Hypothyroidism primary subclinical code according to ICD 10. Postoperative hypothyroidism

RCHR ( Republican Center healthcare development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols Ministry of Health of the Republic of Kazakhstan - 2017

Atrophy thyroid gland(ACQUIRED), Congenital hypothyroidism without goiter (E03.1), Congenital hypothyroidism with diffuse goiter (E03.0), Unspecified hypothyroidism (E03.9), Other specified hypothyroidism (E03.8), Other chronic thyroiditis(E06.5), Myxedematous coma (E03.5), Post-infectious hypothyroidism (E03.3), Congenital iodine deficiency syndrome (E00), Thyroiditis, unspecified (E06.9)

Endocrinology

General information

Brief description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

Hypothyroidism- clinical syndrome caused by persistent deficiency of thyroid hormones or a decrease in them biological effect at the tissue level.

INTRODUCTORY PART

ICD-10 code(s):

ICD-10 (children)
Code	Name
E00	Congenital iodine deficiency syndrome
E00.0	Congenital iodine deficiency syndrome, neurological form, endemic cretinism, neurological form
E00.1	Congenital iodine deficiency syndrome, myxedema form, endemic cretinism: hypothyroid. myxedema form
E00.2	Congenital iodine deficiency syndrome, mixed form, Endemic cretinism, mixed form
E00.9	Congenital iodine deficiency syndrome, unspecified, Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS.
E03	Other forms of hypothyroidism
E03.0	Congenital hypothyroidism with diffuse goiter, congenital goiter (non-toxic): NOS parenchymal Excluded: transient congenital goiter with normal function(P72.0)
E03.1	Congenital hypothyroidism without goiter, aplasia of the thyroid gland (with myxedema) Congenital: atrophy of the thyroid gland. hypothyroidism NOS
E03.3	Post-infectious hypothyroidism
E03.4	Thyroid atrophy (acquired), Excludes: congenital thyroid atrophy (E03.1)
E03.5	Myxedema coma
E03.8	Other specified hypothyroidisms
E03.9	Hypothyroidism, unspecified, myxedema NOS
E06	Thyroiditis
E06.5	Thyroiditis: chronic: . NOS. fibrous. woody. Riedel
E06.9	Thyroiditis, unspecified

Date of protocol development/revision: 2013 (revised 2017).

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
VG	-	congenital hypothyroidism
Gastrointestinal tract	-	gastrointestinal tract
svT3	-	free triiodothyronine
SSS	-	cardiovascular system
T4 general	-	total T3
T4 sv	-	free T4
TG	-	thyroglobulin
TPO	-	thyroid peroxidase
TSH	-	thyroid-stimulating hormone
thyroid gland	-	thyroid gland

Protocol users: doctors general practice, therapists, pediatricians, endocrinologists, obstetricians-gynecologists, otorhinolaryngologists, neurologists, hematologists, cardiologists, psychiatrists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies, or high-quality (++) cohort or case-control studies with very low risk of bias, or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population .
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+), the results of which can be generalized to the relevant population or RCT with very low or low risk of bias (++ or +), the results of which cannot be directly distributed to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice.

Classification

Clinical classification hypothyroidism:
Primary:
Hashimoto's thyroiditis:
− with goiter;
− “Idiopathic” atrophy of the thyroid gland; presumably the final stage of autoimmune diseases - Hashimoto's thyroiditis or Graves' disease;
− neonatal hypothyroidism due to transplacental transfer of thyroid-blocking antibodies;
· Radioiodine therapy for Graves' disease.
· Subtotal thyroidectomy for Graves' disease, nodular goiter, or thyroid cancer.
· Consumption of excess amounts of iodide (algae, X-ray contrast agents).
· Subacute thyroiditis (usually transient).
· Iodide deficiency.
· Congenital defects in the synthesis of thyroid hormones.
· Medicinal substances (lithium, interferon-alpha, amiodarone).

Secondary:
· Hypopituitarism due to pituitary adenomas, removal or destruction of the pituitary gland.

Tertiary:
· Hypothalamic dysfunction (rare).

Peripheral resistance to thyroid hormones

Classification primary hypothyroidism by severity:

Severity	Laboratory changes	Clinical picture
Subclinical	TSH - elevated, st. T4 - normal or reduced	Asymptomatic or only nonspecific symptoms
manifest	TSH - elevated, st. T4 - reduced	Present characteristic symptoms hypothyroidism
Complicated (severe)	TSH - elevated, st. T4 - reduced	Detailed clinical picture of hypothyroidism. There are heavy complications: “polyserositis”, heart failure, cretinism, myxedematous coma, etc.

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints:
· weakness;
· chilliness;
lethargy;
· drowsiness;
· “unreasonable” weight gain;
paresthesia;
· constipation;
· hair loss;
· violation menstrual cycle(often menorrhagia) and reproductive function;
· convulsions.

Physical examination:
Excess weight, dense local or general edema up to anasarca (in severe cases - hydrothorax, hydropericardium, ascites), decreased timbre of voice, dry and cold skin, brittle hair, enlarged facial features, periorbital edema, narrowing of the palpebral fissures, tongue with teeth marks.

CNS:
Chronic fatigue, drowsiness, apathy, depression or “myxedematous psychosis”, lethargy, slowed movements and speech, dysarthria, inability to concentrate, decreased memory and hearing, hypo- or amymia.

Cardiovascular system:
expansion of the borders of the heart in diameter, decreased myocardial contractility, bradycardia, diastolic arterial hypertension, increase in total peripheral resistance, decrease in cardiac output.

Lungs:
Slow shallow breathing, impaired response of the respiratory center to hypoxia and hypercapnia. Respiratory failure is the main cause of death in patients with myxedema coma.

Gastrointestinal tract:
Slow peristalsis, constipation, possible fecal impaction and intestinal obstruction.

Kidneys:
Decreased GFR, fluid retention, possible water intoxication.

Neuromuscular disorders:
Painful muscle cramps, paresthesia and muscle weakness.

Reproductive system:
Impaired secretion of LH, FSH, anovulation and infertility in women, menorrhagia.

Laboratory research:
The thyroid hormonal profile is determined by the level of damage to the hypothalamus-pituitary-thyroid axis:

Increased levels of antibodies to TPO and/or TG in cases of hypothyroidism due to Hashimoto's thyroiditis.

Anemia due to impaired hemoglobin synthesis, deficiency of iron, vitamin B12 and folate (due to loss during menorrhagia and impaired absorption in the intestine), etc.
Hypercholesterolemia, increased LDL, lipoprotein A and homocysteine.

Instrumental studies:
· Ultrasound of the thyroid gland: often - a decrease in the volume of the organ, changes characteristic of AIT, nodal and cystic formations;
· ECG: decreased voltage of QRS complexes, T and P waves, sinus bradycardia, impaired repolarization processes in the ventricular myocardium;
· X-ray of organs chest: increase in heart size due to interstitial edema of the myocardium, swelling of myofibrils, dilatation of the left ventricle and effusion in the myocardium, hydropericardium is possible;
· MRI or CT scan of the pituitary gland indicated for central hypothyroidism;
· EchoCG with severe heart failure.

Indications for specialist consultation:
· consultation with a cardiologist - for CHF and suspected ischemic heart disease;
· consultation with an ophthalmologist, neurosurgeon, neurologist - for central hypothyroidism;
· consultation with a hematologist - for moderate and severe anemia.

Diagnostic algorithm:(scheme)

Differential diagnosis

Differential diagnosisand justification additional research in adult patients with suspected hypothyroidism:

Diagnosis	Rationale for differential diagnosis	Surveys	Diagnosis exclusion criteria
Nephrotic syndrome	General: presence of edema	TSH, svT3, svT4 Definition total protein, creatinine and urea levels in the blood, GFR, TAM, kidney ultrasound.	Lack of clinical and laboratory signs kidney damage
Acromegaly	Enlargement of facial features	TSH, svT3, svT4 Determination of levels of growth hormone, IGF-1 in the blood, MRI of the pituitary gland with contrast enhancement.	Normal levels of growth hormone and IGF-1 in the blood, no changes on MRI of the pituitary gland. Presence of changes in the thyroid profile characteristic of hypothyroidism

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment (outpatient clinic)

TREATMENT TACTICS AT AN OUTPATIENT LEVEL: all patients with this diagnosis are treated at an outpatient level

Non-drug treatment: No

Drug treatment:
The main drug is levothyroxine sodium 25, 50, 75, 100, 125, 150 mcg in the table.
Starting daily dose with manifest hypothyroidism:
· in patients under 60 years of age - 1.6-1.8 mcg/kg;
· in patients with concomitant diseases cardiovascular systems s and over 60 years old - 12.5-25 mcg, followed by an increase of 12.5-25 mcg every 6-8 weeks.
Take in the morning on an empty stomach no later than 30 minutes before meals. After taking thyroid hormones, avoid taking antacids, iron and calcium supplements for 4 hours.
The selection of a maintenance dose is carried out under the control of general condition, pulse rate and determination of the blood TSH level in case of primary hypothyroidism, st. T4 - with a central form.
The first determination is made no earlier than 6 weeks from the start of therapy, then once every 3 months until the effect is achieved.
After achieving a clinical and laboratory effect, to determine the adequacy of the dose of levothyroxine, a TSH or fT4 study is performed once every 6 months.

Replacement doses of T4 for adults are 50-200 mcg/day, on average 125 mcg/day.
After thyroidectomy for thyroid cancer, suppressive doses are used - 2.2 mcg/kg per day.

List of additional medicines - individually (according to indications).

Surgical intervention:No.

Further management:
Therapy with levothyroxine sodium drugs is lifelong replacement therapy under the supervision of a physician.

Indicators of treatment effectiveness:
An indicator of the effectiveness of treatment is the achievement of normal TSH levels in the blood. The target TSH level is determined individually, taking into account the patient’s age (adult - young, mature, elderly, senile) and concomitant pathology.

Treatment (inpatient)

TREATMENT TACTICS AT THE INPATIENT LEVEL: hospitalization is indicated only when complications occur: heart failure, adrenal insufficiency, liver failure, etc.

Patient observation card, patient routing ( schemes, algorithms): No.

Non-drug treatment: No.

Drug treatment: the main drug is levothyroxine sodium 25, 50, 75, 100, 125, 150 mcg in the table.
Take in the morning on an empty stomach no later than 30 minutes before meals.

List of essential medicines (having a 100% probability of use):

List of additional medications (less than 100% probability of use): the choice is determined by the accompanying syndrome.

Surgical intervention: No.

Further management:
· lifelong replacement therapy with thyroid drugs.

Indicators of treatment effectiveness:
The classic indicator of treatment effectiveness is the achievement of normal TSH levels in the blood.
In reality, the target TSH level should be determined individually, taking into account age and concomitant diseases. In elderly and old age, and also in the presence of severe concomitant diseases, may be higher than standard values.

Hospitalization

INDICATIONS FOR HOSPITALIZATION, INDICATING THE TYPE OF HOSPITALIZATION

Indications for planned hospitalization:
· newly diagnosed hypothyroidism in elderly and senile people to initiate hormone replacement therapy;
· decompensated hypothyroidism in the absence of effect from outpatient treatment.

Indications for emergency hospitalization:
· gradual increase in drowsiness with transition to stupor (myxedema/hypothyroid coma), dynamic intestinal obstruction, pneumonia, myocardial infarction, thrombosis of cerebral arteries, gastrointestinal bleeding, convulsions with hyper- and hypocalcemia, hypothermia, hyponatremia (water intoxication).

Information

Sources and literature

1. Minutes of meetings of the Joint Commission on the quality of medical services of the Ministry of Health of the Republic of Kazakhstan, 2017
   1. 1) D. Gardner, D. Shobeck. Basic and clinical endocrinology, 2016. 2) Clinical protocol for the diagnosis and treatment of hypothyroidism in adults, Astana, 2014. 3) Sviridenko N.Yu., Abramova N.A. Endocrinology: national guide / ed. I.I. Dedova, G.A. Melnichenko- M.: GEOTAR-Media, 2016, - 1112 pp. 4) Zeltser M.E., Bazarbekova R.B. Directory of endocrinologist. 1st edition, Almaty, 2014, 368 pp. 5) TinsleyHarrison. Internal diseases. Book six. – M, 2005, 415 pp. 6) Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) Jonklaas, Bianco, et al. Thyroid 24(12): 1670-1751, 2014.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of protocol developers with qualification information:
1) Dosanova Ainur Kasimbekovna - candidate of medical sciences, assistant of the department of endocrinology of JSC Kazakh Medical University continuing education».
2) Rimma Bazarbekovna Bazarbekova - Doctor of Medical Sciences, Professor, Head of the Department of Endocrinology of JSC “Kazakh Medical University of Continuing Education”, Chairman of the RPO “Association of Endocrinologists of Kazakhstan”.
3) Smagulova Gaziza Azhmagievna - candidate of medical sciences, head of the department of propaedeutics of internal diseases and clinical pharmacology RSE at the University of West Kazakhstan State Medical University named after M. Ospanov.

Indication of absence conflict interests: No.

Reviewers: Nurbekova Akmaral Asylovna - Doctor of Medical Sciences, Professor of the Department of Internal Medicine No. 2 of the RSE at the Kazakh National Medical University named after S.D. Asfendiyarov."

Note conditions revision protocol: review of the protocol 5 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

Attached files

Attention!

• By self-medicating, you can cause irreparable harm to your health.
• The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you.
• The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
• MedElement website and mobile applications"MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are solely information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
• The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.

Hypothyroidism is a pathology caused by insufficient functioning of the thyroid gland. According to ICD 10, there are many varieties, which are assigned a separate code. All diseases that have one or another code differ in etiology and pathogenesis.

The ICD-10 code for this disease is:

• E 02 – Subclinical hypothyroidism as a result of iodine deficiency.
• E 03 – Other forms of hypothyroidism.

According to ICD 10, “other forms” most often mean congenital thyroid insufficiency with or without diffuse goiter, post-medication and post-infectious hypothyroidism, thyroid atrophy, myxedematous coma and other types of the disease. There are more than 10 such varieties in total.

Main symptoms of the disease

The clinical picture of thyroid insufficiency is characterized by a slowdown in all life processes in the body. Low levels of thyroid hormones produce energy in the human body with less intensity. This is why patients constantly feel cold.

Due to the low stimulating effect of thyroid hormones, patients are highly prone to infectious diseases. They feel constant fatigue, headaches, and discomfort in muscles and joints. The skin becomes dry, hair and nails become brittle.

Postoperative hypothyroidism develops after surgery to remove the thyroid gland. Patients are concerned about the following symptoms:

• Decreased body temperature;
• Weight gain;
• Swelling on the body;
• Drowsiness, lethargy, mental retardation;
• Damage to the digestive system;
• Anemia;
• Decreased libido;
• Disorders of the heart and respiratory system.

The main directions of treatment of thyroid insufficiency

Treatment for this disease depends on clinical form. The primary form of the disease always requires treatment replacement hormones. Treatment of peripheral hypothyroidism is very difficult; in certain cases it is difficult to treat.

The compensated form of thyroid disease sometimes does not require specialized therapy at all. But in the presence of decompensation, the patient is prescribed hormonal drugs. The dose and the drug itself are selected strictly individually.

Sometimes they have a good effect homeopathic medicines. They allow the body to overcome a dangerous illness. True, such treatment is very long and assumes that the patient will take the medicine many times a day.

Hypothyroidism- a disease caused by insufficient secretion of thyroid hormones by the thyroid gland. Distinguish between primary and secondary hypothyroidism. Primary develops when the thyroid gland is damaged and is accompanied by an increase in TSH levels (90% of cases hypothyroidism) . Secondary occurs when the hypothalamic-pituitary system is damaged with insufficient release of thyrotropin-releasing hormone and TSH and a subsequent decrease in thyroid function. Tertiary develops when the hypothalamus is damaged with the development of thyrotropin-releasing hormone deficiency.

Code by international classification diseases ICD-10:

• E02 - Subclinical hypothyroidism due to iodine deficiency
• E03 - Other forms of hypothyroidism

Statistics

5-10 cases per 1000 in the general population. The predominant age is over 40 years. The predominant gender is female (7.5:1).

Hypothyroidism: Causes

Etiology

Primary hypothyroidism. Chronic autoimmune thyroiditis is the most common cause hypothyroidism. Idiopathic atrophy of the thyroid gland. Antithyroid antibodies are often detected, which allows us to consider this disease an atrophic form of chronic thyroiditis. Treatment of diffuse toxic goiter. The incidence may reach 50% in patients treated with radioactive iodine. Hypothyroidism also occurs after subtotal thyroidectomy or use of antithyroid drugs. Iodine deficiency. Secondary hypothyroidism may be caused by any of the conditions leading to hypopituitarism.

Genetic aspects

Cretinism (congenital myxedema) is severely inherited hypothyroidism, manifested in childhood (#218700, mutation of the TSH gene TSHB, 1p13, r; or *275120, mutation of the thyroliberin gene TRH, 3p, r). Characterized by a lag in mental development and slower physical development and growth. Short limbs, large head with a wide flattened nose, widely spaced eyes and a large tongue. Dysgenesis of the epiphyses with anomalies of the centers of ossification in the femoral and humerus and other parts of the skeleton. Early recognition and treatment can prevent permanent mental and physical impairment. Primary hypothyroidism may be a component of type II autoimmune polyglandular syndrome.

Rare inherited forms: . Hypothyroidism in combination with ectodermal dysplasia and agenesis corpus callosum(225040, r or À) . Hypothyroidism in combination with ectodermal dysplasia and ciliary dyskinesia (225050, r). Hypothyroidism in combination with ectopia of the thyroid gland (225250, r). Athyroid hypothyroidism in combination with cleft palate, choanal atresia and other developmental defects (241850, r). Inherited TSH receptor resistance (*275200, TSH gene defect TSHR, 14q31, r).

Risk factors

Old age. Autoimmune diseases.

Pathomorphology

The thyroid gland can be either reduced or enlarged.

Hypothyroidism: Signs, Symptoms

Clinical picture

Weakness, drowsiness, fatigue, slow speech and thinking, constant feeling cold due to a decrease in the effect of thyroid hormones on tissues and a slowdown in metabolism.

Puffiness of the face and swelling of the extremities, which do not leave pits when pressed, are caused by the accumulation of a mucous substance rich in mucopolysaccharides in the tissues. The phenomenon is described by the term myxedema, sometimes used as a synonym for severe hypothyroidism.

Weight gain reflects a decrease in metabolic rate, but no significant increase occurs because appetite is reduced.

Changes from other systems. On the part of the cardiovascular system - decrease cardiac output, bradycardia, pericardial effusion, cardiomegaly, tendency to decrease blood pressure. From the lungs - hypoventilation and pleural effusion. From the gastrointestinal tract - nausea, flatulence, constipation. From the kidneys - a decrease in GFR due to decreased peripheral hemodynamics and increased ADH levels. On the skin side - hair loss, dryness and fragility, often jaundice skin due to excess circulating b-carotene, which is slowly transformed into vitamin A in the liver. From the peripheral nervous system- slow Achilles and other deep tendon reflexes. From the eyes - periorbital edema, ptosis, refractive error. From the blood side - as a rule, normochromic (in children hypochromic) normocytic anemia and pseudohyponatremia. A tendency to hypercoagulation is noted due to increased plasma tolerance to heparin and an increase in the level of free fibrinogen. Menstrual irregularities (metrorrhagia or amenorrhea).

Hypothyroidism: Diagnosis

Laboratory diagnostics. Reduced concentrations of total T4 and T3 in the blood serum. Reduced uptake of radioactive iodine by the thyroid gland. Elevated serum TSH concentration: the earliest and most sensitive sign of primary hypothyroidism; for secondary hypothyroidism On the contrary, a decrease in TSH concentration is characteristic. In case of severe hypothyroidism- anemia, pseudohyponatremia, hypercholesterolemia, increased CPK, LDH, AST.

Drugs that affect results. Thyroid hormone preparations. Cortisone. Dopamine. Phenytoin. Large doses of estrogens or androgens. Amiodarone. Salicylates.

Diseases affecting results. Any serious illness. Liver failure. Nephrotic syndrome.

Differential diagnosis

Nephrotic syndrome. Chronic nephritis. Depressive syndrome. Chronic heart failure. Primary amyloidosis.

Hypothyroidism: Treatment Methods

Treatment

Diet

is built along the path of increasing the protein content and limiting fats and carbohydrates (mainly easily digestible ones - honey, jam, sugar, flour products); for obesity - diets No. 8, 8a, 8b.

Drug of choice- levothyroxine sodium. Treatment is carried out to normalize TSH levels. Take in a dose of 50-100 mcg once in the morning on an empty stomach 30 minutes before meals. The dose is increased every 4-6 weeks by 25 mcg/day. The maintenance dose for most patients is 75-150 mcg/day (adjusted according to the content of TSH and thyroid hormones).

Alternative drugs

thyrocomb, levothyroxine sodium + liothyronine.

Observation

Every 6 weeks until stabilized, then every 6 months. Assessment of CVS functions in elderly patients.

Complications

Hypothyroid coma. In patients with ischemic heart disease treatment hypothyroidism may cause chronic heart failure. Increased susceptibility to infections. Megacolon. Hypothyroid chronic psychosyndrome. Addison's crisis and bone demineralization during intensive treatment hypothyroidism. Infertility.

Course and prognosis

If treatment is started early, the prognosis is favorable. If left untreated, hypothyroid coma may develop.

Pregnancy

During pregnancy, monitoring of the free T4 fraction is necessary. Replacement therapy may require correction. TSH levels should be tested monthly during the first trimester. IN postpartum period— assessment of TSH levels every 6 weeks; Postpartum autoimmune thyroiditis may develop.

Concomitant pathology

Pseudohyponatremia. Normochromic normocytic anemia. Idiopathic deficiency of adrenal hormones. SD. Hypoparathyroidism. Severe pseudoparalytic myasthenia gravis. Vitiligo. Hypercholesterolemia. Prolapse mitral valve. Depression.

Age characteristics in the elderly. The clinical picture is often blurred. Diagnosis is based on laboratory criteria. Sometimes they watch increased sensitivity to thyroid hormones. This group of patients has an increased risk of complications from the cardiovascular system and other systems, especially if correction hypothyroidism carried out intensively. Therefore, treatment is started with small doses of levothyroxine sodium (25 mcg), which are then increased to the full maintenance dose over 6-12 weeks.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Atrophy of the thyroid gland (ACQUIRED), Autoimmune thyroiditis (E06.3), Congenital hypothyroidism without goiter (E03.1), Congenital hypothyroidism with diffuse goiter (E03.0), Unspecified hypothyroidism (E03.9), Other specified hypothyroidism (E03. 8), Other chronic thyroiditis (E06.5), Myxedema coma (E03.5), Post-infectious hypothyroidism (E03.3), Congenital iodine deficiency syndrome (E00), Congenital iodine deficiency syndrome, unspecified (E00.9), Thyroiditis, unspecified ( E06.9)

Pediatrics, Pediatric Endocrinology

General information

Brief description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

Hypothyroidism- a clinical syndrome caused by a deficiency of thyroid hormones, characterized by a slowdown of all metabolic processes.

INTRODUCTORY PART

ICD-10 code(s):

ICD-10 (children)
Code	Name
E00	Congenital iodine deficiency syndrome
E00.0	Congenital iodine deficiency syndrome, neurological form, endemic cretinism, neurological form
E00.1	Congenital iodine deficiency syndrome, myxedematous form, endemic cretinism: . hypothyroid. myxedema form
E00.2	Congenital iodine deficiency syndrome, mixed form, Endemic cretinism, mixed form
E00.9	Congenital iodine deficiency syndrome, unspecified, Congenital hypothyroidism due to iodine deficiency NOS Endemic cretinism NOS
E03	Other forms of hypothyroidism
E03.0	Congenital hypothyroidism with diffuse goiter, goiter (non-toxic) congenital: NOS parenchymal Excluded: transient congenital goiter with normal function (P72.0)
E03.1	Congenital hypothyroidism without goiter, aplasia of the thyroid gland (with myxedema) Congenital: atrophy of the thyroid gland. hypothyroidism NOS
E03.3	Post-infectious hypothyroidism
E03.4	Thyroid atrophy (acquired), Excludes: congenital thyroid atrophy (E03.1)
E03.5	Myxedema coma
E03.8	Other specified hypothyroidisms
E03.9	Hypothyroidism, unspecified, myxedema NOS
E06	Thyroiditis
E06.3	Autoimmune thyroiditis
E06.5	Thyroiditis: chronic: . NOS. fibrous. woody. Riedel
E06.9	Thyroiditis, unspecified

Date of protocol development/revision: 2013 (revised 2017).

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
VG	-	congenital hypothyroidism
Gastrointestinal tract	-	gastrointestinal tract
svT3	-	free triiodothyronine
SSS	-	cardiovascular system
T4 general	-	total T3
T4 sv	-	free T4
TG	-	thyroglobulin
TPO	-	thyroid peroxidase
TSH	-	thyroid-stimulating hormone
thyroid gland	-	thyroid gland

Protocol users: general practitioners, pediatricians, endocrinologists, cardiologists, psychiatrists, neurologists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population .
WITH	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). The results of which can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice.

Classification

Clinical classification of hypothyroidism in children:

Reasons	Frequency (% per number of newborns)
Primary hypothyroidism: 1. Thyroid dysgenesis; Agynesia (atherosis); Hypogenesis (hypoplasia); Dystopia. 2. Dyshormonogenesis: TSH receptor defect; Iodine transport defect; Defect of the peroxidase system; Defect in thyroglobulin synthesis.	85-90; 1:4000 5-10; 1:30 000-1:50 000
Central hypothyroidism (secondary, tertiary): 1. Combined deficiency of pituitary hormones; 2. Isolated TSH deficiency.
Peripheral resistance to thyroid hormones	Unknown
Transient hypothyroidism	unknown

One of the most common thyroid diseases in children is congenital hypothyroidism ( VG), which is based on complete or partial deficiency of thyroid hormones, leading to a delay in the development of all organs and systems.
VG- a heterogeneous group of diseases caused either by morphofunctional immaturity of the hypothalamic-pituitary system or thyroid gland, or their damage in the prenatal period.

Classification of primary hypothyroidism by severity:

Severity	Laboratory changes	Clinical picture
Subclinical	TSH - increased, St. T4 - normal or reduced	Asymptomatic or only nonspecific symptoms
manifest	TSH - increased, St. T4 - reduced	Characteristic symptoms of hypothyroidism are present
Complicated (severe)	TSH - increased, St. T4 - reduced	Detailed clinical picture of hypothyroidism. There are heavy complications: “polyserositis”, heart failure, cretinism, myxedematous coma, etc.

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria:
It should be noted that the clinical symptoms described below are more typical for children with primary congenital hypothyroidism.
In secondary hypothyroidism, both congenital and acquired, the clinical picture of the disease is openwork; in these conditions, signs of central nervous system damage come to the fore. To identify it, the study of the thyroid hormonal profile is of key importance.

Complaints and anamnesis:
Newborns:
· breathing problems;
· cyanosis;
· jaundice;
sluggish sucking;
· hoarse cry;
· umbilical hernia.
Children and teenagers:
· growth slowdown;
· decline in academic performance;
· disorders of sexual development;
· constipation;
· drowsiness;
· chilliness;
· dry skin;
Poor hair and nail growth.

Physical examination:
In newborns it is possible:
· post-term pregnancy (more than 40 weeks);
· high birth weight (more than 3500 g);
· swollen face, lips, eyelids;
· half-open mouth with a wide, “spread” tongue;
· localized swelling in the form of dense “pads” in the supraclavicular fossa, dorsal surfaces of the hands, feet;
· signs of immaturity in a full-term pregnancy;
· low, rough voice when crying, screaming;
· late passage of meconium;
· late loss of the umbilical cord, poor epithelization umbilical wound;
· prolonged jaundice.
A sharp lag in the rate of ossification (absence of proximal epiphyses of the tibial and distal epiphyses femur).
However, the classic clinical picture of hypothyroidism in newborns occurs with a frequency of no more than 10-15%. In this regard, to diagnose congenital hypothyroidism in newborns, it is advisable to use the Apgar scale, which helps to identify CH in early dates.

Apgar score for diagnosing congenital hypothyroidism in newborns

Clinical sign	Number of points
Umbilical hernia	2
Puffy face	2
Constipation	2
Female gender	1
Paleness, hypothermia of the skin	1
Enlarged tongue	1
Muscular hypotonia	1
Jaundice longer than 3 weeks	1
Peeling and dry skin	1
Open posterior fontanel	1
Pregnancy lasted more than 40 weeks	1
Birth weight more than 3500 g	1

If the score is more than 5, congenital hypothyroidism should be suspected.

Later- at the age of 3-4 months the following symptoms appear:
· decreased appetite;
· difficulty swallowing;
· poor weight gain;
· flatulence;
· constipation;
· dryness;
· pallor;
peeling of the skin;
Hypothermia (cold hands, feet);
· brittle, dry, dull hair;
· muscle hypotonia.

In children with CH of older age (after 5-6 months and older), in the absence of treatment, severe short stature comes to the fore (height below the 3rd percentile or below 2 standard deviations (< -2,0 SDS) от средней по популяции для данного хронологического возраста и пола), прогрессирующее замедление скорости роста (скорость роста более чем на 1 SD ниже (при хронологическом возрасте >1 year) for a given chronological age and gender.
Body proportions in children with hypothyroidism are close to chondrodystrophic (the “upper/lower segment” ratio is greater than normal values).
Characteristic features include underdevelopment of the facial skeleton, a wide sunken bridge of the nose, and hypertelorism; late closure of the greater and lesser fontanels; delayed teething and their late replacement.
Severe delay in psychomotor and speech development. Children are lethargic, can lie quietly for hours, without showing concern when there is a wet diaper or hunger, are not interested in toys, and begin to sit and walk late.
Adynamia and muscle hypotonia are pronounced: a convex abdomen with an umbilical hernia, divergence of the rectus abdominis muscles, posture with lumbar lordosis, protruding buttocks and bent knees, frequent constipation, flatulence.

Characteristic complex of respiratory symptoms:
· difficult nasal breathing, stridor;
cyanosis of the nasolabial triangle;
· low, rough voice, frequent colds.

The skin is dry, yellowish, flaky due to decreased secretion of sweat and sebaceous glands, have a “marble” pattern, feel good to the touch. Hair is brittle, dry, lacks shine, and falls out rapidly. Seborrhea of ​​the scalp, forehead, and eyelids is typical. Nails are brittle and cracked. There is slow growth of hair and nails.

Muffling of heart sounds, bradycardia (in the first months of life, heart rate may be normal), functional murmur, expansion of the boundaries of the heart, decreased blood and pulse pressure.

The above symptoms can be “formatted” into the following clinical syndromes.
Exchange-hypothermic syndrome:
· constant feeling of chilliness;
· decrease in body temperature;
· hyperlipoproteinemia (increased levels of cholesterol and triglycerides);
· moderate increase in body weight (due to the accumulation of glycoaminoglycans and water retention).

Trophic disorders of the skin and its appendages:
The development of this syndrome is associated with a violation of glycosaminoglycan metabolism, which results in an increase in tissue hydrophilicity.
Characteristic:
· myxedematous dense swelling of the face and extremities;
· enlargement of the lips and tongue with tooth marks on the lateral edges;
· “old-looking face” with coarsened features;
· the skin is thick, dry, cold, pale with a yellowish tint, does not gather in folds, peels off on the elbows;
· hair is dull, brittle, falls out on the head, eyebrows, limbs, and grows slowly. Total alopecia may occur;
· nails are thin, with longitudinal or transverse striations.

Signs of damage to the nervous system and sensory organs:
· chronic fatigue;
· drowsiness;
· apathy;
· depression or “myxedematous psychosis”;
· lethargy;
· hypo- or amymia;
· slowing of movements and speech;
· dysarthria;
· inability to concentrate;
memory loss;
Impaired hearing and smell due to swelling of the mucous membranes ear canals and nose.
due to swelling and thickening vocal cords the voice becomes rough and low.

Signs of damage to the cardiovascular systems:
· expansion of the borders of the heart in diameter;
· decreased myocardial contractility;
· bradycardia;
· diastolic arterial hypertension;
· increase in total peripheral resistance;
Decrease in cardiac output.

Signs of lung damage:
· slow shallow breathing;
· impaired response of the respiratory center to hypoxia and hypercapnia. Respiratory failure is the main cause of death in patients with myxedema coma.

Signs of gastrointestinal damage:
· slowing down peristalsis;
· constipation;
· dyskinesia of the biliary tract, possible fecal impaction and intestinal obstruction.

Signs of kidney damage:
· decrease in GFR;
· fluid retention;
Possible water intoxication.

Neuromuscular disorders:
· painful muscle cramps, paresthesia and muscle weakness.

Signs of damage to the reproductive system:
Delayed sexual development; in girls, oligo-opsomenorea, amenorrhea, anovulatory cycles, galactorrhea (Van-Wyck-Hennes-Ross syndrome) are possible.
Due to hyperprolactinemia, often accompanied by hyperthyrotropemia, there is a disturbance in the production of LH and the reception of gonadotropins in the gonads.
(Van Wyck-Grambach syndrome).

Hematopoietic disorders:
Disorders of erythropoiesis, caused both by the actual deficiency of thyroid hormones and by a decrease in the formation of erythropoietins.
In addition, with hypothyroidism, B12 deficiency and iron deficiency anemia. Disturbances in platelet function are characteristic: decreased adhesive-aggregation function.

In areas with severe iodine deficiency, CH may manifest as endemic cretinism.

There are two forms of endemic cretinism:
· neurological;
· myxedematous.
The most common is endemic neurological cretinism, in the clinic of which neurological (pyramidal and extrapyramidal) and intellectual impairments come to the fore. Clinical signs Hypothyroidism is absent or mildly expressed.
And, conversely, myxedematous endemic cretinism is characterized by severe symptoms of hypothyroidism (see above).

Laboratory research:
· gene defects leading to congenital hypothyroidism: TTF1, TTF2, PAX-8, PROP-1, Pit-1, TSH-R, NIS, TPO, PDS, TG, TR-, TR-α - if possible.
The thyroid hormonal profile is determined by the level of damage to the hypothalamus-pituitary-thyroid axis:

Increased levels of antibodies to TPO and/or TG in cases of hypothyroidism due to Hashimoto's thyroiditis.

The vast majority of the territories of the Republic of Kazakhstan suffer from iodine deficiency.
In this regard, as well as in connection with the weak severity of clinical symptoms of hypothyroidism in the first days and weeks of a child’s life, in Kazakhstan, as in all developed countries of the world, a state system of neonatal screening for CH has been introduced since 1994.
Screening allows you to make a diagnosis in the first days of a child’s life, before the appearance of a detailed clinical picture of the disease, and to avoid severe consequences illnesses, primarily delays in the mental and physical development of the child. The main goal of screening for CH is the early identification of newborns with elevated TSH levels in the blood.

Examination and further observation of children is carried out in three stages:
I - maternity hospital;
II - medical genetic laboratory;
III - children's clinic.

Stage I - maternity hospital:
For all full-term newborns, on the 4th-5th day of life (for premature babies on the 7th-14th), 6-8 drops of blood are taken from the heel and applied to a special porous filter paper. All blood samples are sent to a specialized medical genetic laboratory.

Stage II - medical genetic laboratory:
In infants and older children, the TSH standards given in the table below should be used.

Standards for TSH levels in children

All specimens with TSH levels greater than 20 mIU/mL should be retested. Repeated detection of TSH levels above 20 mIU/ml with high degree probability indicates the presence of CH and indicates the need for replacement therapy with thyroid drugs.

Transient hypothyroidism in newborns deserves special attention - this is a state of temporary (transient) hypothyroxinemia, accompanied by an increase in the level of TSH in the blood.
A transient increase in TSH levels in most cases is associated with the functional immaturity of the hypothalamic-pituitary system in the postnatal period. The risk of developing transient hypothyroidism is high in premature infants and low birth weight infants.
This condition most often occurs in following cases:
iodine deficiency or excess in the mother;
· children born from mothers with autoimmune diseases thyroid gland (possible transplacental transfer of antibodies that block the TSH receptor);
· children whose mothers received large doses of antithyroid drugs during pregnancy for Graves' disease; such children, as a rule, have a goiter at birth, which tends to decrease as they are excreted medicines from the blood of a child;
· children with intrauterine (and postnatal) malnutrition, with intrauterine viral and bacterial infections.

At the initial screening stage, it is almost impossible to distinguish between congenital and transient hypothyroidism. The distinction between these conditions must be carried out at stage III of screening, that is, in outpatient settings, when re-determining serum levels of TSH and fT4 during treatment with thyroid drugs.

In the case of a child’s late visit to the doctor in the presence of a minimal clinical picture of CH and doubtful hormonal indicators a decision is made in favor of prescribing levothyroxine.

Stage III - clinic:
Based on the results of TSH determination, indicating hypothyroidism, the clinic doctor prescribes thyroid hormone replacement therapy.
Doses of levothyroxine are selected individually based on clinical and laboratory data.

Further control studies of TSH and fT4 levels should be carried out in the first year of life every 2-3 months, after a year every 3-4 months.
During the first 6 weeks from the start of replacement therapy, control studies of fT4 levels only are carried out every 2 weeks.
It is advisable to start monitoring the levels of TSH and fT4 simultaneously no earlier than 6 weeks from the start of treatment.
In children of the first year of life, the focus is only on the TSH level due to possible violation its feedback regulation may lead to the prescription of unnecessarily high doses of levothyroxine.

In cases normal levels fT4 (individually for each laboratory), the dose of levothyroxine can be considered adequate.
· Study of the state of “red blood”. Anemia is possible due to impaired hemoglobin synthesis, deficiency of iron, vitamin B12 and folic acid;
· Lipid profile study. Characterized by hypercholesterolemia, increased LDL, lipoprotein A and homocysteine.

Instrumental studies:
· Ultrasoundthyroid gland: a- or hypoplasia of the organ; ectopia; multinodular goiter; with primary acquired hypothyroidism, changes characteristic of AIT, nodular and cystic formations are possible;
· ECG: decreased voltage of QRS complexes, T and P waves, sinus bradycardia, impaired repolarization processes in the ventricular myocardium;
· , as well as brushes used not only for diagnosis, but also to assess the adequacy of the therapy for CH.
X-ray of knee joints and feet helps determine the duration of intrauterine hypothyroidism. Absence of ossification centers (epiphyseal dysgenesis) of the distal femurs, proximal ends of the tibias and cuboid bones stop is indirect evidence of congenital hypothyroidism (bone ossification is present in most healthy full-term newborns).
X-ray of hands reveals a delay in the appearance of ossification nuclei, their asymmetry, and a violation of the sequence of appearance. Typically, there is a sharp lag in bone age from the passport age, while bone age is delayed even in to a greater extent than growth.
· MRI or CT scan of the pituitary gland indicated for central hypothyroidism;
· EchoCG with severe heart failure.

Indications for specialist consultation:
· consultation with an ophthalmologist, neurosurgeon, neurologist - for central hypothyroidism;
· consultation with a hematologist - for moderate and severe anemia.

Diagnostic algorithm:(scheme)

Differential diagnosis

Differential diagnosis and rationale for additional studies:

Diagnosis	Rationale for differential diagnosis	Surveys	Diagnosis exclusion criteria
Nephrotic syndrome	General: presence of edema	TSH, svT3, svT4 Determination of total protein, creatinine and urea levels in the blood, GFR, TAM, kidney ultrasound.	Absence of clinical and laboratory signs of kidney damage Presence of changes in the thyroid profile characteristic of hypothyroidism
GH deficiency	Stunting	Test for STG reserves TSH, svT3, svT4 X-ray of the left hand with the wrist joint, MRI of the pituitary gland with contrast enhancement	Identification of sufficient STG reserves. Presence of changes in the thyroid profile characteristic of hypothyroidism Bone age lags behind passport age more than physical development Absence of structural changes in the pituitary gland on MRI
Achondroplasia	Stunted growth with shortened limbs, sunken bridge of the nose	TSH, svT3, svT4	Presence of changes in the thyroid profile characteristic of hypothyroidism Psychomotor development appropriate for age or no obvious delay

Treatment abroad

Hypothyroidism- a disease caused by insufficient secretion of thyroid hormones by the thyroid gland. There are primary and secondary hypothyroidism. Primary develops when the thyroid gland is damaged and is accompanied by an increase in TSH levels (90% of cases of hypothyroidism). Secondary occurs when the hypothalamic-pituitary system is damaged with insufficient release of thyrotropin-releasing hormone and TSH and a subsequent decrease in thyroid function. Tertiary develops when the hypothalamus is damaged with the development of thyrotropin-releasing hormone deficiency.

Code according to the international classification of diseases ICD-10:

Statistics. 5-10 cases per 1000 in the general population. The predominant age is over 40 years. The predominant sex is female (7.5:1).

Reasons

Etiology. Primary hypothyroidism. Chronic autoimmune thyroiditis is the most common cause of hypothyroidism. Idiopathic atrophy of the thyroid gland. Antithyroid antibodies are often detected, which allows us to consider this disease an atrophic form of chronic thyroiditis. Treatment of diffuse toxic goiter. The incidence may reach 50% in patients treated with radioactive iodine. Hypothyroidism also occurs after subtotal thyroidectomy or the use of antithyroid drugs. Iodine deficiency. Secondary hypothyroidism can be caused by any of the conditions leading to hypopituitarism.

Genetic aspects

Cretinism (congenital myxedema) is a severe hereditary hypothyroidism that manifests itself in childhood (#218700, mutation of the TSH gene TSHB, 1p13, r; or *275120, mutation of the thyroliberin gene TRH, 3p, r). Characterized by mental retardation and slower physical development and growth.. Short limbs, large head with a wide flattened nose, widely spaced eyes and a large tongue.. Dysgenesis of the epiphyses with abnormalities of the centers of ossification in the heads of the femur and humerus and other parts of the skeleton. Early recognition and treatment can prevent permanent mental and physical impairment. Primary hypothyroidism may be a component of type II autoimmune polyglandular syndrome.

Rare inherited forms: .. Hypothyroidism in combination with ectodermal dysplasia and agenesis of the corpus callosum (225040, r or À) .. Hypothyroidism in combination with ectodermal dysplasia and ciliary dyskinesia (225050, r) .. Hypothyroidism in combination with ectopia of the thyroid gland (225250 , r) .. Athyroid hypothyroidism in combination with cleft palate, choanal atresia and other developmental defects (241850, r) .. Inherited TSH receptor resistance (*275200, TSH gene defect TSHR, 14q31, r).

Risk factors. Old age. Autoimmune diseases.

Pathomorphology. The thyroid gland can be either reduced or enlarged.

Symptoms (signs)

Clinical picture

Weakness, drowsiness, fatigue, slowed speech and thinking, a constant feeling of cold due to a decrease in the effect of thyroid hormones on tissue and a slowdown in metabolism.

Puffiness of the face and swelling of the extremities, which do not leave pits when pressed, are caused by the accumulation of a mucous substance rich in mucopolysaccharides in the tissues. The phenomenon is described by the term “myxedema,” sometimes used as a synonym for severe hypothyroidism.

An increase in body weight reflects a decrease in metabolic rate, but a significant increase does not occur, because appetite is reduced.

Changes from other systems.. From the cardiovascular system - decreased cardiac output, bradycardia, pericardial effusion, cardiomegaly, a tendency to decrease blood pressure.. From the lungs - hypoventilation and pleural effusion.. From the gastrointestinal tract - nausea, flatulence, constipation.. On the kidney side - a decrease in GFR due to reduced peripheral hemodynamics and increased ADH levels. On the skin side - hair loss, dryness and fragility, often yellowness of the skin due to an excess of circulating b-carotene, which is slowly transformed into vitamin A in the liver. From the peripheral nervous system - slow Achilles and other deep tendon reflexes. From the eyes - periorbital edema, ptosis, refractive errors. From the blood - as a rule, normochromic (in children, hypochromic) normocytic anemia and pseudohyponatremia. A tendency to hypercoagulation is noted due to increased plasma tolerance to heparin and an increase in the level of free fibrinogen. Menstrual irregularities (metrorrhagia or amenorrhea).

Diagnostics

Laboratory diagnostics. Reduced concentrations of total T 4 and T 3 in the blood serum. Reduced uptake of radioactive iodine by the thyroid gland. Elevated serum TSH concentration: the earliest and most sensitive sign of primary hypothyroidism; Secondary hypothyroidism, on the contrary, is characterized by a decrease in TSH concentration. In severe hypothyroidism - anemia, pseudohyponatremia, hypercholesterolemia, increased CPK, LDH, AST.

Drugs that affect results. Thyroid hormone preparations. Cortisone. Dopamine. Phenytoin. Large doses of estrogens or androgens. Amiodarone. Salicylates.

Diseases affecting results. Any serious illness. Liver failure. Nephrotic syndrome.

Differential diagnosis. Nephrotic syndrome. Chronic nephritis. Depressive syndrome. Chronic heart failure. Primary amyloidosis.

Treatment

TREATMENT

Diet is built along the path of increasing the protein content and limiting fats and carbohydrates (mainly easily digestible ones - honey, jam, sugar, flour products); for obesity - diets No. 8, 8a, 8b.

Drug of choice- levothyroxine sodium. Treatment is carried out to normalize TSH levels. Take a dose of 50-100 mcg once in the morning on an empty stomach 30 minutes before meals. The dose is increased every 4-6 weeks by 25 mcg/day. The maintenance dose for most patients is 75-150 mcg/day (adjusted according to the content of TSH and thyroid hormones).

Alternative drugs: thyrocomb, levothyroxine sodium + liothyronine.

Observation. Every 6 weeks until stabilized, then every 6 months. Assessment of CVS functions in elderly patients.

Complications. Hypothyroid coma. In patients with coronary artery disease, treatment of hypothyroidism can cause chronic heart failure. Increased susceptibility to infections. Megacolon. Hypothyroid chronic psychosyndrome. Addison's crisis and bone demineralization during intensive treatment of hypothyroidism. Infertility.

Course and prognosis. If treatment is started early, the prognosis is favorable. If left untreated, hypothyroid coma may develop.

Pregnancy. During pregnancy, monitoring of the free T4 fraction is necessary. Replacement therapy may require adjustment. TSH levels should be tested monthly during the first trimester. In the postpartum period, assess TSH levels every 6 weeks; Postpartum autoimmune thyroiditis may develop.

Concomitant pathology. Pseudohyponatremia. Normochromic normocytic anemia. Idiopathic deficiency of adrenal hormones. SD. Hypoparathyroidism. Severe pseudoparalytic myasthenia gravis. Vitiligo. Hypercholesterolemia. Mitral valve prolapse. Depression.

Age characteristics in the elderly. The clinical picture is often blurred. Diagnosis is based on laboratory criteria. Hypersensitivity to thyroid hormones is sometimes observed. This group of patients has an increased risk of complications from the cardiovascular system and other systems, especially if the correction of hypothyroidism is carried out intensively. Therefore, treatment is started with low doses of levothyroxine sodium (25 mcg), which are then increased to the full maintenance dose over 6-12 weeks.

Synonyms. Hypothyroidism. Gall's disease.

ICD-10. E02 Subclinical hypothyroidism due to iodine deficiency. E03 Other forms of hypothyroidism

Notes Hypothyroidism was first described by V. Gall in 1873. Before any surgical intervention, patients should be brought into a euthyroid state.