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Dept. of Human
Nutrition,
AIIMS
e mail : kapilumesh@hotmail.com
History of IDD
Endemic
goiter in
Iodine Deficiency Disorders is known to be a significant
public health problem in 118 countries. At least 1572 million people worldwide
are estimated to be at risk of IDD i.e. who live in areas where iodine
deficiency is prevalent (total Goiter rates above 5%), and at least 655 million
of these are considered to be affected by Goiter. A recent WHO/ UNICEF/ICCIDD
report estimates that currently
about 29% of the world's
population live in areas of iodine deficiency and need some form of iodine
supplementation. Most of these are in
developing countries in
About 200 million people are at the
risk of IDD in
Etiology
Iodine is one
of the essential elements required for normal
human growth and development. Its daily
per capita requirement is 150
micrograms. Soils from mountain ranges, such as the
The
contribution of different food groups to the daily intake
of iodine are cereals 40 percent, milk and milk products 37
percent, flesh foods
11 percent, pulses 10
percent and Vegetables 2
percent. Cereals and pulses together
contribute significantly to the daily intake of iodine .
Iodine
deficiency thus results mainly from geological rather than social and economic conditions. It cannot be
eliminated by changing dietary
habits or by eating specific
kinds of foods grown in the same area . Besides
nutritional iodine deficiency, a variety of
other environmental, socio-cultural and
economic factors operate to
aggravate iodine deficiency
and related thyroid dysfuncitons. These include poverty related
protein-energy malnutrition, ingestion of
goitrogens through unusual diets (particularly by the poor),
bacteriologically contaminated drinking water,
as well as bulky
high residue diets
which interfere with intestinal absorption of iodine.
There is
also evidence to believe that
intensive cropping, resulting in large
scale removal of biomass from the soil, as well as widespread use of alkaline fertilizers, rapidly deplete the
soil of its iodine content. Since
both intensive cropping and use
of alkaline fertilizers are
widely practiced in almost all
states of the country, it is not surprising that
nutritional iodine deficiency and
endemic goiter are seen wherever they are looked for in India
Several environmental and genetic factors interfere with the
above processes of
thyroxin synthesis leading
to goiter formation. The genetic factors, which are rare, mainly
affect the enzymes involved
in thyroxin synthesis.
Environmental factors are amongst the most common factors that interfere
in thyroxin synthesis and
lead to goiter formation.
The most important environmental
factors are (i) environmental
iodine deficiency (ii) goitrogens.
However, the most frequent cause of
goiter in
Besides iodine
deficiency and goitrogens, a variety of other factors can
adversely affect efficient thyroxin
synthesis and iodine utilisation
in the body, resulting in
aggravation of goiter. These
include, protein energy
malnutrition, dietary
factors that interfere with iodine absorption etc.
Environmental iodine deficiency coupled with a variety of ancillary factors
compromises thyroxin biosynthesis which results in prevalence of endemic goiter
.
Iodine deficiency
in food and water leads to less
iodine to thyroid gland which is the exclusive organ for
synthesis of two very important iodine
containing hormones T3 (Tri iodo thyronine) and T4 (Thyroxin). As a result, the thyroid gland becomes hyper active
to produce the requisite amounts
of T3 and T4
thereby enlarging itself by
hyperplasia phenomenon under compulsion
and this enlargement of the thyroid gland is known as goiter. In the past,
goiter was said to be a cosmetic
problem however the recent research
studies have shown that goiter is one
of the several disorders that the body
is subjected to suffer due to iodine deficiency. All the disorders are currently being
categorised under a term Iodine deficiency
disorders (IDD). The relationship
between dietary iodine intake and severity of IDD is shown in Table-II.
The major
factors responsible for iodine deficiencies are :
Iodine deficiency has been called the world's major
cause of preventable mental retardation. Its severity can vary from mild
intellectual blunting to frank cretinism, a
condition that includes gross mental retardation, deaf mutism, short
stature, and various other defects. In areas of severe iodine
deficiency, the majority of individuals risk some degree
of mental impairment. The damage to the developing brain results in
individuals poorly equipped
to fight disease,
learn, work effectively, or
reproduce satisfactorily.The spectrum
of disorders caused
due to iodine deficiency affects all the stages of life- from
fetus to
adult (Table III).If a
pregnant woman diet do not
contain adequate iodine, the
fetus cannot produce enough thyroxin and fetal growth is retarded.
Hypothyroid fetuses often perish in the
womb and many infants die within
a week of birth. The current data on the embryology of the brain suggest that
the critical time for the effect of iodine deficiency
is the mid second trimester i.e.
14-18 weeks of pregnancy. At this time
neurons of the cerebral cortex
and basal ganglia are formed. It is also
the time of formation of `Cochlea'
(10-18 weeks) which is also severely
effected in endemic cretinism. A deficit in iodine
or thyroid hormones occuring during this critical period of
life results in the slowing down
of the metabolic activities of all the
cells of the fetus and irreversible alterations in the
development of brain.
The growth and
differentiation of the central
nervous system are closely
related to the presence of iodine and thyroid hormones.
Hypothyroidism may lead to cellular
hypoplasia and reduced
dendritic ramification gemmules
and interneuronal connections.
Hypothyroid children are intellectually subnormal and may also
suffer physical impairment. They lack
the aptitudes of normal children of similar
age, and are often incapable of
completing school. Studies have documented that
in areas with an incidence of mild to moderate IDD, IQs of school
children are, on
average, 10 –12 points below
those of children living in areas
where there is no iodine deficiency. Foetal thyroid
start secreting thyroxin early in the
2nd trimester in intra-uterine
life. From then on till the end of
the first year of post-natal life, thyroxin plays
a very important role
in the growth and functional maturation
of the fetal brain. Thyroxin
deficiency during this critical
period can result in impaired brain development which cannot be
corrected later by giving iodine or thyroxin.
The thyroid
gland in its present form evolved
over the course of millions of
years of biological evolution. The molecule of
thyroxin has four atoms of iodine.
Therefore, iodine is an essential
element required for the synthesis of
thyroxin. The thyroid gland has
very efficient mechanisms for extracting iodine from the
circulation, where it may be present in
as low a concentration as
0.01 micrograms per 100 ml of
plasma. The minimum daily requirement of iodine by thyroid gland in man is
estimated to be 100 micrograms. To
extract this amount of iodine from the
circulation, the thyroid daily clears several
hundreds of liters of
plasma of its iodine. This work
can increase further by
several times in
severely iodine
deficient environments
because of the very low
concentrations of iodine present in the circulation in such conditions. To cope up
with this increased work load, the thyroid enlarges in size, under the
influence of thyroid stimulating hormone (TSH), secreted from the pituitary
gland. The efficient compensatory
mechanism triggered by low
thyroxin feedback at the hypothalamic
centers lead to increased
TSH secretion from the pituitary and cause remarkable enlargement of the thyroid gland
resulting in goiter . Iodine as iodide (I-the ionic form) is transported
into the cells by the
iodide pump. This process is called
`trapping'. The trapped `iodine'
is enzymatically oxidised to free iodine and chemically linked
to a protein in
the thyroid cell
called thyroglobulin. In fact
the iodine is attached to the tyrosines
(an amino acid) of the thyroglobulin molecule.
The thyroglobulin so iodinated is secreted into the thyroid follicles. Thyroxin is formed, iodinated
and stored in the thyroglobulin
molecules. Under the influence of
TSH, the thyroxin stored as
thyroglobulin in the thyroid acini is released, in accordance with the
needs of the body. Synthesis of thyroxin in the thyroid cells involve availability of enough iodine to the thyroid, as well as action of a variety of
enzymes in the thyroid. If
any of these process
is affected thyroxin synthesis is
impaired and goiter formation results.
Endemic cretinism is the extreme clinical
manifestation of severe hypothyroidism during
fetal, neonatal and
childhood stages of development.
It is characterised
by severe and irreversible mental
retardation, short stature,
deaf-mutism, spastic
dysplegia and squint. In early eighties in many seriously endemic Tarai districts of north
Cretinism seen
in endemic areas is
predominantly of two types
(a) Neurological cretinism, where
only the
neurological manifestations of
thyroxin deficiency early in life
(in utero) and dysplegia
and squint. This is presumably
because, in such
individuals hypothyroidism was confined to the in-utero or neonatal
stages of life. (b) Myxedematous cretinism where besides having
mental retardation, have myxoedema
and dwarfism. This variant
of cretinism is presumably because of continuing hypothyroidism through all phases of life.
ii)
Cretinoids
Besides the
few who manifest as cretins, in an endemic goiter area, a large number of
individuals with lesser degrees of mental
retardation, speech and
hearing defects, psychomotor retardation, as
well as gait
defects may be
seen. Such individuals are
known as cretinoids.
The prevalence of cretinoids may be tenfold or more, than
fully manifested cretins in severely
endemic regions.
iii) Other syndromes due to foetal iodine deficiency
There is preliminary
scientific evidence suggesting that severe
iodine deficiency can lead
to fetal wastage such
as abortion, still births, and
congenital abnormalities. However, hard
evidence available in this regard is limited.
iv)
Neonatal and childhood hypothyroidism
When the
cause of endemic goiter in the Himalayas
was investigated in the late
fifties, modern techniques for precise
measurement of thyroid
hormones were not available. In
the sixties, and seventies, when radio-immunoassay techniques became available for
sensitive and precise
measurement of these hormones, it
was discovered that more
than 30%
the goitrous subjects in
endemic areas were functionally
decompensated and hypothyroid despite
the `adaptive' enlargement of
the thyroid. Subsequently, in
early eighties by screening the cord
blood of over 20,000 newborns, it was discovered that one out of every 10 new borns from the Tarai regions
of UP were hypothyroid at birth.
iv) Adult
Hypothyroidism
A large number of goitrous adults in an endemic region can have varying degrees of
hypothyroidism leading to a variety of clinical symptomatology and
complications related to hypometabolic states.
These symptomatology can
seriously hamper human energy and
work capacity with resultant erosion of
economic productivity of endemic
regions. Indeed such
factors may possibly be
contributing to the
known socio-economic
backwardness of endemic regions.
v) Goiter and
its complications
These are well known medical and surgical problems which are also
included in the syndrome of IDD.
Besides, there is emerging epidemiological evidence
linking endemic goiter
with incidence thyroid cancer.
Following the successful trial of iodized salt in
the Kangra valley, Himachal Pradesh, a National Goiter Control Program was
launched by the Government of
Objectives : National IDD Control Program
has the following objectives:
Beneficiaries
All people
residing in endemic and non-endemic
areas for IDD. The
population in known endemic
area are given priority.
Activities and
Services provided under the NIDDCP:
The following
activities are conducted under the
NIDDCP:
i. Production and Distribution of Iodised Salt
On the
recommendations of Central Council of Health in 1984, the Government took policy decision to iodise the
entire edible salt in
the country. This
policy decision was implemented w.e.f. April, 1986 in phased manner. Subsequently
the e iodised salt production was
liberalized to private sector. Six
hundred fourth one private
manufactures have been licensed
by Salt Commissioner . These have annual production capacity
of iodised salt of more than 60
lakh tons (which is adequate
for the entire country). The
annual production of iodised salt has increased
from 5 lakh metric tons in 1985-86 to 45
lakh metric tons in
1998-99. This is expected to
further rise furthur to 52
lakh metric tones in near future which is the projected national requirments .
Budget is
provided to Salt
Deaprtment for monitoring
the quality control of iodised salt
produced at production
level. The Salt Commissioner in
consultation with the Ministry of the
Railways arranges for the transportation of iodised salt from the production centres
to the consuming States under priority
category `B', a priority second
to that for defence
.The Salt Deaprtment has been initiating action to improve packaging
of iodised salt to prevent iodine loss
during transit. The State Government have been advised to include iodised salt
under Public Distribution System (PDS).
ii. Notification for banning use of non-iodised salt
To ensure use of only iodised salt the sale
of non-iodised salt has
been completely banned
under Prevention of
food Adulteration Act, 1954, in all states and union
territories. However there
is no ban notification in state
of Kerala. Realizing
the importance of iodine
deficiency in relation
to human resource development, NIDDCP has been included in 20 point Program of the Prime Minister for monitoring the
progress.
iii.
Establishment of Goiter Cell :
For effective
monitoring and proper implementation of
NIDDCP, all the States and UTs have been advised to establish IDD
control Cell in the
State Health Directorate.
Government of
iv. Information
education and communication activities
Central Government provides cash grants to the states
and UTs for production of health
education material and
carrying out health education
activities on IDD
as well as
for undertaking IDD surveys.
To intensify the IEC
activities a communication
package by way of video films, posters/danglers and radio/TV spots
has been produced. TV video
Spots are being regularly telecasted through the
National Network of Doordarshan about
the consequences of Iodine Deficiency
and the benefits of consuming
iodised salt.
The standards
for iodised salt have been laid
down under PFA, 1954.
These stipulate the iodine content of salt at the
production and consumption level to be
at least 30 and 15 ppm, respectively. Under a GOI-UNICEF project intensive monitoring and
IEC activities have
been undertaken in
selected districts of India.
v.
Intersectoral Co-ordination :
It has
been realised that
NIDDCP activities require integrated efforts of multiple
agencies like Industry, Railways,
Health, Education, Food
and Civil Supplies, Information
and Broadcasting etc. The focus of NIDDCP activities has now been shifted from
only health department
to multi and interdisciplinary participation.
vi.
Laboratory Support:
A National Reference Laboratory for monitoring
of IDD
has been set up at the
Bio-chemistry division of National
Institute of Communicable Diseases,
Delhi for training
medical and paramedical personnel and monitoring the iodine content
of salt and urine.
District level IDD monitoring laboratories are
being setup in all
the States for estimation of iodine content of salt and urinary
iodine excretion. These two laboratory investigations are the most effective tools for proper monitoring the implementation of
IDD Control Program. For
ensuring the quality
control of iodised
salt at consumption level,
testing kits for "on the spot" qualitative testing have
been distributed to
all District Health Functionaries for creating awareness
about consumption and use of iodised salt.
vii.
Training under NIDDCP Programs :
Every year,
training Programs are conducted in management
and monitoring of National Iodine
Deficiency Disorders Control Program for
the Regional Directors of Health and
Family Welfare and the State level technical officers by the Directorate General of Health
Services. Training Programs for laboratory technicians from
the state level IDD monitoring
laboratories are also organised by the Directorate General of Health Services
every year.
viii Evaluation:
The status of salt iodisation in different states
has been extensively assessed
by different research
studies and by national level
surveys in recent years . The NFHS‑2 was one of the klargest suvey which covered
all the states in the country with a representative sample of households . Thee
degree of iodization of salt used in
households was assessed. It was found that more than 70% population was
consuming iodised salt. ( Table IV).The research studies conducted has identified following areas which
require strengthening :-
Regular IDD surveys are not conducted by the State/UT Governments to monitor the progress/identify new areas of endemicity.
Safety of Iodised Salt
Iodine
requirements have been
calculated based on (i)
average daily physiological loss of iodine in the urine which is 100-200 mcg/ day and (ii) balance studies
to get equilibrium or positive
balance which is 44-162 mcg/ day. These studies have estimated a safe daily intake of iodine between
a minimum of 50 mcg and a maximum of at least 1000
mcg. The generally accepted
desirable adult intake is 100-300 mcg/day. In
The average salt intake among adults is about 10g/day, and at the current level of fortification of salt with 15 ppm of iodine at the consumer level , the iodised salt provides an additional amount of about 73.5 mcg only (considering the losses during cooking and biologically available). The remaining requirement of iodine is met from the dietary sources. Thus, the total intake of iodine is much below the safe limit and therefore the iodised salt is unlikely to cause any harmful effects even in populations who are not iodine deficient. Also It has been documented that at all intake levels, a proportionate amount of iodine is excreted in the urine.
The recent
research studies conducted by Human Nutrition Unit ,AIIMS
Assessment of
IDD
Probability Proportionate to Size(PPS) cluster
sampling methodology is recommended. The
thirty
clusters is should be covered and should
be selected as follows. Firstly all population
units/villages in the area to surveyed is listed
along with the population. Secondly ,the cumulative frequency table is prepared and the
total population in the survey area is calculated. Then by dividing
total population with 30, the sampling
interval is calculated. Subsequently the first
cluster is selected
at random and subsequent clusters are calculated by
adding sampling interval. The
number of subjects to be surveyed within each
cluster depends on the following :i. estimated prevalence of IDD, ii.
level of precision desired, iii. variability of prevalence between clusters
ii. Selection of Target Groups for
IDD Survey
The survey should be conducted in
a sample of population which should be representative of the population. The school
age children reflect the IDD status of
the community, are vulnerable to deficiency and respond to the iodine
supplementation intervention and hence have been recommended for the survey
iii.
Indicators for Assessing IDD:
The common indicators for
assessment of IDD are i. Clinical indicators
and Biochemical indicators. It
is recommended that the assessment of iodine content of salt consumed by the
subjects should also be included in the survey as data on this aspect provides the guideline
for developing the intervention for prevention of IDD simultaneously.
iv. Clinical
Indicators
Thyroid size
The size of the thyroid gland changes inversely in response to alterations in iodine intake, with a lag of 6-12 months in children and young adults (i.e <30 years of age). The traditional method for determining thyroid size is inspection and palpation. Palpation of the thyroid is important in assessing Goiter prevalence. Costs is minimal. It is relatively easy to conduct. The training of personnel can be done. Children 6-12 years of age should be studied. Very young children have smaller thyroid and it is more difficult it is to perform palpation. It is recommended that if the proportion of children attending school is less than 50%,spot surveys should be done on two groups of children of the same age, i.e those who attend school and those who do not, to ascertain if there is any significant difference between the two. If so, both groups should be studied separately, in all clusters, or an appropriate adjustment should be made in the rate found among school children.
A modification of the previous Goiter
classification system, which defined five grades, is recommended. The previously
used grades 1A and 1B are thus combined into one, and
grades 2 and 3 are
combined into another
(Table V).
Table VI gives
the epidemiological criteria for establishing IDD severity based
on Goiter prevalence in school age children. It is
recommended that a total
Goiter rate (TGR, Goiter
grades 1 and 2 ) of 5% or more in primary school children
(age range approximately 6 to 12
years) be used to signal the presence of
a public health problem. This recommendation is based on the observation that
in a normal, iodine replete
population the prevalence of
Goiter should be quite low. The
cut off
of 5% allows some
margin of inaccuracy of Goiter assessment and
for Goiter that may occur in iodine replete population due to other causes
such as goitrogens and autoimmune thyroid diseases.
The previously recommended 10%
cut off level
has been revised downwards since it has been shown that Goiter prevalence
rates between 5% and
10% may be
associated with a
range of abnormalities, including
inadequate urinary iodine
excretion and/or sub normal
levels of TSH among adults,
children and neonates.
The specificity and sensitivity
of palpation are low in grades 0
and 1 due to a high
inter observer variation.
As demonstrated by studies of
experienced examiners,
misclassification can be as high as 40%. Measurement of urinary
iodine levels (in an adequate sample) essential to decide
whether an iodine
deficiency problem is
of public health
importance.
v. Biochemical Indicators
Urinary
Iodine
Since most iodine that is absorbed is excreted, therefore the urinary iodine level is a good marker of a previous day's dietary iodine intake. However, since an individual's level of urinary iodine varies daily and even during a given day, data can be used only for making a population based estimate. Experience has shown that the iodine concentration in early morning urine specimens (child or adult) provides an adequate assessment of a population's iodine status; 24-hour samples are not necessary. Acceptability is very high and spot urine specimens are easy to obtain. Urinary iodine assay methods are not difficult to learn or use, but meticulous attention is required to avoid contamination with iodine at all stages. Special rooms, glassware and reagents should be set aside solely for this purpose.
Small amount (0.5-1.0ml) of urine is required. Specimens are collected in tubes, which are tightly sealed with screw tops they do not require refrigeration or the addition of a preservative. Iodine content remains stable throughout transport to the laboratory. The tightly sealed specimens can be refrigerated in the laboratory for several months before actual determinations are made. Should evaporation occur, iodine concentration will increase.
Since casual specimens are used, it is desirable to measure about 300 from a given population group to allow for varying degrees of subject hydration and other biological variations between individuals, as well as to obtain a reasonably small confidence interval. Smaller sample sizes are adequate to establish at the outset that iodine deficiency is the cause of the endemic Goiter. The cut off points proposed for classifying iodine deficiency into different degrees of public health significance are shown in Table VII. Frequency distribution curves are necessary for full interpretation, since urinary iodine values from populations are usually not normally distributed and therefore the median value should be used rather than the mean. The indicator of iodine deficiency "elimination" is a median value for iodine concentration of 100 ug/l, i.e 50% of the samples should be above 100 ug/l, and not more than 20% of samples should be below 50 ug/l. As an IDD prevention Program progresses, Goiter rates become progressively less useful, and urinary iodine levels progressively more useful, as elimination criteria.
New frontiers in
the field of IDD
A disturbing
finding in recent years is the emergence of new goiter-endemic areas in the
irrigated plains of country. The precise
factors underlying this have not been identified; but it is
being suspected that
the modern practice
of intensive agricultural technology
could have resulted in the diminished bioavailability of soil
iodine and the consequent
diminished content of iodine in food and water. The
possible role of an
excessive use of
fertilisers, pesticides and food additives has also been suspected.
The possibility that
goitrogens may be involved
in the emergence
of new goiter-endemic areas
is suggested by the finding of
high levels of urinary excretion of
thiocyanate in a significant proportion of subjects
in these areas. Peroxidase
inhibiting goitrogens have been suspected
to interfere with the effective utilisation of iodine by the thyroid
gland. Such goitrogens could be either
present in foods or as food contaminants. The possible role of
selenium deficiency in aggravating the
goiter problem also requires investigations. It
is becoming clear that problems of iodine
deficiency are acquiring new dimensions
in the context of intensive agricultural technology and ecological and
environmental factors incidental to 'development' In combating these new dimensions we may have
to look for strategies
other than (and over
and above ) the
conventional approach of the
fortification of common salt with
iodine.
Table
I
|
State |
Total No. of Districts |
No. of District Surveyed |
No. of District Endemic |
|
Andhra
Pradesh |
23 |
7 |
6 |
|
Arunachal
Pradesh |
10 |
10 |
10 |
|
|
18 |
18 |
18 |
|
Bihar |
38 |
22 |
21 |
|
Goa |
2 |
2 |
2 |
|
Gujarat |
19 |
16 |
8 |
|
Haryana |
16 |
8 |
8 |
|
Himachal
Pradesh |
12 |
10 |
10 |
|
Jammu
& Kashmir |
15 |
14 |
11 |
|
Karnataka
|
20 |
17 |
6 |
|
Kerala
|
14 |
14 |
11 |
|
Madhya
Pradesh |
45 |
16 |
16 |
|
|
31 |
29 |
21 |
|
Mizoram |
4 |
4 |
4 |
|
Manipur
|
8 |
8 |
8 |
|
Meghalaya
|
5 |
2 |
2 |
|
Nagaland
|
7 |
7 |
7 |
|
Orissa |
30 |
2 |
2 |
|
Punjab |
12 |
3 |
3 |
|
Rajasthan
|
27 |
3 |
3 |
|
|
4 |
4 |
4 |
|
Tamilnadu |
21 |
12 |
12 |
|
Tirpura
|
3 |
3 |
3 |
|
Uttar
Pradesh |
67 |
34 |
29 |
|
|
18 |
5 |
5 |
|
Andman &
Nicobar Islands |
2 |
Survey not done |
Survey not done |
|
|
1 |
1 |
1 |
|
Dadar &
Nagar Haveli |
1 |
1 |
1 |
|
|
1 |
1 |
1 |
|
Daman
& Diu |
1 |
1 |
1 |
|
Lakshwadeep
|
1 |
Survey not done |
Survey not done |
|
|
4 |
Survey not done |
Survey not done |
|
Total
No. of District |
480 |
282 |
241 |
RELATIONSHIP BETWEEN IODINE INTAKE AND IDD
-------------------------------------------------- -------------------
Nutritional Status
Daily iodine intake
(micrograms)
------------------------------------------------------------- ---------
Associated
with cretinism 20 or less
Associated
with goiter 20 - 50
Marginal 50 - 100
Normal 100 - 300
More than
normal 300 and above
---------------------------------------------------------------------
Table
III
The Spectrum of Iodine Deficiency
Disorders
________________________________________________________________
Stage in Life Health
Effects
________________________________________________________________
Foetus Abortions
Stillbirths
Congenital
Anomalies
Increased
Perinatal Mortality
Increased
Infant Mortality
Neurological Cretinism :
mental
deficiency
-
deaf-mutism
-
spastic diplegia
-
squint
Myxedematous Cretinism :
-
mental deficiency
-
dwarfism
Psychomotor
Defects
Neonate Neonatal
goiter
Neonatal hypothyroidism
Child and Adolescent Goiter
Juvenile
hypothyroidism
Impaired
mental function
Retarded
physical development
Adult Goiter
with complications
Hypothyroidism
Impaired
mental function
____________________________________________________________________
STATUS OF SALT IODISATION IN
1998-99 NFHS SURVEY - 2
|
Percent
distribution of households by degree of iodization of salt, according to
state, |
||||||
|
State |
Not iodized |
7 ppm |
15 ppm |
30 ppm |
Missing |
Total percent |
|
North
Haryana
Himachal Pradesh Jammu
& Kashmir
Rajasthan Central Madhya
Pradesh Uttar
Pradesh East Orissa Northeast
Arunachal Pradesh
Manipur
Meghalaya
Mizoram
Nagaland West SOUTH Andhra
Pradesh
Karnataka Kerala Tamil Nadu |
28.4 21.6 16.8 32.6 0.7 100.0 6.1 4.5 13.5 75.7 0.1 100.0 19.5 9.2 13.9 57.1 0.2 100.0 3.2 6.2 14.9 75.6 0.1 100.0 24.8 22.3 27.5 25.4 0.0 100.0 16.7 7.8 13.7 61.6 0.3 100.0 37.1 15.3 21.9 24.4 1.3 100.0 25.0 16.3 14.4 42.3 2.1 100.0 22.7 26.9 19.6 29.2 1.6 100.0 22.9 30.1 26.6 20.4 0.0 100.0 29.6 35.1 18.2 16.8 0.4 100.0 11.3 26.5 25.8 36.0 0.5 100.0 0.8 15.0 46.9 37.2 0.1 100.0 1.8 18.2 32.7 46.9 0.3 100.0 2.3 9.7 15.4 72.5 0.1 100.0 6.7 30.0 24.9 38.1 0.3 100.0 0.7 8.0 27.9 63.3 0.0 100.0 10.9 21.2 25.5 41.7 0.7 100.0 3.1 17.5 31.8 47.3 0.3 100.0 37.3 20.2 4.0 37.9 0.6 100.0 29.5 14.2 14.9 41.2 0.2 100.0 32.0 6.9 11.0 49.1 1.0 100.0 36.8 35.7 10.2 17.2 0.1 100.0 24.1 32.4 12.9 30.5 0.1 100.0 47.6 13.2 5.6 33.7 0.0 100.0 62.7 15.8 8.1 13.1 0.3 100.0 |
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ppm: Parts per million |
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Table V
Simplified
classification of Goiter
_____________________________________________
Grade O : 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 (PNV) when the neck is in
the normal
position. It moves upward in the
neck as the
subject swallows.
Nodular alteration(s) can
occur even
when the
thyroid is not visibly enlarged.
Grade
2 : A swelling in the
neck that is visible
(V) when the neck is in a
normal position
and is consistent
with an enlarged
thyroid when
the neck is
palpated.
________________________________________________________________________
Epidemiological
criteria for assessing the severity of IDD
based on the prevalence of Goiter in
school age children
_________________________________________________________
Prevalence
of Goiter Mild IDD Moderate IDD Severe IDD
_________________________________________________________
TGR 5.0-19.9% 20.0-29.9% >30.0%
Table. VII
Epidemiological
criteria for assessing severity of IDD
based on median urinary
iodine levels.
________________________________________
Median value Severity of IDD
________________________________________
< 20 Severe IDD
20-49 Moderate IDD
50-99 Mild IDD
> 100 No deficiency
________________________________________