Transcript Vitamin A Deficiency

Nutritional Epidemiology:
Micronutrient malnutrition
Asst. Prof. Dr. Sumattana Glangkarn
Micronutrient malnutrition: a public health problem
 Micronutrient malnutrition (MNM) is widespread in the
industrialized nations, but more in the developing regions
 Can affect all age groups, but young children and women
of reproductive age tend to be among those most at risk of
developing micronutrient deficiencies
 MNM has many adverse effects on human health, even
moderate levels of deficiency (detected by biochemical or
clinical measurement)
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 Nutrition problems in Thailand include;
- Protein energy malnutrition (PEM)
- MNM; Iron deficiency anemia (IDA)
Iodine deficiency disorder (IDD)
Vitamin A deficiency.
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Iron-deficiency anemia
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Iron-deficiency anemia (IDA) is the most common nutritional
disorder in the world
Women in the reproductive age group and young children in
tropical and subtropical regions
IDA affects over 2 billion people in the world
Average prevalence is higher in pregnant women (51%) than nonpregnant women
High prevalence in south and south-east Asia
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Stage of iron depletion
Stage I
Stage II
Stage III
Decrease in
iron stores
Biochemical
indicators of low
iron stores
Iron-deficiency
anemia
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 Ferritin
Transferrin saturation
 Erythrocyte protoporphyrin
 Hemoglobin
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องค์ ประกอบของฮีโมโกลบิน
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Iron nutritional status
Biochemical and hematological tests
 Serum iron concentration
 Total iron binding capacity
 Transferrin saturation
 Protoporphyrin
 Serum ferritin
 Transferrin receptors
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Serum iron concentration
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In IDA, serum iron may either be low or even normal
The normal value between 50 and 175 µg/dl
There is a considerable diurnal variation; the levels are highest in
the morning and lowest during the night
It is reduced in inflammation, malignancy and during
menstruation
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Total iron binding capacity
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Total iron binding capacity (TIBC) and transferrin saturation
indicate iron supply to issues
The normal value is about 300 µg/dl
TIBC is lowered in chronic disease and raised in iron deficiency
Transferrin saturation
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This is a ratio of serum iron and TIBC, normal value is 33%
In iron deficiency, there is a decreased saturation, while in chronic
diseases the saturation is normal
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Protoporphyrin
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Protoporphyrin is the precursor of heme
Free red blood cell (RBC) protoporphyrin is raised when there is
an insufficient supply of iron for heme synthesis
It is high in IDA, caused by lead toxicity and other sideroblastic
anemia
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Serum ferritin
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Serum ferritin reflects the status of total body iron stores
A value below about 10 ng/ml is considered as diagnostic of iron
deficiency
Its levels are raised in inflammation, infections and liver disease
Serum ferritin is a sensitive indicator of iron stores, particularly in
areas where the incidence of infections is very high; the
developing countries of south-east Asia
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Transferrin receptors
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Transferrin receptors become elevated on cell surfaces and in
plasma whenever there is insufficient iron supply to cells or iron
depletion.
Because of the cost implications for multiple biochemical tests, the
parameter used to indicate iron status in population studies of
IDA is measured by hemoglobin.
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Hemoglobin (Hgb)
ค่ าปกติ (g/dl)
ชาย
หญิง
เด็ก
ทารก
แรกคลอด
14-18
12-16
11-16
10-15
14-24
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Hematocrit : Hct
Hct. = 3 (Hgb)
ค่ าปกติ (/100 ml.)
ชาย
หญิง
เด็ก
ทารก
แรกคลอด
42-52
37-47
31-43
30-40
44-64
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Centrifuge
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Clinical features of iron-deficiency anemia
The symptoms of IDA depend on the rate at which anemia
develops in an individual
 Symptoms may relate to rate of fall in hemoglobin
 Lowering of hemoglobin affects oxygen carrying capacity; in
IDA, any physical exertion leads to shortness of breath
 Initially, most patients complain of increasing lethargy and fatigue
 More unusual symptoms are headache, tinnitus and disturbance in
test
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As the severity of deficiency increases, the patients develop pallor
of conjunctiva, tongue, nailbeds and soft palate
 In IDA of longer duration, there may be papillary atrophy of the
tongue and, the nail may become spoon shaped (koilnychia)
 In children, chronic IDA may lead to behavioral changes; they
may have impairment of cognitive function and short attention
spans and appear withdrawn
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Conjunctiva
Normal appearing conjunctiva
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Spoon finger
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Iron metabolism
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Human body requires iron for the synthesis of the oxygen transport
proteins, hemoglobin and myoglobin in the body
Total body iron in men ~ 3.8 g, in women ~ 2.3 g.
Approximately 2/3 of total iron is functional, serving either a metabolic or
an enzymic function; in the form of hemoglobin, circulating with in RBC
The factor influencing iron balance are intake of iron, iron stores and iron
loss
Adult males require ~ 1 mg of absorbed iron daily to replace the losses in
gut secretions, epithelial cells, urine and skin
In menstruating females this can increase to 1.4
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Factor influencing iron absorption
Type of food consumed; meat, eggs
 Interactions between foods; iron absorption enhancers (vitamin
C), iron absorption inhibitors (i.e. calcium phosphate, bran)
 Regulatory mechanisms in the intestinal mucosa
 Bioavailability; utilization of ingested iron for metabolic
functions
 Amount of iron stores: liver, reticuloendothelial, bone marrow
 Rate of production of red blood cells
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Iron losses
In healthy individuals occur primarily in feces (0.6 mg/day),
bile and desquamated mucosal cells, and in minute quantities
of blood
 Urinary losses are small
 Women of reproductive age, in addition to the basal losses;
lose iron in menstruation
 The median menstrual blood loss is about 30ml/day, an
additional requirement of 0.5 mg of iron per day
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In the tropical countries, hookworm infestation is a major
cause of gastrointestinal blood loss contributing to iron
deficiency in older children and adults.
 In the developed world, among adults, chronic use of drugs
such as aspirin, bleeding tumors and ulcers contribute to iron
losses.
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Risk factors for anemia
Poor iron stores
 Dietary inadequacy
 Increased demands
 Malabsorption and increased losses
 Hemoglobinopathies; thalassemia, sickle cell anemia (nonnutritional factor)
 Drug and other factors; anticancer drug, radiation therapy
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Prevention and control of iron-deficiency anemia
Provision of iron supplements
 Fortification of commonly consumed food with iron
 Nutrition education
 Horticulture-based approaches to improving the iron
bioavailability of common foods
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Iodine and Iodine-deficiency Disorders
The epidemiology of iodine deficiency disorders (IDD) is
currently in a transitional phase because of the great
progress seen during the 1990s in the battle against IDD
 Mainly in the form of national salt iodization programs
 The diagnosis of iodine deficiency should be seen as a
group, community or population diagnosis rather than an
assessment on the individual level; interpretation of IDD
status
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Definition of iodine status of a population
Iodine status
Median urinary iodine
concentration (µg/l)
Severe iodine deficiency
<20
Moderate iodine deficiency
20-49
Mild iodine deficiency
50-99
Ideal iodine intake
100-200
More than adequate iodine intake; increased
risk hyperthyroidism
Excessive iodine intake
201-299
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>300
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Thyroid size by palpation
Grade 0: no palpable or visible goiter
 Grade 1: a mass in the neck that is consistent with an
enlarged thyroid that is palpable but not visible when the
neck is in the normal position (Ia), but move upwards in the
neck as the subject swallows and visible when neck fully
extended (Ib)
 Grade 2: a swelling in the neck that is visible when the neck
is in a normal position and is consistent with an enlarged
thyroid when the neck is palpated
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Thyroid size by ultrasonography is a safe, noninvasive,
specialized technique, which provides a more accurate
measurement of thyroid volume than palpation
 Thyroid-stimulating hormone (TSH) and thyroglobulin can
be used as indicators to assess IDD, or as surveillance
indicators
 Thyroid hormones thyroxine (T4) and triiodothyronine (T3)
tests are cumbersome, more expensive and less sensitive
than other indicators
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WHO/UNICEF/ICCIDD recommended dietary intake for
iodine (2001)
Category
Intake (µg/day)
Infants, 0-59 months
90
Schoolchildren, 6-12 years
120
Children > 12 years and adults
150
Pregnant and lactating women
200
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Management of iodine deficiency
 Use of iodized salt
 Iodination of drinking water
 Fortification of infant formulas
 Fortification of other food
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Vitamin A Deficiency
Xerophthalmia
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Vitamin A Deficiency
Vitamin A deficiency is the most common cause of childhood
blindness
 Causing 250,000-500,000 children to go blind every year, half of
whom will die within the year
 Vitamin A deficiency disorders occur when body reserves are
depleted to the limit at which physiological functions are
impaired
 Xerophthalmia; the pathological eye signs of Vitamin A
deficiency
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Sources of vitamin A
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Common dietary sources of performed vitamin A are liver, milk and
milk products, eggs and fish
The richest sources are liver oils of fish, such as shark, halibut and
cod, and of marine mammals, such as polar bear
The livers of ox, sheep, calves or chicken also contain vitamin A at
concentrations comparable to cod liver oil
Eggs, milk and other dairy products: butter and cheese, are all
moderate sources
Provitamin A carotenoids are found in yellow and orange fruit and
vegetables, and in dark green leafy vegetables
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Consequences of vitamin A deficiency
 Xerophthalmia represents the ocular consequences of
vitamin A deficiency that include night blindness
(XN), conjunctival xerosis (X1A), Bitot’s spots
(X1B), corneal xerosis (X2), ulceration (X3A) or
necrosis/keratomalacia (X3B)
 Immunocompetence: effects on the immune system,
infection
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Epidemiology
Magnitude of the problem
Vitamin A deficiency is, after PEM and iron-deficiency anemia,
the most widespread and serious nutritional disease among
young children
 In 1994, global estimate indicated that 2.8 million preschool
children are clinically affected by vitamin A deficiency
 Asia and Africa account for nearly 90% of the global problem
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Risk factors
As a public health problem, vitamin A deficiency occurs within
an environment of social, economic and ecological deprivations
in which people live in the transitional and developing
economics of the world
 It is imperative to understand the local conditions when
designing appropriate and effective intervention programs to
improve the situation
 Some underlying factors: age, gender, physiological status, diet,
disease patterns, socioeconomic conditions
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Age
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Varying levels of vitamin A deficiency, from subclinical forms to the
severe form of blinding malnutrition (keratomalacia), can occur at any
age
However, vitamin A deficiency, particularly severe deficiency, affects
children of preschool age
The requirements for growth are high, while the dietary intake of
vitamin A is often low
Children under 12 months of age, corneal disease is relatively rare
event, largely because breast-feeding is protective
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Gender
In healthy human adults, both plasma retinol and RBP (retinol
binding protein) are found at levels 20% higher in males than
females
 Nevertheless, males have generally been found to be at higher
risk of night blindness and Bitot’s spot than female during the
preschool and early school-age years
 Less gender difference in severe xerophthalmia
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Physiological status
Vitamin A needs are increased during periods of rapid growth,
younger children are the most vulnerable group
 The demands for vitamin A are also increased during the period
of gestation and lactation
 Night blindness during pregnancy and lactation is especially
common in south Asia (15-20% of all pregnancies)
 Studies have shown, breast milk of women with poor vitamin A
could subsequently contribute to increased susceptibility of the
infants
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Diet
The basic underlying cause of vitamin A deficiency is a diet
lacking adequate amounts of vitamin A, either preformed or
provitamin A carotenoids, to meet the requirement
 Vitamin A deficiency is common wherever diets are of
relatively low quality
 Breast-feeding, the quality of complementary feeding and the
quality of the children diet are all important factors in maintain
vitamin A status ; xerophthalmia protective
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Diet
Epidemiological studies support a progressive of appropriate
complementary feeding that has been shown to guard children
from xerophthalmia through the preschool year
 Intake of yellow fruit (mango and papaya) is strongly protective
in the second and third years of life
 Dark green leafy vegetables play a more important role from the
third year onwards
 After infancy, routine consumption of animal foods with
preformed vitamin A (eggs, dairy products, fish and liver) is
highly protective
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Disease patterns
 Vitamin A deficiency increase the risk of infectious
morbidity; diarrhea, respiratory infection, measles
 Intestinal worms such as Giardia and Ascaris have been
reported to lead to reduced absorption of vitamin A
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Socioeconomic conditions
 Vitamin A deficiency is confined largely to relatively
impoverished countries
 Studies have shown that households with mildly
xerophthalmic children have smaller landholdings, poorer
housing conditions, fewer draft and grazing animals, and
lower economic standing
 Low education levels of the father or mother are a further
risk factor
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Prevention
 Food-based approaches, including dietary
diversification, nutrition education and fortification
of staple and value-added food
 Supplementation with vitamin A capsules
 Breast-feeding, treatment of infectious diseases
 Modification of the political, socioeconomic, physical
environment
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Food fortification
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Food fortification refers to the addition of micronutrients to
processed foods.
Salt iodization was introduced in the early 1920s in both
Switzerland and the USA.
From the early 1940s onwards, the fortification of cereal products
with thiamine, riboflavin and niacin became common practice
Margarine was fortified with vitamin A in Denmark.
Milk with vitamin D in the United States
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