Thyroid gland diseases
Thyroid gland diseases. The
diagnosis, the differential diagnosis, preventive maintenance and treatment of
goiter
Iodine deficiency diseases (IDD) are pathological states
caused by reduced iodine contains in organism.
About 740 million of the world population are ill with IDD.
kinds of IDD:
Ø
Hypothyroidism,
Ø Diffuse euthyroid goiter or nontoxic,
Ø
Nodular and multinodular
euthyroid goiter,
Ø
Functial autonomy of the thyroid
gland.
The
main phatology is Goiter – diffuse. Now we use modern classification of
increasing of the thyroid gland.
Degrees of Thyroid Gland Size
Abnormalities
·
0 degree - goiter is hidden and not palpable;
·
I degree - goiter is palpable, but hidden; or one or more nodules are palpable
in the thyroid gland;
·
II degree - goiter is palpable and visible.
Factors of
Etiology.
-
Main factor is iodine insufficiency, f.e. in water, in food
-
Goitrogenes factors,
which inhibit transportation of iodides to the thyroid gland
-
Low level of microelements,
such as Zn, Co, Se, Mg, Cu and high level of Ca
-
Ionize radiation and
environment pollution with radionuclides
-
Infectious diseases
-
Helmintic invasion
-
Lack of Vitamin A - reduction
-
Hereditary factors connected with disorders of syntheses thyroid hormones
Differenceeted natural
stumogenes of food products contained in tapioca, soy,
peanut, turnip. Some flavonoids provoked disorders of metabolism iodine, f.e. african millet, sorghum, bobs.
What do
analysis of presence of iodine deficiency? Analyses of iodine deficiency can be made according to concentration
of iodine in urine. There are some degrees of iodine deficiency:
Endemic goiter severity criteria (WHO, 1994)
Indices,
at children and adults
|
Standard
|
Severity
degree
|
||
Mild
|
Middle
|
Severe
|
||
goiter
rate during palpation(%)
|
less
than 5
|
5-19,9
|
20-29,9
|
more
than 30
|
Thyroid
gland volume rate more than 97 percentiles (%)
|
less
than 5
|
5-19,9
|
20-29,9
|
more
than 30
|
Median
of iodine excretion with urine (ug/1)
|
more
than 1 00
|
50-90
|
20-49
|
less
than 20
|
Median
of thyroglobulin concentration in blood (ng/ml)
|
less
than 10
|
10-19.9
|
20-39.9
|
more
than 40
|
Median
of TSH level in blood more than 5 mu/1 newborns), %
|
less
than 3
|
13-19.9
|
20-39.9
|
more
than 40
|
Pathogenesis.
The
Iodine Deficiency caused the secretory ability of the thyroid gland and
promotes goitrogenesis. The decrease of thyroid
hormone in blood leads to increasing of TSH hormone production and to the
development of iodine deficiency hypothyrosis. As a result it promotes
follicles hypertrophy, strengthening of bloodstream in a gland and iodine
absorption - compensatory mechanisms. After that thyroid gland hyperplasia
develops. This adaptive mechanisms allow to support an euthyroidism for the
long time in the conditions of insufficient iodine supply. Goiter, as the basic
manifestation of iodine insufficiency, is also a display of adaptation
possibilities of organism.
Thyroid hormone increases in pubertal age, during pregnancy, at the
serious somatic or infectious diseases. At this situations develop hyperplasia
thyroid gland acquires a nodular character. Nodules and adenomas appear in a
gland. A diffuse endemic goiter grows into diffuse-nodular goiter. Adenomas and
nodules are able to grow into thyrotoxic in case of sufficient iodine supply.
Iodine-induced thyrotoxicosis develops following this mechanism. In
these conditiones functional autonomy of the thyroid gland is developing. At
iodine deficiency, number of autonomously-functioning thyrocytes is increasing,
they formed into nodular and multinodular forms, often with thyrotoxicosis.
In
pathogenesis of clinical displays of endemic goiter certain role is played by
natural immunity inhibition.
Clinical features.
Appear increasing of thyroid gland. The
degree of increasing can be different. Usually the increase is diffuse, but sometimes it is diffuse-nodular. With mild and
moderate iodine deficiency the increase of the thyroid gland takes place
slowly, achieving maximal sizes during 10-15 years and more. Clinically the
goiter is usually euthyroid, with gradual development of the hypothyroidism.
Goiter is only the external display of iodine deficiency. Clinical
features are caused by a hypothyroidism. Fatigue, deceleration of psychical
reactions, dysmenorrhea, galactorrhea, abnormalities of the reproductive
ability arc connected with hypothyroidism.
Characteristic signs of hypothyroidism:
• constipations,
• physical and mental fatigue,
• somnolence, chillness,
• growth of body weight,
• anemia.
In
severe cases endemic cretinism develops which is manifested by disorders of the
nervous system.
Diagnosis. -
Thyroid hormones in blood is decreasing.
-
TSH in blood plasma is
increasing.
-
Goiter size.
-
Testing of ioduria.
-
Ultrasound examination of the
thyroid gland enables to determine its size and presence of nodules.
On indication: - Nodules formations are punctuated.
- Scanning with
radioactive iodine.
Treatment.
1. Diffuse
endemic goiter prescribe iodides in daily dose up to 200μg, in
case of a big
goiter (2nd degree) L-thyroxin is prescribed to decrease TSH
concentration in blood. The dosage of L-thyroxin is from 25 to 100 μg per day. Patient's
condition must be strictly monitored and controlled to achievement an
euthyroidism.
Surgical intervention is
necessary for patients with large goiters or in case of presence syndrome of
compression and dysfunction.
2. Nontoxic Nodular and Multinodular goiter. There are three methods of
treatment: surgical, medicamental, and active supervision of the nodule.
- Medical tactics
depends on functional condition of the nodule, cellular compound, growth
velocity. The medicamental treatment of nodular goiter by L - thyroxine is
applied in case of hypothyrosis. The purpose of the treatment is a replacement
therapy, achievement of euthyrosis, inhibition of further enlargement of nodes.
- Surgery is applied in case of node malignization, autonomic adenomas,
quickly enlarged retrosternal nodes, compression of trachea or esophagus,
mediastinum.
- Active supervision is applied to patients with nodes (10-30 mm in diameter) without
signs of proliferation, which does not enlarge during dynamical ultrasound
investigation, usually these are mature and elderly people.
Prevention.
Iodine deficiency may be prevented by realizing mass, group and individual iodine prophylaxis.
Mass prophylaxis is carried out for all inhabitants
of an iodine deficient area. Iodized
salt consumption is a tried and tested method. Iodination is made by
using potassium iodide, 20 -40 mg/kg of salt, that provides matriculation of
150 μg of iodine every day. For mass prevention oily dine solution (lipiodol)
is also used. Ingestion of this product provides a body with a sufficient
amount of iodine for 6 to 12 months and intramuscular introduction - for 1 to 3
years.
For individual and group prevention iodine preparations are used, primarily antistrumin, 1
tablet 1-2 times a week, as well as iodides (Iodide-Farmak, IodBalance and Iodomarin)
-10 and 200 μg in tablets.
Group prevention is an additional introduction of iodides on the back-ground of the mass
prophylaxis for the categories of people with an increased iodine requirement: pregnant women, nursing mothers,
adolescents.
Individual prevention is prescribed
to some patients in case of an increased iodine requirement. These patients will
include: women one year before a scheduled pregnancy, recovers after severe
somatic or infectious diseases, after antibiotic therapy courses or sulfonamide
treatment, persons with affected alimentary organs, if abnormal iodine
absorption may occur.
Iodine
requirement for different age categories
Children under 1
years old
|
50 μg/day
|
Children 1-6
years old
|
80 μg /day
|
Children 6-12
years old
|
120 μg /day
|
Children older
than 12years old
and adults
|
150 μg /day
|
Pregnant women
and
nursing mothers
|
150 to 200 μg /day
|
Thyrotoxicosis.
Thyrotoxicosis (synonym:
Basedow's, Graves' s - diffuse toxic goiter) is a disease characterized by
excessive production of thyroid hormones (hyperthyroidism) and by diffuse
enlargement of the thyroid gland. Changes in other organs caused by
influence of thyroid hormones and autoimmune disorders.
Graves' disease is
mostly a disease of women of 20-50.
Etiology.
Thyrotoxicosis
occurs in consequence of the thyroid-stimulating globulins formation, which
compete with TSH receptors on a surface of thyreocytes and induce a cell growth
and excessive secretion of thyroid hormones.
Factors that lead to autoimmune disorders can be:
§ excessive amount
of iodine,
§ treatment by
lithium,
§ infectious
diseases (a flu, quinsy, chronic tonsillitis, a scarlet fever, whooping cough,
rheumatism, encephalitis).
Some viruses can
form complexes with thyreocytes surface proteins, changing its structure and
antigenic characteristics.
As provocative moments of disease
manifestation can act
• an excessive
insolation,
• a mental trauma,
• pregnancy and
postnatal period.
Pathogenesis.
Thyrotoxicosis is
classified as a disease which develops due to the mechanism of hypersensitivity
of the slow type.
Genetic defect is located in organ-specific CD-8 -
lymphocytes (T-supressors). Because
of the suppression of "forbidden" T-lymphocytes clones is not carried
out they survive and cooperate with organ-specific antigenes of a thyroid
gland.
Clones of lymphocyte that are sensibilized to the
antigenes of a thyroid gland stimulate B-lymphocytes to synthesis of antibodies
to thyroid-stimulating hormone receptor. Thyroid-stimulating immunoglobulins
of class G cooperate with follicular epithelium receptors and induce
thyreocytes to excessive production of thyroid hormones and to hypertrophy and
hyperplasia.
It is impossible
to explain completely a pathogenesis of diffuse toxic goiter by action of
thyroid-stimulating immunoglobulins. They are also found at subacute and
autoimmune thyroiditis. In these cases they do not stimulate but depress the
function of a thyroid gland. In pathogenesis of a diffuse toxic goiter a major
importance is given to lymphocytic infiltration of the gland which produces a
tumor necrosis factor and alpha interferon.
Pathogenesis of
clinical symptoms of diffuse toxic goiter is connected with increased
cathabolic impact of excessive amount of thyroid hormones.
Clinical features.
Most prominent clinical symptoms of disease are:
-
increasing irritability,
-
nervousness,
-
tachycardia,
-
weight loss with normal nourishment,
-
weakness,
-
a tremor of all
body,
-
sweating,
-
heat intolerance,
-
diarrhea,
-
tearfulness.
The skin is wet
and warm. In some patients an uneven hyperpigmentation
of all body is observe. In some patients a pretibial
swelling (thyroid acropathy, pretibial
myxedema) is observed. The skin is characterized by swelling of pretibial
areas, brownish in color.On feet the leather skin is horned, crawls over
phalanxes of fingers.
The eyes signs are
characteristic to the majority of patients with a diffuse toxic goiter – Ophtalmopathia.
v Palpebral fissures are widely
opened with expression of surprise - Delremplin's
symptom.
v The exophtalmus is determined, more often on both eyes. Exophotalmus
can affect one eye, for instance a rare
winking - Shtelwag's symptom;
v Retraction of upper lid, owing to what during the movement of an eyeball
downwards between upper lid and an iris appears a white strip of sclera - Gref's symptom or during the movement of an eyeball upwards -
Coher's symptom.
v Disorders of
convergence of eyeballs is called - Moebius's
symptom.
The most typical clinical symptoms of thyreotoxicosis
are changes in cardiovascular system.
The most common is sinus tachycardia.
The pulse rate reaches 100 beats per a minute and more. May be: - extresystole,
- atrial fibrillation.
Symptoms of
thyrotoxicosis and their frequency
Symptom
|
Frequency
(%)
|
Goiter
|
85-100
|
Tachycardia
|
85-100
|
Sweating
|
70-90
|
Heat
intolerance
|
70-80
|
Tremor
|
70-90
|
Increased
systolic blood pressure
|
60-80
|
Weight
loss
|
60-80
|
Hyperkinesia
|
60-80
|
Muscle
weakness
|
60-80
|
Eye
signs
|
50-70
|
Diarrhea
|
20-10
|
Ophtalmopathia
|
30-50
|
Increased
appetite
|
40-60
|
Atrial
fibrillation
|
10-30
|
Pretibial
myxedema
|
2-3
|
Dysmenorrhea
|
3-5
|
Vitiligo
|
1-2
|
The systolic blood pressure increased and diastholic blood
pressure is reduced. It is connected with increase cardiac output (systolic
blood pressure) and peripheral vasodilatation (diastolic blood pressure).
Borders of relative heart dullness are displaced to the left, heart tones are
loud and strengthened. A systolic murmur may be often heard. The origin of
murmur is connected with enlargment of atrioventricular ostiums and bloodstream
acceleration. The gemodinamic changes includes increased stroke and minute
volumes of bloodstream, volume of circulating blood, bloodstream. Heart insufficiency
develops in 15-20 % of cases, mainly in patients with atrial fibrillation.
Thyreotoxic cardiomiopathy develops under influence of excessive amount of
thyroid hormones and catecholamines, which received a clinical name
«hyperthyroid heart».
Electrocardiographic examination
shows the signs of a left ventriclar hypertrophy. High waves R, S and T,
shortening of interval S-T, sinus tachycardia are fixed. As soon as heaviness
of «hyperthyroid heart» increases the waves size decreases and wave T becomes
twophase or negative, the depression of S-T segment and atrial fibrillation are
observed.
Changes of muscular system are shown by thyrotoxic miopathy.
Significant muscular.
Half
of patients suffer from changes of digestive system. Defecation becomes more
frequent, it can be up to 20 times a day. Weight loss is one of the most
typical symptom of thyrotoxicosis. It is caused by increased catabolism due to
high amount of thyroid hormones.
Characterize
presents of psychic and nervous symptoms in clinical picture, f.e. a
nervous hysteria. Patients appear to be nervous, anxious, irritate with no
reason, start crying. Changes of mood are often. Tremor of fingers of the
extended hands (Mari's symptom) is typical. Tremor is constant. In case
of serious clinical course of thyrotoxicosis depression, delirious conditions
and delirium are possible.
On the part of skeletal system an intensification of osteoporosis
is possible as a result of stimulating impact of thyroid hormones on
osteoclasts.
Dysfunction of other glands of internal secretion, in particular,
reproductive glands is frequently observed during thyrotoxicosis. Half
of women with thyrotoxicosis have deranged menstrual cycle and dysmenorrhea. In
case of mild forms of thyrotoxicosis menorrhea. The menstrual cycle becomes
single-phase with insufficiency of lutein phase.
Males has atrophic changes in testis, prostate
gland, reduced libido and potency. These specified symptoms are temporal,
reverse development occurs after the liquidation of thyrotoxicosis.
Function of adrenal glands is intensified, as a result -
hypocorticoidism develops, and chronic suprarenal insufficiency (Addison's
desease).
Patients with thyrotoxicosis may have reduce tolerance to
carbohydrates even to development of a diabetes.
The thyrotoxic crisis develops within several hours to one day.
Symptomatology:
·
Excitation increases
·
Tachycardia - 200 beats per a
minute
·
Extrasystole
·
Atrial fibrillation
·
Systolic arterial blood pressure
increases
·
Diastolic arterial blood pressure
decreases.
·
Sweating is increased
·
The skin is warm and wet to touch
·
The body temperature increases and
can arise up to 40 °C
·
Psychical and emotional excitation
·
Psychical excitation - acute
psychosis with a disorientation, delirium, hallucinations
·
The diarrhea
·
Vomiting
·
Muscular weakness up to adynamia
·
Patients can lose consciousness -
Thyreotoxic coma
·
Other complectation - acetone
appears, ketonurine
·
Acute hepatic insufficiency
·
Reduction of diuresis up to anury
·
The systemic alkalosis,
hypokaliopenia
Diagnosis is based on the establishment of excessive production of thyroid
hormones (hyperthyroidism) and on diffuse enlargement of the thyroid gland.
The most typical
clinical signs are:
-
excitability,
-
irritability,
-
weight loss,
-
weakness,
-
tachycardia,
-
atrial fibrillation,
-
sweating,
-
tremor of all body.
A goiter
in a patient diffuse hyperplasia
Functional activity of
a thyroid gland
1.
Level of thyroid hormones increased.
2.
Depression of TSH.
Thyroid gland volume is determined by ultrasound studies. In case
of toxic goiter a thyroid gland is diffusely enlarged.
Treatment.
Thyrotoxicosis can be treated by medications, surgery or by using a
radioiodine.
Antithyroid drugs is always used - mercasolile,
thyrosol, thiamazole, metisole. These medicaments block formation of organic
iodine in a thyroid gland, they inhibit the process of condensation of
iodotyrosines into triiodothyronine and thyroxine.
In case of intolerance to mercasolil, other
medicaments with thyrostatic actions are prescribed,
a)
iodides,
b)
Lughole’s iodine solution is
prescribed up to 50 drops a day.
Beta-blockers are prescribed with antithyroid
medicaments.
·
propranolol is 120 mg per day
·
atenolol (50-100 mg per 24 day),
·
metoprolol (100-200 mg per day),
·
bysoprolol (5-10 mg per day).
Glucocorticoids can be also used in case of
relative suprarenal insufficiency. The prednisolonum is prescribed in an
initial dose of 20-30 mg, reducing each five days to 5 mg or other
glucocorticoids in an adequate dose.
Treatment of a
thyrotropic crisis includes:
-Elimination of provoking factors (whenever it is possible);
-Blockade of thyroid hormones synthesis;
-Blockade of peripheral action of hormones;
-Maintenance of vital functions of an organism;
-Removing thyroid hormones and thyroidstimulating
immunoglob-ulines from an organism.
Blockade
of thyroid hormones synthesis is reached by oral introduction of mercasolil or
through nasogastral probe. Initial dose of mercasolil is 60 mg, further dose is
30 mg each 4 hours. Preparations of iodine are prescribed in 2 hours after
introduction of mercasolil. It excludes use of iodides for thyroid hormones
synthesis.
Intravenous drip-feed of 1000 ml of 5 % solution of glucose with 1 ml of
Lughole’s iodine solution is prescribed. 10 % natrium iodides solution is
injected, by 1 ml intravenously each 3 hours. Lughole’s iodine solution can be
given by oral introduction or through nasogastral probe by 30—40 drops each 3
hours.
Peripheral action of hormones is blocked by B-blockers, that is why a
pro-pranolol is injected intravenously from 1 up to 3 mg each 3 hours.
Glucocorticoids are also intravenously dropwise injected. Hydrocortison is
prescribed up to 500 mg per day or prednisolonum - 200 mg per day, dexamethazon
up to 20 mg per day. Strengthening of thyroid hormones excretion from an
organism is reached by assignment of phenobarbital, in dose up to 200 mg per
day.
Body temperature of patients is reduced by covering them with bubbles of
ice, cold blowing, by assignment of acetoamiphenum (paracetamol).
Excessive amount of thyroid hormones released from an organism with the
help of plasmapharesis, hemadsorbtion. The water regimen of an organism is
supported by introduction of a 5 % solution of glucose and 0.9 % solution of
natrium chloridis.
Hypothyroidism
Hypothyroidism is a disease, caused by a persistent
reduction of thyroid hormone impact on a target organs.
Classification.
Nowadays the
following forms of hypothyroidism are distinguished:
1.
Primary hypothyroidism – as a result pathology in a thyroid gland.
2.
Central hypothyroidism (hypothalamic-pituitary). Hypothyroidism develops due to a defeat of a
pituitary gland (secondary hypothyroidism) or hypothalamus (tertiary
hypothyroidism).
3.
Peripheral hypothyroidism, caused by resistance of tissues to thyroid hormones action
4.
Subclinical hypothyroidism is
a syndrome, which is characterized by increasing plasma level of TSH on a
background of a normal level of thyroxine and triiodothyronine.
5.
Transient hypothyroidism. Hypothyroidism, which developed on a background of some diseases
(conditions) or reception of medical preparations and inclined to spontaneous
disappearance of its displays after elimination of etiological factors.
Etiology.
It is known that primary hypothyroidism makes approximately 95 % of all
cases of hypothyroidism. Often it is an outcome of autoimmune thyroiditis, it
may be a display of congenital defects of thyoroid hormones biosynthesis, the
heaviest iodine deficiency, medicamentous or toxic effects.
Pathogenesis.
The pathogenetic basis of hypothyroidism is an disorder of metabolism.
Metabolism is reduced, especially in organs and tissues, which quickly grow and
updated:
• erythropoesis is slowed down and anemia occurs
•
Free fatty acids, triglyceridis,
cholesterol are collected in organism because of lipids metabolism delay
•
Proteins metabolism - accumulation
of glycosaminglycans - a mucinous swelling.
Clinical features.
The disease develops slowly and gradually. Weakness, drowsiness,
sluggishness, memory impairment, chill, constipations are typical complaints of
patients. Frequently patients with anemias.
Clinical
symptoms
|
Frequency
%
|
Weakness
|
90-70
|
Dryness
of the skin
|
90-70
|
Drowsiness
|
90-70
|
Speech
delay
|
90-70
|
Chill
|
90-70
|
Face
puffiness
|
90-70
|
Increased
tongue
|
90-70
|
Hair
loss
|
90-70
|
Increased
borders of relative heart dullness
|
90-70
|
Bradycardia
|
70-50
|
Memory
impairment
|
70-50
|
Pallor
of a skin
|
70-50
|
Yellowish
discoloration of the skin
|
70-50
|
Weight
increase
|
70-50
|
Lack of
breathe
|
70-50
|
Hoarseness
of the voice
|
70-50
|
Hearing
impairment
|
30-20
|
Cardiovascular system. Abradycardia
in case of a significant anemia tachycardia occurs. The borders of relative
heart dullness are displaced due to dystrophic changes in myocardium and
accumulation of liquid in a pericardium. The diastolic pressure increases. On
electrocardiography the interval R-R is increased, voltage of waves is reduced,
there can be a depression of S-T segment, inversion of T wave.
Significant changes in gastrointestinal system are observed. A
decreased motility of the. The tongue is increased. The secretion is decreased,
the absorption of vitamin B12 is disturbed, this process aggravates
anemia.
Essential changes are revealed in nervous system, both in
peripheral and in central. A hypothyroid patient is slow in thought, they less
able to concentrate and memorize. The mental potential of a person decreases.
Some of patients feel fears, disturbing-depressive syndrome is formed.
Changes in peripheral nervous system –as a result tunnel
syndrome.
The bronchitis
and prolonged pneumonias are.
The changes of muscles and joints - edema of synovial structures
and capsules of joints of hands and legs – as a result pseudomyopathic syndrome
occurs.
Anemia – decrease of hemoglobin synthesis,
reduction of iron absorbtion in digestive system, vitamin Bp and
folic acid deficiency.
Myxedema
coma.
The
reason of its development is untreated hypothyroidism.
Reasons: - cold
exposures,
-
respiratory diseases,
-
surgical interventions,
-
narcosis,
-
food and medicamental
intoxications,
-
medical drugs, that oppress central
nervous function (neuroleptics, tranquilizers, sedatives).
In patogenesis : - hypercapnia,
-
hypoxia,
-
water and electrolytic imbalance,
-
hypothermia.
Hypoxia is caused by pulmonary hypoventilation. Adiposity, edema of
body, hydrothorax, ascites, mucinous swelling of alveoluscs promote hypoxia
development. Decreas of kidney’s bloodstream - hypercapnia - coma develops
gradually.
Clinic features.
·
Weakness,
·
Apathy,
·
Drowsiness occurs,
·
Movements become slower.
Appearance
of patients with hypothyroidism is rather specific: puffy face with specially
strongly pronounced swelling lips, ears and eyelids. The skin is dry, pale,
rough with scales and it feels cold. The skin practically can not be taken in
folds because of significant mucinous swelling.
The body temperature is reduced. Bradycardia. Boundaricss of heart
dullness arc displaced.
Diagnosis and the differential diagnosis.
Ø
Hypothyroidism is diagnosed on its
clinical symptoms and laboratories results of hormones in plasma of blood.
Ø
Reduction of triiodothyronine
Ø
Thyroxine and increasing of TSH.
Instrumental diagnostics.
Ø
Increased time of Achilles tendom
reflex - the limits of 270 ± 30 Msec.
Ø
An atrophy of a thyroid gland - ultrosound.
Treatment.
Hypothyroidism is treated by synthetic analogues of thyroid hormones:
Levothyroxine and Liothyronin. There are also combined preparations of
Levothyroxine with Liothyronine and a potassium iodide (Thyrocomb, Thyrotom,
Novothyral e.a.)
Thyrocomb (70 ug of the Levothyroxine, 10 ug
of the Liothyronine, 160 ug of the potassium iodide).
Thyrotom (40 ug of the Levothyroxine, 19 ug
of the Liothyronine).
Thyrotomorte (120 ug of the L-thyroxine, 30 ug
of the L-triiodothyronin).
Novothyral (120 ug of the Levothyroxine, 20 ug
of the Liothyronine).
Euthyrox with 25, 50, 75, 100, 125, 150,
175, 200 ug of levothyroxine.
Levothyroxine is the most used preparation - for
adults is 1.6-2.2 ug /kg/ per day. The treatment begins with 1/4 of a day.
Calculated dose increasing each 2 weeks twice and
gradually leading up to a necessary effective therapeutic dose. The treatment
begins from 25 ug of the Levothyroxine per day leading up to 100-150 ug per
day. All the dose is taken in the morning after a breakfast. The efficiency of
the treatment is estimated by a regress of clinical symptoms regression and
normalization of the TSH.