What is Hypothyroidism?
Hypothyroidism is a clinical syndrome that develops due to a deficiency of thyroid hormones. According to the pathogenesis, hypothyroidism can be primary (due to the pathology of the thyroid gland itself) and secondary (due to TSH deficiency), with more than 99% of cases occurring in primary acquired hypothyroidism. The prevalence of hypothyroidism in the general population is about 2%, and in some age groups (elderly women) it can reach 6-8%.
Acquired hypothyroidism is one of the most common endocrine diseases. The main reason for persistent primary hypothyroidism is chronic autoimmune thyroiditis, followed by iatrogenic hypothyroidism, which develops as a result of thyroid surgery or radioactive 131I therapy.
The epidemiology of hypothyroidism is largely determined by the fact that its most common cause is autoimmune thyroiditis. Firstly, autoimmune thyroiditis, like most other thyroid diseases, is 10 or more times more common in women. Secondly, this disease is characterized by a long course and leads to hypothyroidism after many years and decades from its onset. In this regard, hypothyroidism is most common among women over the age of 50-60. If the prevalence of hypothyroidism in the general population is about 1%, among women of childbearing age – 2%, then among women over 60 this indicator in some populations can reach 10-12% or more.
Causes of Hypothyroidism
Of greatest clinical importance is hypothyroidism, which developed as a result of chronic autoimmune thyroiditis, as well as iatrogenic hypothyroidism (postoperative, in the outcome of therapy with radioactive 131I). Iatrogenic hypothyroidism accounts for at least 1/3 of all cases of hypothyroidism. In these diseases, hypothyroidism in most cases is persistent irreversible. Along with this, for many diseases of the thyroid gland (destructive thyroiditis), as well as when exposed to a number of substances (large doses of iodine, thyreostatics), transient hypothyroidism can develop, which self-confines either during the natural course of these diseases, or upon termination of exposure to the factor that caused it (withdrawal thyreostatics). In some cases, the genesis of primary hypothyroidism remains unclear (idiopathic hypothyroidism).
One of the causes of primary hypothyroidism can be severe iodine deficiency. Mild and moderate iodine deficiency cannot lead to hypothyroidism in adults under normal conditions. In newborns, due to moderate, and sometimes even slight iodine deficiency, due to the combination of a low iodine content in the thyroid gland and a high level of thyroid hormone metabolism, transient neonatal hyperthyrotropinemia may develop. Pregnant women with iodine deficiency may develop relative gestational hypothyroxinemia. Nevertheless, the last two phenomena should not be fully identified with hypothyroidism syndrome.
The reason for the relatively rare secondary hypothyroidism, as a rule, is various destructive processes in the hypothalamic-pituitary region. Most often, we are talking about macroadenomas of the pituitary gland and suprasellar structures, as well as surgical interventions for these diseases.
Pathogenesis during Hypothyroidism
With a deficiency of thyroid hormones, changes develop in all organs and systems without exception. Since the main function of thyroid hormones is to maintain the main metabolism (cellular respiration), when they are deficient, there is a decrease in oxygen consumption by tissues, as well as a decrease in energy expenditure and utilization of energy substrates. For the same reason, with hypothyroidism, there is a decrease in the production of a number of energy-dependent cellular enzymes that ensure their normal functioning. The universal change that is found in severe hypothyroidism is mucinous edema (myxedema), the most pronounced in connective tissue structures. Myxedema develops due to excessive accumulation in the interstitial tissues of hyaluronic acid and other glycosaminoglycans, which, due to their hydrophilicity, retain excess water.
Symptoms of Hypothyroidism
The clinical picture of hypothyroidism is determined by its etiology, patient age, and the rate of development of thyroid hormone deficiency.
The main problems in the clinical diagnosis of hypothyroidism are:
- lack of specific (occurring only in hypothyroidism) symptoms;
- high prevalence of symptoms similar to hypothyroidism in the general population, which are associated with other chronic somatic and mental diseases. In approximately 15% of adults with normal thyroid function, up to several symptoms characteristic of hypothyroidism can be detected;
- the absence of a direct relationship between the degree of deficiency of thyroid hormones and the severity of clinical manifestations (in some cases, the symptoms may be completely absent with obvious hypothyroidism, in others they are significantly pronounced even with subclinical hypothyroidism).
As indicated, the clinical picture of hypothyroidism as a whole is characterized by polysystemicity, but complaints and symptoms from a single system dominate in individual patients, and therefore, the patient is often diagnosed with a mask disease.
With severe and persistent hypothyroidism, the patient develops a fairly characteristic “myxedematous” appearance, which is characterized by general and periorbital edema. The face is puffy, pale jaundice, the look alienated, facial expressions poor (masked face).
In addition, there is a thinning and tarnishing of the hair, their increased loss. In general, patients are lethargic, slowed down or even inhibited. For severe hypothyroidism, speech retardation is very characteristic; sometimes it seems that the patient has something in his mouth (tongue is plaited). Swelling of the laryngeal mucosa is manifested by a low or even hoarse timbre of the voice. The patient may stumble on the utterance of individual words, after which, after making certain efforts, pronounces them more clearly. Classically, with hypothyroidism, swelling of the tongue is described, on which tooth prints can be seen. Swelling of the mucous membrane of the Eustachian tube may occur with some hearing loss. A common complaint is dry skin.
Among the changes on the part of the nervous system, mention should be made of a decrease in memory and intelligence, drowsiness, and depression. In children older than 3 years and in adults, changes in the nervous system are not irreversible and completely stop against the background of replacement therapy. In contrast, congenital hypothyroidism in the absence of replacement therapy leads to irreversible neuropsychic and physical disorders. On the part of the peripheral nervous system, changes rarely develop, although in some patients, myxedema phenomena provoke the development of tunnel syndromes (carpal tunnel syndrome).
A general decrease in the level of basal metabolism is manifested by a certain tendency of patients with hypothyroidism to gain weight, while hypothyroidism itself never leads to the development of severe obesity. With extremely severe hypothyroidism, hypothermia can develop. Patients often complain of chilliness (they freeze all the time). In the genesis of this symptom, along with a decrease in basal metabolism, centralization of blood circulation, characteristic of hypothyroidism, is important.
The most common changes in the cardiovascular system are a tendency to bradycardia, mild diastolic hypertension and the formation of effusion in the pericardial cavity. Most patients with hypothyroidism develop atherogenic dyslipidemia.
On the part of the digestive system, constipation is a common symptom. In addition, biliary dyskinesia, hepatomegaly may develop; a slight decrease in appetite is characteristic. With severe hypothyroidism, hypochromic anemia can develop.
Very often, especially in women, changes in the reproductive system come to the fore. With hypothyroidism, various menstrual irregularities can occur: from amenorrhea to dysfunctional uterine bleeding. Both men and women experience a decrease in libido. In the pathogenesis of changes in the reproductive system, secondary hyperprolactinemia is of particular importance. Severe hypothyroidism is almost always accompanied by infertility, but a less pronounced deficiency of thyroid hormones in some women (about 2% among all pregnant women) may not prevent pregnancy, which in this case is accompanied by a high risk of her termination or birth of a child with impaired development of the nervous system.
With prolonged hypothyroidism, hyperstimulation of the pituitary thyrotrophs can result in the formation of a secondary adenoma. After compensation of hypothyroidism on the background of substitution therapy as a result of a decrease in the volume of the pituitary gland, the formation of an “empty” Turkish saddle may occur.
The most severe, but currently extremely rare complication of hypothyroidism is hypothyroid (myxedema) coma. Hypothyroid coma, as a rule, develops in elderly patients with long-term undiagnosed hypothyroidism, severe concomitant diseases with a low social status and lack of care. Intercurrent diseases (often infectious), cooling, injuries, the appointment of drugs that depress the central nervous system provoke the development of hypothyroid coma. Clinically, hypothyroid coma is manifested by hypothermia, hypoventilation with hypercapnia, hypervolemia, hyponatremia, bradycardia, arterial hypotension, acute urinary retention, dynamic intestinal obstruction, hypoglycemia, heart failure, progressive inhibition of the central nervous system. Mortality in myxedema coma reaches 80%.
Diagnosis of Hypothyroidism
Diagnosis of hypothyroidism, that is, evidence of a decrease in thyroid function, is quite simple. It involves determining the level of TSH and T4, while the detection of an isolated increase in TSH indicates subclinical hypothyroidism, while a simultaneous increase in TSH and a decrease in T4 indicates clear or manifest hypothyroidism. A much larger problem is the determination of the indications for this study, since the non-specificity of the clinical picture of hypothyroidism is determined by the fact that even “clear symptoms” may not be confirmed by hormone testing, along with this, in some cases, hypothyroidism, even accompanied by a significant increase in the level TSH and a decrease in T4, sometimes asymptomatic. If we talk about subclinical hypothyroidism, then in the vast majority of cases it does not have manifestations that would allow him to be suspected. When comparing these facts, a logical question arises about the appropriateness of screening determination of thyroid function in order to diagnose hypothyroidism, which is supported by many recommendations.
Risk groups for the development of hypothyroidism
- Thyroid Disease
- Pernicious anemia
- Primary adrenal insufficiency
- Past thyroid dysfunction
- Thyroid surgery or 131I therapy
- Pernicious Anemia
- A number of drugs (lithium carbonate, iodine preparations, including amiodarone and contrast agents)
- Atherogenic dyslipidemia
- Increased levels of creatine phosphokinase and lactate dehydrogenase
Manifest hypothyroidism is an absolute indication for prescribing replacement therapy with levothyroxine (L-T4), regardless of any additional factors (age, concomitant pathology). Only the treatment initiation option (initial dose and rate of increase) can differ. An absolute indication for replacement therapy in subclinical hypothyroidism is its detection in a pregnant woman, or planning for pregnancy in the near future.
The principles of substitution therapy for secondary hypothyroidism are similar, except that the quality of its compensation is assessed at the T4 level. Treatment of hypothyroid coma implies intensive measures, including the administration of thyroid hormone preparations, glucocorticoids, and the correction of hemodynamic and electrolyte disorders.
The quality of life of patients with compensated hypothyroidism, as a rule, does not suffer significantly: the patient has no restrictions, except for the need for daily intake of L-T4.
Prevention of acquired hypothyroidism consists in improving the methods of surgical interventions on the thyroid gland, the correct selection of doses of antithyroid drugs in the treatment of diffuse toxic goiter, the targeted and timely treatment of thyroiditis, as well as in the use of rational doses when using elemental iodine or its compounds as medicines.