 9.8 0.5 11.0

86 Thanigaivel 1.5 1--5 M 2 PT Y 3 3 5 V Y N N N N N Y Y N Y N N N N N N 84.5 0.85 9.6 13.44 Y N N N Y Y N N N 6.6 >=7 12200 5.94 25.6 43 11.2 26 16.9 6.5 0.3 19.38 482 3.87 500.98 15.1 678 21.18 4 10 MHA N 5.7 1.2 7.2

87 Prashanth 6 5--10 M 3 T Y 3 0 3 V N N N Tb abd Y Y Y Y N N N N N N N N 108 1.08 13.7 11.75 Y N Y N Y Y N Y N 10.1 9--11 4900 4.51 33.6 74 22.3 30 16.9 1.48 0.6 71.28 261 21.45 332.38 36 476 16.75 14 50.5 NHA N

88 Pushpak 5 1--5 M 3 T Y 6 6 12 NV Y N N N N N N N Y N N N N N N N 103 1.03 16 15.08 Y N Y N Y Y N N Y 10.8 9--11 9500 4.16 33.2 79.7 25.9 33 13.6 1.86 1.5 35.4 222 13.73 257.82 131.8 452 21.9 21 24.4 NNA N

89 Deepika 10 5--10 F 2 T Y 1 1 3 NV Y N N N N N N Y N Y N N N N N N 148 1.48 27.5 12.55 Y N N N N N Y N Y 10.3 9--11 8000 4.32 36.5 84.5 23.8 28 12.4 2.24 1.2 12.83 254 4.81 266.93 1139 772 13.35 12 90 NNA N
Seizure
90 Sanjay 3 1--5 M 3 T Y 1 2 6 NV N N N disorder N N Y Y N N N N N N N N 106 1.06 16 14.24 Y N N N N Y N N N 10.2 9--11 7000 4.32 38.5 84.5 28.8 29 10.4 2.16 0.5 56.4 386 12.74 442.6 13.1 375 10.9 8 24 NNA N

bronchopne
91 Vishal 6 5--10 M 3 T Y 4 5.5 4 NV N Y N umonia N N Y Y Y N N N N N N N 104 1.04 14.8 13.68 Y N N N N Y N N N 9.8 9--11 11400 4.02 31.9 79 24.4 31 12.4 4.96 0.9 47.6 264 15.27 311.8 37 684 6.33 11 21 NNA N

simplefebril
92 Vimalraj 3 1--5 M 4 PT Y 1 1 8 NV Y Y N eseizures N N Y Y N Y N N N N N N 81 0.81 8.2 12.50 Y N N N N Y Y Y N 10.8 9--11 9600 4.52 36.4 80 24.1 30 12 2.97 0.7 24.87 293 7.83 317.67 51.3 492 11.85 22 58.9 NNA N

93 Kamalesh 10 5--10 M 3 T Y 8 12 8 NV N Y Y N N N Y Y N Y N N N N N N 135 1.35 22.5 12.35 Y N Y N Y Y N N N 6.2 >=7 10000 3.77 20.4 56.6 16.2 29 20.7 3.97 1 15.14 412 3.54 427.14 66 452 13.8 18 0.28 MHA N 5.3 1.4 9.3

94 Elavarasan 3 1--5 M 3 PT Y 8 9 8 NV N N N N N N Y N N N N N N N N N 105 1.05 12.3 11.16 Y N N N N N Y Y N 7.3 7--9 16500 5.09 24.4 47.9 14.3 29 20.1 2.43 0.8 31.3 455 6.44 485.8 4.5 915 12 10 7 MHA N 8.0 2.0 9.1

95 Rithika 2.5 1--5 F 2 T Y 8 8 8 NV N N N N N Y N Y N N N N N N N N 76 0.76 11.3 19.56 Y N N N N N N Y N 9.2 9--11 14500 4.46 29.7 6.7 19.6 30 12.8 3.19 0.5 22 408 5.12 429.9 65 452 14.2 15 4 MHA N 9.8 1.0 11.5

96 Maana sree 1 1--5 F 2 T Y 6 0 6 NV N N N N N N N N N N N N N N N N 73 0.73 7.6 14.26 Y N Y N Y N N N N 8.7 7--9 18600 4.39 28 64 19.7 31 13.1 2.9 0.6 23.41 440 5.05 463.11 72 522 13.04 12 6.5 MHA N 9.6 1.0 10.5

97 Ranjith 1.5 1--5 M 2 T Y 7 12 7 NV N N N Vfever N N N N N N N N N N N N 85 0.85 9.1 12.60 Y N N N N N N N N 7.9 7--9 8200 4.52 27.2 65 22.2 28 13.4 4.3 0.6 27 452 5.64 479 10 652 20.2 6 12 MHA N 9.4 2.0 11.5

98 Harini 10 5--10 F 2 T Y 4 4 6 NV Y Y N N N N N N Y Y N N N N N N 132 1.32 25.6 14.69 Y N N N N N Y Y N 9.8 9--11 8900 4.46 29.2 65.5 21.9 33 16.5 3.26 0.8 15.8 380 3.99 395.5 2.8 743 5.4 21 0.13 MHA N 11.6 0.8 12.0

99 Monika 1 1--5 F 3 T Y 6 6 6 NV Y N N N N N N N N N N N N N N N 94 0.94 8.4 9.51 Y N N N N N N N N 9.7 9--11 11500 4.2 28.5 67.9 23 34 15.4 3.44 0.7 31.46 412 7.09 443.46 57.8 228 9.29 22 4.02 NNA N

100 Jagatheesh 2 1--5 M 2 T Y 3 3 7 NV Y N N Vfever Y Y N Y N N N N N N N N 91 0.91 14 16.91 Y N N N N N N N N 10.4 9--11 10000 4.8 34.2 75.4 21.6 29 16 3.2 0.7 56.12 390 12.59 445.62 28.1 695 10.72 2 12 NNA N

101 Mahathi 1.5 1--5 F 2 T Y 6 6 6 NV N N N Vfever N N N N N N N N N N N N 76 0.76 7.8 13.50 Y N N N Y Y N N N 10.8 9--11 15500 4.69 37.7 80 23.3 29 12 1.87 0.8 48 317 13.16 364.7 33.4 625 11.83 19 9.4 NNA N

102 Sasikumar 2 1--5 M 3 T Y 4 4 4 NV N Y N N N N N N N N N N N N N N 127 1.27 25.3 15.67 Y N N N Y Y N N N 5 >=7 8600 3.47 16 46 11.6 25 12.2 4.28 1.1 17.13 500 3.32 516.63 2.9 834 6.29 9 5 MHA N 6.7 2.0 7.5

simplefebril
103 Shanthi 10 5--10 F 3 T Y 0 1 5 NV N N N eseizures Y N N Y Y N N N N N N N 118 1.18 25.5 18.31 Y N N N Y N N N N 10.1 9--11 8000 3.75 32.9 88.8 26.8 31 11.5 1.46 1.7 110.4 120 47.95 230.34 54.5 505 4.54 23 5 NNA N

104 Karthikrraj 10 5--10 M 2 T Y 6 0 6 NV Y Y N N N N N Y N Y N N N N N N 142 1.42 33.6 16.66 Y N N N N N N N N 9 7--9 10500 3.76 29.9 80 23.9 30 12.8 3.3 0.4 39.27 243 13.93 281.87 132.8 325 3.47 85 32.3 NNA N

105 Shamini 2 1--5 F 3 T Y 5 6 5 NV Y N N N N N Y Y N Y N N N N N N 78 0.78 9 14.79 Y N N N Y Y N N Y 8.2 7--9 11100 4.2 27.9 66 19.5 29 12.5 2.5 1.1 20.36 380 5.09 400.06 18.6 485 7.59 15 12.3 NHA N

106 Bhakyalakshmi 8 5--10 F 2 T Y 5 5 5 NV Y N N N N N N Y Y Y N N N N N N 122 1.22 18.6 12.50 Y N N N Y N N N N 10.8 9--11 9700 4.76 40.6 85 26.1 31 12.8 3.98 0.4 80.74 350 18.74 430.74 28.7 247 4.76 12 6.6 NNA N

107 Swathi 8 5--10 F 2 T Y 5 5 5 NV N N N N N N N Y Y N Y N N N N N 122 1.22 24.5 16.46 Y N N N N Y N N N 10.5 9--11 6700 4.75 37.9 80 24.2 30 14 3.8 0.8 90.2 218 29.25 308.4 30.3 476 8.9 9 5 NNA N

108 Suryaprakash 8 5--10 M 3 T Y 3 0 3 NV Y Y N N N N N Y N Y N N N N N N 124 1.24 20 13.01 Y N Y N N N N N N 10.4 9--11 4300 4.41 34.1 77 23.7 31 12.6 1.82 0.9 80.45 233 25.63 313.85 55 321 12.4 5 5.3 NNA N

109 Sivasubavishnu 2 1--5 M 3 T Y 5 0 5 NV N N N N N N Y Y N N N N N N N N 80 0.8 9 14.06 Y N N N N N N N N 9.2 9--11 6900 3.92 29.3 74 23.1 31 11.2 2.67 0.8 28.73 341 7.78 369.43 25.2 267 14.8 12 19.5 NHA N

110 Rabitha 10 5--10 F 3 T Y 4 0 4 NV Y N N N N N N Y N N N N N N N N 131 1.31 33.6 19.58 Y N N N N Y N N N 10.5 9--11 8300 4.78 35.2 73.6 24.8 34 14.6 3.1 1 57.24 439 11.54 495.91 4.4 274 7.96 12 0.28 NNA N

111 Dhanyasree 1.5 1--5 F 2 T Y 6 18 6 NV N Y N N N N Y N N Y N N N N N N 83 0.83 9.6 13.94 Y N N N Y Y N N N 10.2 9--11 10400 4.25 32.1 75.5 24 32 17.1 5.2 0.6 45.76 306 13.02 351.36 31.1 431 14.52 5 6 NNA N

112 Vidyut 2 1--5 M 2 T Y 7 12 7 V Y Y Y N N N N N N N N N N N N N 84 0.84 18.2 25.79 Y N N N N N N N N 9.2 9--11 5800 3.9 28.4 73 23.5 32 11.2 2.95 0.5 32 410 7.24 442 23.1 156 13.79 11 6.77 MHA N 10.6 0.5 11.8

113 Mithun 4 1--5 M 2 T Y 3 3 3 V N Y Y N N N N Y N Y Y N N N N N 103 1.03 15.9 14.99 Y N N N Y N N N N 6.5 >=7 16400 5.45 24.7 45 12 27 16.2 5.75 1.8 10.1 587 1.69 597.1 2.6 461 12.21 15 1.58 MHA N 7.8 1.0 10.2

114 Samreen fathima 5.5 5--10 F 2 T Y 1 1 12 NV Y Y N N N N N Y N Y N N N N N N 102 1.02 16 15.38 Y N N N Y Y N N N 9.1 9--11 8300 5.6 29.5 52.7 16.2 31 16.7 2.36 5 74.35 259 22.32 333.11 39.9 670 12.39 11 0.22 MHA N 10.6 0.8 12.1
115 Divakar 6 5--10 M 3 T Y 4 4 6 V N Y Y N N N N Y N Y N N N Y Y N 112 1.12 17.8 14.16 Y N N N Y N N N N 10 9--11 11100 4.41 30.6 69.4 22.8 33 15.4 3.44 0.8 20.11 382 5.00 402.01 4.5 436 8.15 17 0.43 MHA N 10.4 0.5 11.7

116 Keerthirajan 7 5--10 F 2 T Y 4 6 4 NV Y N Y N N N N Y Y Y N N N N N N 108 1.08 18 15.43 Y N N N N N Y Y N 10.6 9--11 6500 4.29 34.3 80 24.7 31 12.9 2.33 1 50.21 428 10.50 478.21 8.2 172 28.2 14 18 NNA N

117 Subramani 10 5--10 M 3 T Y 10 0 11 NV N Y N N N N Y Y N Y Y N N N Y N 131 1.31 24.3 14.16 Y N N N Y Y N N N 4.7 >=7 5800 3.88 18.2 46.8 12 26 26.1 3.5 0.9 19.43 486 3.84 505.66 1.3 295 13.3 41 0.25 MHA N 10.5 1.3 11.9

118 Santhosh 5 1--5 M 2 T Y 6 12 6 V Y Y N N N N N Y N N N N N N N N 110 1.1 18.4 15.17 Y N N N N N N N N 10 9--11 12800 4.75 30.1 63 18.9 298 18 5.25 0.5 26.17 457 5.41 483.53 19 595 16.75 7 1.78 MHA N 7.4 1.2 8.0

119 Pradeep 3.5 1--5 M 2 T Y 5 6 5.5 NV Y Y N N N N N N N Y N N N N N N 95.5 0.96 11.5 12.61 Y N N N Y N Y Y N 8.6 7--9 13000 4.42 26.3 59.5 19.4 33 16.6 3.13 1 38.2 384 9.05 422.2 12 482 14.8 12 6 NNA N

120 Narendar 5 1--5 M 2 T Y 6 6 7 V N Y Y Vfever N N N N Y Y N N N N N N 101 1.01 14 13.72 Y N Y N N N Y N Y 10 9--11 5400 3.61 29 80.4 27.4 34 12.2 3.66 1 57.82 272 17.54 329.62 483 380 17.25 55 12 NNA N

121 Sahana 4 1--5 F 2 T Y 5 5 5.5 NV N Y N N N N N N N N N N N N N N 87 0.87 11 14.53 Y N N N Y N N N N 10.2 9--11 11900 4.59 30.3 76.8 20.2 26 14.6 2.74 0.4 53.92 371 12.69 425.02 71.2 431 10.65 36 8 NHA N

122 Shaheel 5 1--5 M 2 T Y 6 6 6 NV N N N N N N Y Y Y Y N N N N N N 104 1.04 11.2 10.36 Y N N N N N N N N 10.6 9--11 8100 4.33 34.4 79.3 25.3 32 13.5 3.5 0.6 70.15 262 21.10 332.45 5 187 5.72 10 10.2 NNA N

123 Karthik 7 5--10 M 2 T Y 6 0 6 NV N Y N N N N N Y Y Y N N N N N N 109 1.09 16.3 13.72 Y N Y N N N N Y N 9.5 9--11 8500 4.33 30.5 70.5 22 31 18.5 5.73 1.5 37.46 306 10.90 343.66 62.9 360 12.82 40 12 MHA N 10.6 2.0 11.4

124 Thangaraj 10 5--10 M 3 T Y 1.5 1.5 3 NV Y N N N N N N Y N Y N N N N N N 128 1.28 22 13.43 Y N Y N N N N N N 9.9 9--11 6300 4.36 34.6 79.4 22.8 29 12.4 3.5 0.2 74.53 246 23.27 320.23 230.1 792 14.82 49 5 NNA N

125 Arulraj 2.5 1--5 M 3 T Y 5 24 5 NV N N N N N N N N N N N N N N N N 91 0.91 12.1 14.62 Y N N N N Y N N N 9.7 9--11 10200 3.99 28.4 71.2 24.2 34 15.6 3.17 1 26.86 432 5.85 458.86 4.85 300 13.64 28 15.8 NNA N

126 Abishek 2.5 1--5 M 3 PT Y 7 12 7 NV Y N N N Y N N Y N Y N N N N N N 83 0.83 10.2 14.81 Y N Y N N Y N N Y 7.4 7--9 20000 4.2 43 68 11.6 17 16.3 3.64 0.7 43.69 418 9.46 461.99 12.2 714 25.2 22 8.7 NNA N

127 Liza mondal 2 1--5 F 2 PT Y 6.5 6.5 7 NV N Y N N N N N N N N N N N N N N 84 0.84 10.2 14.46 Y N N N Y Y N N N 10 9--11 8700 5.06 32.8 65 19.8 31 16.3 3.43 0.6 71.15 320 18.21 390.65 8.6 852 16.4 25 1.25 NNA N

128 Vishnu 5 1--5 M 2 T Y 6 30 6 NV Y N Y N N N N N N Y N N N N N N 118 1.18 18 12.93 Y N N N N N N N N 10.1 9--11 8900 4.09 30.9 76 24.6 33 16.2 2.76 1 74.52 245 23.34 319.32 19.6 402 9.1 16 3 NNA N

129 Varunikasri 2.2 1--5 F 2 T Y 6 6 6 NV Y Y Y N N N N N N N N N N N N N 81 0.81 10 15.24 Y N N N N N N N N 9 7--9 10400 5.03 30.4 16.4 19.7 33 16 3.63 0.4 30.7 492 5.87 522.72 32 ### 11.24 54 1.06 MHA N N N N

130 Hansika 1 1--5 F 2 PT Y 3 0 3 NV N N N N N N Y Y N Y N N N N N N 72 0.72 8 15.43 Y N N N Y Y N N N 7.9 7--9 7800 4.27 26.8 63 18.5 30 12.8 2.8 0.1 18.3 397 4.40 415.7 13.1 18 4.5 16 22 MHA N 7.9 0.5 7.9

131 Balavignseh 8 5--10 M 2 T Y 3 12 3 NV N Y N N N N N Y N N N N N N N N 102 1.02 18.6 17.88 Y N Y N N N N N N 10.1 9--11 8400 3.81 30.8 80.8 26.6 33 13.3 2.8 0.5 53.86 368 12.76 421.98 178 727 11.18 66 11 NNA N

132 Raagav 2.3 1--5 M 3 T Y 3 3 6 NV N Y Y Walri N N N N N Y N N N N N N 86 0.86 11.5 15.55 Y N N Y Y N N N N 9.4 9--11 29100 5.19 31.2 60 18.1 30 16.3 4.14 0.3 53.96 411 11.61 464.77 12.6 740 3.8 13 0.6 NNA N

133 Sharon roselin 1.2 1--5 F 2 T Y 6 6 6 NV N Y Y loosestool N N Y Y N Y N N N N N N 80 0.8 9 14.06 Y N N N Y Y N N N 7.9 7--9 11900 8.3 88.2 66 18.7 28 16.2 4.7 0.5 35.12 483 6.78 518.07 5.9 496 12.2 14 13 MHA N 8.6 1.5 9.2

134 Swetha 10 5--10 F 3 T Y 6 6 6 NV N N N N N N N Y Y Y Y N N N N N 138 1.38 25.8 13.55 Y N Y N N N Y N Y 7.2 7--9 4000 3.79 23.9 63.1 19.1 30 22.2 0.75 1 29.7 490 5.71 519.82 20.2 433 15.82 57 2 MHA N N N N

bronchopne
135 Raakesh 4 1--5 M 3 T Y 6 6 7 NV Y N N umonia N N Y Y Y Y N N N N N N 92 0.92 14.3 16.90 Y N N N Y Y N N Y 10.2 9--11 10200 4.22 34.8 82.7 26.4 32 13 2.28 0.6 19.8 206 8.78 225.6 1000 282 14.4 28 14 NNA N

136 Sathya 10 5--10 F 2 T Y 5 0 5 V Y Y N N N N N Y N Y Y N N N N N 116 1.16 19.5 14.49 Y N N N N Y Y Y N 6 >=7 12200 3.08 16 52.1 13.6 26 25.5 5.29 2.4 20.8 225 8.46 245.92 4.12 178 15.7 24 18 MHA N 6.7 2.0 8.1

Breathholdi
137 Samuel 1.3 1--5 M 2 T Y 3 3 8 V N Y N ngspell N N N Y N N N N N N N N 74 0.74 10.4 18.99 Y N N N Y N N N N 7.7 7--9 9600 4.28 26.8 63 18 29 18.2 4.52 0.6 12.82 534 2.35 546.63 4.39 390 12.42 9 6 NNA N

138 Abishek 1.9 1--5 M 2 T Y 3 4 4 NV N Y N N N N Y Y N N N N N N N N 82 0.82 10.2 15.17 Y N Y N N Y N N N 8.6 7--9 11000 4.53 30.3 67 19 28 17.8 4.12 1 27.78 406 6.41 433.38 12.89 482 11.4 31 6 MHA N 9.8 0.5 11.8

139 Mohana 6.3 5--10 F 3 T Y 6 6 6 NV N N N N N N N N N Y Y Y N N N N 108 1.08 14.8 12.69 Y N Y N N Y N Y N 9.9 9--11 15200 4 31.6 79 24.7 31 18.5 2.78 0.5 74.35 253 22.75 326.85 65.5 276 10.39 12 18 NNA N

140 Karthik 2 1--5 M 2 T Y 8 0 9 V N N N N N N N N N N N N N N N N 73 0.73 8.3 15.58 Y N N N Y Y N N N 9.9 9--11 15000 5.02 34 68 19.7 29 13.5 4.7 0.5 37.46 308 10.84 345.66 19.4 177 12.8 9 5 NHA N

141 Ramya 10 5--10 F 3 T Y 7 7 8 NV N Y Y N N N N Y N Y N N N N N N 143 1.43 34 16.63 Y N N N N N N N N 9.3 9--11 10200 3.78 31.7 84 24.6 29 17.8 3.76 0.4 50.21 429 10.48 479.21 7.72 172 28.2 15 18 NHA N

142 Amit kumar 4 1--5 M 3 T Y 5 6 5 NV Y N N N N N Y Y Y Y N N N N N N 105 1.05 14.7 13.32 Y N N N Y Y Y Y Y 8.6 7--9 8700 5.75 32 56 14.9 27 19.2 2.57 0.5 17.35 261 6.23 278.45 172 303 10.2 66 58.2 MHA N 9.5 0.8 10.8

143 Smruti sikta veura 2.5 1--5 F 2 PT Y 6 18 6 NV Y N N N N N Y Y N Y N N N N N N 89 0.89 10.9 13.76 Y N Y N N Y Y Y Y 10.2 9--11 9300 4.46 31.9 71.5 22.9 32 13.7 2.16 0.8 34.63 217 13.76 251.73 180 834 12.2 54 28.4 NNA N

144 Dhanasri 1.2 1--5 F 2 T Y 5 5 8 V N N N N N N N N N N N N N N N N 71 0.71 16 31.74 Y N N N Y N N N N 10.9 9--11 6300 4.4 34.1 77.6 24.9 32 13.5 2.9 1 63.18 379 14.28 442.44 68.4 330 14.42 11 10 NNA N

145 Vishwa 1 1--5 M 2 T Y 6 8 6 V N N N N N N Y N Y N N N N N N N 70 0.7 8.07 16.47 Y N N N N N N N Y 8.5 7--9 7800 4.51 26.9 59.6 18.9 32 18.9 4.75 0.7 26.17 457 5.41 483.53 6.45 214 16.75 24 7.2 MHA N 9.5 0.5 11.2

146 Hendric paul 4 1--5 M 2 T Y 4 4 6 NV Y N N N N N N Y N N N N N N N N 105 1.05 13.4 12.15 Y N N N Y Y N N N 8.8 7--9 8200 3.88 28.7 74 22.8 31 13.8 2.48 0.5 18.26 395 4.42 413.26 14.8 364 14.58 10 5.7 MHA N N N N

147 Abinaya 10 5--10 F 2 T Y 1 2 5 NV Y N N N N N N Y Y Y N N N N N N 132 1.32 22.9 13.14 Y N N N N N N N Y 10.8 9--11 8600 4.36 36.9 84 24.6 29 11.3 3.39 1 52.76 533 9.01 585.58 130 303 12.37 27 26.4 NNA N

148 Krithika 2 1--5 F 2 T Y 3 18 3 NV N Y Y N N N N N N Y N N N N N N 80 0.8 9.1 14.22 Y N N N Y Y N N N 7.5 7--9 13600 4.69 26.5 56 15.9 28 12 5.42 2 15.73 426 3.56 442.03 20.6 427 6.8 12 6.26 MHA P 8.2 1.5 9.6

149 Maariselvam 6 5--10 M 4 PT Y 6 12 6 NV N Y N N N N N N Y Y N N N N N N 107 1.07 14.2 12.41 Y N N N N N N N N 10.6 9--11 14800 4.7 36.3 77 23.3 30 12.3 2.8 0.5 58.21 352 14.19 410.33 22.7 588 17.82 25 8 NNA N

150 John jeslin 1.8 1--5 F 2 T Y 5 6 6 NV N N Y N N N N Y N N N N N N N N 79 0.79 9.5 15.22 Y N N N Y N Y Y N 8.8 7--9 12800 4.23 29.3 69 20.7 30 18.2 4.25 0.8 39.16 282 12.19 321.28 12.2 516 15.65 8 12 NNA N
 129

Annexures
 130

ANNEXURE-I
PROFORMA

Name : Insurance No -

Age :

Sex :

Informant :

Reliability :

Address :

Socio –economic Details

Mother’s education

Father’s education

Annual Income

Occupation

Socio –economic Status :

Housing :
 131

History

Term / preterm
Duration of breast feeding
Timing of introduction of cow’s milk /
formula feeds

Introduction of complementary feeds

Veg Non-Veg

Diet
H/o Intake of red meat,
liver and greens

Worm infestation Yes No

H/O Pica Yes No

H/O Pagophagia Yes No

H/O treatment for any infections in the past Yes No

H/O of GI bleed Yes No

Family history of hemolytic anemia Yes No

Presenting complaints with duration:

H/o Irritability Yes

No

H/o Lethargy Yes

No
 132

H/o Poor school performance Yes

No

H/o Easy fatigability Yes

No

H/o Breathlessness Yes

No

H/o Palpitation Yes

No

H/o Chest pain Yes

No

H/o Dizziness Yes

No

H/o Headache Yes

No

Drug History-
 133

EXAMINATION

ANTHROPOMETRY VITAL SIGNS

Temperature
Height
Heart rate
Weight
Respiratory rate
BMI
BP mmHg)

GENERAL EXAMINATION

Pallor Yes No

Icterus Yes No

Generalized lymphadenopathy Yes No

Edema Yes No

Koilonychia Yes No

Leuconychia Yes No

Glossitis Yes No

Cheilitis Yes No

SYSTEMIC EXAMINTION
CVS -

RS -

ABDOMEN -

CNS -
 134

INVESTIGATIONS

Parameters Values Reference range

1 to 23 months: 10.5 -14 g/dl
Hemoglobin 2 to 9 years : 11.5 - 14.5 g/dl
10 to 17 years : 12.5 -15 g/dl
1 to 23months: 6000 -14000
cells/cu.mm

2 to 9 years : 4000 –
WBC count
12000cells/cu.mm

10 to 17 years : 4000 -
10500cells/cu.mm

6m to 2 years: 3.7 -5.3 million/cu.mm

RBC count 2 to 6 years: 4.9 – 5.3 million/cu.mm

6 to 12 years: 4 – 5.2 million/cu.mm

1 to 23 months: 32 -42 %
PCV 2 to 9 years : 33 -43%
10 to 17 years : 36 -45%

1 to 23 months: 72 – 88 fL
MCV 2 to 9 years : 76 – 90 fL
10 to 17 years : 78 – 95 fL

1 to 23 months: 24 – 30 pg
MCH 2 to 9 years : 25 – 31 pg
10 to 17 years : 26 – 32 pg

MCHC 32.0 – 36.0 %

RDW 10.0 – 15.0 %

 135

Platelet count 154000 – 400000 /cu.mm

Reticulocyte count <1%

Serum Iron 50.00 – 120.00 µg/dL

TIBC 250.00 – 400 µmol/L

Transferrin
15 - 55%
saturation

Serum Transferrin 208 – 400 mg/dl

Serum Ferritin 6.0 – 67.0 ng/mL

Serum B12 140.00 – 700.00 pg/mL

Serum Folic acid 1.8-9.0 ng/mL

ESR 5-15 mm/Hr

HsCRP 0.01-2.80mg/l

Peripheral smear study :

Stool for occult blood :

DIAGNOSIS:

TREATMENT DETAILS:

FOLLOW U P DETAILS

DATE Hb values Remarks

 136

ANNEXURE II
PATIENT CONSENT FORM

Study title: PROFILE AND OUTCOME OF NUTRIONAL ANEMIA IN

CHILDREN ATTENDING THE PEDIATRIC DEPARTMENT OF A TERTIARY
CARE HOSPITAL IN CHENNAI

Study center: ESI-PGIMSR, K.K.Nagar, Chennai

Participant name: Age: Sex:
I.P.No:

I confirm that I have understood the purpose of procedure for the

above study. I have the opportunity to clarify all my queries and doubts
and they have been answered to my satisfaction. Investigator explained
very well about the procedure and I am made aware of the safety,
advantage and disadvantage of the technique.

I understand that my participation in the study is purely voluntary

and that I am free to withdraw at any time without giving any reason.

I have understood that the investigator, regulatory authorities and

the ethics committee will have access to my health records both in respect
to current study and any further research that may be conducted in
relation to it, even if I decide to withdraw from the study. I have
understood that my identity will not be revealed in anyway and
information released to third parties or published, unless as required
under the law. I agree not to restrict the use of any data or results that
arise from the study.

Without any compulsion I am willing to give consent for the

participation of my child in this study.

Date: Signature / thumb impression of patient

Place:

Patient name:

Signature of the investigator:

Name of the investigator:

 137

ANNEXURE III
Sample size Calculation
The following were the statistical considerations.
Single Proportion – Absolute Precision
Expected Proportion 0.75
Precision (%) 7
Desired confidence level (1- 95
alpha) %
Required sample size (n) 147

The required sample size for this study was 147 participants. 3
cases were taken as lost to follow up. So, 150 participants were enrolled.
Therefore, total sample size was 150 for this study.

The following were the sample size calculations for the interventional
study.

Single Mean - Paired t-test

Pre-test mean 8
Post-test mean 9
Standard deviation in Pre-test 2.2
Standard deviation in Post-test 2
Effect size 0.47619
Power (1- )% 90
Alpha Error (%) 5
1 or 2 sided 2
Required sample size 48
2 sided: Null hypothesis: There is no difference between before and

after treatment.

So, a total sample size of 50 was taken for follow up study

including lost to follow up. The Master software (version 1.0) was used to
calculate sample size.