Pure goitre pathology

2021-01-27 12:00 AM

There are many ways to add iodine, but iodizing salt is the most preferred method of iodine supplementation in an iodine-deficient population.


The epidemiological goitre is also known as a local goitre or a circulating goitre: When the physiological requirement of iodine is insufficient in the population, a series of abnormalities arise, including damage to thyroid function and, when severe iodine deficiency causes epidemiological goitre or dullness, decreased intelligence and increased perinatal and neonatal mortality. These complications are a major hindrance to the development of the population and are grouped together as a common name due to iodine deficiency.

The goitre has since been defined as a localized or general enlargement of the thyroid gland in more than 10% of the population.

The definition of a sporadic goitre is an enlarged thyroid gland that is wholly or partially benign with no symptoms of hypothyroidism or hyperthyroidism, is not caused by inflammation, and is not of a local nature (i.e., region without epidemiology.), pathogenic factors do not influence in the general population.

The many different causes of a large thyroid gland are probably common to both sporadic and epidemiological goitre.


Single goitre is more common in women than men, and the incidence is high in some localities. In the world, there are geographical regions lacking iodine: such as mountainous areas with a very high risk of goitre: snow-covered areas, Himalaya (Himalaya, Andes)

However, it is also found to lack iodine in areas with low amplitude, very far from the ocean such as the Central African continent, the European continent today. There are no exact figures for how much of the human race is at risk of developing the disorder due to an iodine deficiency.

One estimate is considered probable> 800 million, of which 3 million are epidemiologic.

In Vietnam, according to a survey by the Ministry of Health (1993) on urinary iodine in children 9-11 years old, there is 94% lack of iodine.

Whole disease

Lack of iodine

Meet in special geographic areas such as mountainous areas and some of the areas mentioned above.

Female hormonal disorders: occurs in women with puberty, pregnancy, perimenopause.

Due to the anti-thyroid

White cabbage or synthetic antithyroid drugs or substances that inhibit iodine loading such as Thiocyanate, Perchlorate.

Cassava also causes goitre epidemiology, because cassava contains Glucoside cyanogénique, Linamarin, which when hydrolysed to release cyanuric, in the body cyanurate is detoxified into thiocyanate, which thiocyanate inhibits the pump of thyroid iodine and increases vocalisation. Iodine excretion by the kidneys, resulting in a lack of body iodine.

Due to abnormal synthesis of thyroid KTT

Due to lack of enzymes affects the biosynthesis of thyroid KTT.

Due to a congenital bias in thyroxine synthesis, abnormal iodoprotein is produced.

Using high doses of iodine causes inhibition of thyroid hormone synthesis due to the effectiveness of Wolff Chaikoff (transient effect).

Loss of iodine

Prolonged diarrhoea, nephrotic syndrome (decreased protein loading iodine), pregnancy (increased urinary iodine excretion).

Mechanism of pathogenesis

In goitre, decreasing thyroxin stimulates the pituitary to increase TSH secretion, causing goitre and increase the production of thyroid hormones, this is just a compensatory phenomenon, a reaction to supply the body with enough thyroxin, so the thyroid is not impaired. reduced functionality.

The concentration of iodine in the blood and thyroid decreases, causing an enlarged thyroid to compensate also through the above mechanism.

The problem of goitre is not very well explained, it is thought that the entire thyroid gland begins to enlarge and then shrinks to one or more nuclei. There is another opinion that TSH acts on a small number of thyroid cysts, and the colloid tumour is the result of a tumour or hypertrophic cells.


Clinical symptoms

Mechanical symptoms:

For goitre alone: ​​the patient usually has a euthyroid state.

For epidemiological goitres, it affects the body development, especially in children, reducing intelligence and dullness.

Physical symptoms:

For single goitre: just happen to see a large goitre, or because someone else discovers a tumour in the middle of the neck, has a clear boundary, does not stick to the skin, is painless, soft or firm, moves in rhythm swallowing, when the tumour is large, it can cause insertion; no blowing at the top of the tumour.

For multi-nuclear goitre: consists of many round blocks with diameters from 0.5 to several cm.

Goitre classification has epidemiological properties:

The normal sizes of each TG lobe: 2.5-4cm in height, 1.5-2cm in width, 1- 1.5 in thickness; the weight of TG 10-20g.

Subclinical symptoms

Quantify FT3, FT4 normally.

Normal FT4 = 0.8 - 2.4ng / dl, or 8 - 18pg / ml, or 10 - 30nmol / L.

FT3 = 0.4ng / dl, or 3 - 4pg / ml

Normally, the thyroid secretes T4 is converted to T3 in peripheral tissue under the action of désiodases. T3 is a hormone that acts on target cell receptors. So it is best to measure FT3, FT4, biologically active, and especially FT4 actually assess TG production, while FT3 is specific for peripheral regulation.

The whole T3 and T4 are less honest, due to their susceptibility to alterations by foreign factors affecting protein loading:

Factors that increase protein load or increase total T4: oestrogen, pregnancy, infectious hepatitis, myeloma, collagenase.

T4-reducing factors: malnutrition, hypovolemia, cirrhosis, androgen drugs, high dose corticoids.

Factors that prevent association with protein loading: hydantoin, clofibrate, héparine, phenylbutazone.

TSH is extremely sensitive (TSH us) normal (TSH = 0.3 - 4mUI / L).

TSH controls TG, TSH secretion is very sensitive regulated by peripheral thyroid hormone concentration through a feedback mechanism.

Using the current generation II ultra-sensitive technique of 0.1mUI / L, TSHus <0.1mUI / L is hyperthyroidism. Generation III is 0.01mUI / L, TSH us <0.01mUI / l is hyperthyroidism.

A normal I131 concentration, except in the case of an iodic monolith, requires an additional Werner test to rule out hyperthyroidism.

Normally, the concentration of I131 in the thyroid gland at the time of 2 hours is 15%, at 6 hours is 25%, after 24 hours is 40%.

Scintigraphy: shows thyroid morphology, thyroid function, ability to capture radioactive I131 or 99 Technetium of the owner of the thyroid tissue (this test is necessary for tumour designation): in a single tumour, the iodine is evenly distributed throughout the thyroid gland.

Quantify free T3, T4 normally.

TSH is extremely sensitive normally.

I131 concentration is normal, except in the case of single iodine tumour.

Biopsy: sometimes needed, for benign changes as seen in pathology.

For epidemiological goitre or local goitre, urinary iodine/day measurement, or urinary iodine/creatinine ratio to assess the severity of iodine deficiency:

Mild degree: 50 - 99 (g / day or 50 - 99 (g / g urinary creatinine.

Average level: 25 - 49 (g / day or 25 - 49 (g // g urinary creatinine.

Severity <25 (g / day or 25 (g / g urinary creatinine).

Maximum volume of the thyroid gland (upper limit) in adults 18 ml.


Implementing the quadrants

Epidemiological and clinical conditions are sufficient for diagnosis.

In the case of sporadic goitre, more careful clinical examination and laboratory tests should be done to probe gland function.

Differential diagnosis

Goitre with hypothyroidism: differences only in symptoms of hypothyroidism.

Hyperthyroidism like Basedow, clinically toxic goitre with signs of hyperthyroidism, the special properties of the goitre and subclinical help make diagnosis easy.

Monolithic goitre combined with neurological disorders: having the same symptoms as goitre, easily tired or nervous, fast heart rate but heart rate easily returns to normal when resting or using sedation, soles hands are sweaty but not hot, and the tests probe for normal thyroid function.

Mono-iodic goitre: no sign of hyperthyroidism, only high I131 concentration, but Werner test> 50%, other tests are normal.

Thyroid k: very stiff, may have symptoms of compression and lymph node metastasis, I131 concentration, a biopsy to eliminate.

Subacute and chronic thyroiditis (Hashimoto, Riedel), diffuse goitre, sometimes multiple nuclei, stiffness, increased sedimentation rate, (increased globulin, high autoantibodies against thyroid, TPO resistance KT, organ biopsy armour to eliminate.

Extra-thyroid tumour: not moving with swallowing rhythm.


Haemorrhage in the tumour: the tumour is fast, painful and hot, acute compression mark.

Hyperthyroidism: Usually occurs in the multinodular tumour, perennial tumour, Basedow normalization of the normal gland between the nuclei, often due to too much iodine supply (iodine-Basedow).


Particularly for goitre due to lack of iodine in the pregnant mother: can affect the mental and physical development delay of the fetus.


The principles of treatment

In order to normalize thyroid hormone levels, without requiring the thyroid to overact and enlarge, so if aetiology:

Lack of iodine, provide iodine, not due to lack of iodine, provide more thyroid hormone synthesis.

In single goitre due to lack of iodine, treatment with iodine or thyroid hormone causes the thyroid to shrink more or less, depending on many factors, such as time to appear, tumour size, fibrosis of the tumour.

Among other causes of nontoxic diffuse mononuclear goitre, levothyroxine may be used to reduce the size of the thyroid gland.

Specific treatment

Treatment of single diffuse (non-toxic) goitre:

Surgical treatment:

Minimize surgery because the goitre, in this case, is largely due to the compensatory action, if removed, it is easy to get hypothyroidism, especially rarely indicated for diffuse large tumour. However, surgical intervention can be instituted in the following cases:

The goitre is too large to cause pressure (difficulty swallowing, difficulty breathing, hoarseness). Perennial goitre is susceptible to cancer or suspected cancer. Polycystic tumour

For aesthetic reasons.

After surgery, must regularly check FT4, TSH to detect hypothyroidism in time

. Internally medical treatment:

For goitre due to lack of iodine or local goitre:

Most of them do not or have very little effect on thyroid function, but the main cause is due to lack of iodine, so it is best to put iodine in treatment and prevention, Iodine has many forms:

Iodine as iodur de potassium (IK) (Lugol) 1 mg of KI salt/day for a minimum of 6 months, or iodate de potassium (KIO3).

Need to monitor Iodine-Basedow complications.

However, because the Feedback mechanism is normal, thyroid hormone can be used

to reduce the volume of the thyroid gland. L. Thyroxine tablets are indicated when:

Clinical and ultrasound identifies large goitre.

Thyroxine concentrations decrease and plasma TSH increases.

The volume of the thyroid gland is smaller compared to before treatment

Thyroxine (Levothyroxine, L-Thyroxine, Levothyrox) (T4), 50μg, 75μg, 100μg, the dose depends on the patient's condition 0.5-2 tablets/day

Levothyroxine has a 1/2 life of 7 days, well-absorbed, used in the morning to avoid insomnia.

Triiodothyronine (Liothyronine) (T3) tablets 25 μg, 1-2 tablets/ng, rarely used because of rapid absorption, 1/2 short life, effective only transient. Do not use in patients with hypertension, coronary artery disease.

In young adults, the dose starts at 100 μg / day and is discontinued when the TSH is at the normal-low level

Monitoring for increasing dose gradually to achieve good results, monitoring complications of hyperthyroidism (rapid pulse, thinning).

In elderly patients, an initial dose of 50 μg / day is required, with increasing dose monitoring of angina and electrocardiogram.


Because of the potential for latent autoimmune thyroid disease, thyroxine should be avoided especially when the TSH is in the low limit.

In elderly patients, nodules or fibrosis tumour, the ability to shrink about 1/3, the disease usually decreases after 3-6 months of treatment.

For sporadic goitre not due to lack of iodine:

Still treated with thyroxine dose as above, to reduce thyroid enlargement.

Treatment of multinuclear goitre is not toxic.

Most polynuclear goitre is non-toxic and can be conserved.

Supply of thyroxine rarely causes the thyroid to shrink.

If levothyroxine is used, the starting dose is 50 μg / day, the dose may be increased gradually, but TSH should be monitored.

Contrast or iodine-containing substances should be avoided because of the risk of iodine-Basedow hyperthyroidism due to increased production of thyroid hormone by thyroid nuclei.

Radiation therapy is increasingly indicated because of the smaller gland size, and can selectively remove autonomic nuclei. Dose I131 depends on thyroid size, and on radioactive iodine capture. Usually approximately 100 μCurie / gram of glandular tissue. Treatment can be repeated if needed. In most patients, the thyroid size decreases by about 40-50%.

When acute compression occurs, glucocorticoids or surgery may be needed.

Hypothyroidism after non-toxic multinuclear goitre treatment is less common than after Basedow radiation therapy. However, approximately over 5% of autoimmune hypothyroidism can occur after treatment for nontoxic multinuclear goitre.,.


For region lacking iodine

Iodized salt:

The recommended concentration of iodine mixed into salt is recommended as 1 part of iodine for 10,000-100,000 parts of salt, by based on the consumption of about 5g-10g salt/day, providing about 50-500μg iodine/ng. Currently using iodate is more stable than iodure (IK) due to its stable properties in the humid tropics,

Prevention of goitre by using iodized salt has had good results in some countries such as USA, Switzerland, India, Mexico, Finland, and Czechoslovakia. In the United States, after 30 years of provision of backup iodine’s, the 24-hour radioactive concentration decreased from 40-45% (1960) to 8-30% (1990). However, as recommended by WHO (1996) on the use of iodized salt, it should be noted:

Approximately 20% of the iodine is lost from production to use.

About 20% of the iodine is damaged during food preparation.

The average amount of salt used per day is 10g. How to mix Potassium iodate (iodate de potassium: KIOμ) or potassium iodine (IK) 20-25 mg/kg salt, corresponding to the average requirement is 150-300 μg / day.

Supply is assessed when the urine iodine concentration averages 100-200 μg iodine / l

Oil iodine:


Oral: 1ml contains 480mg iodine, 1ml single dose, 1-2 years prophylaxis.

Intramuscular injection: a dose of 0.5-1ml (1ml contains 480mg of iodine), prevention of goitre and local numbness in 3 - 5 years.

Children <1 year: dose 0.5ml, TB in the buttocks.

Children> 1-year-old and adults TB in hands, a dose of 1ml.

Water iodine phase:

Iodine type of concentrated solution I2, IK or KIO3 put into drinking water needs 150μg / day.


5g I2 + 10g IK in 100ml (or 6mg of iodine contained in 1 drop of Lugol). The duration of action is shorter than the iodine oil, it is recommended for many times a day

There are many ways to add iodine, but iodizing salt is the most preferred method of iodine supplementation in an iodine-deficient population.