Subclinical hypothyroidism is a preclinical stage of hypofunction of the thyroid gland (thyroid gland), characterized by an increase in the level of thyrotropin at normal values of free fractions of thyroid hormones. Specific symptoms of hypothyroidism are absent or expressed minimally (anxiety, mood depression, fatigue, decreased attention and memory). Metabolic syndrome often develops. The diagnosis is confirmed according to the study of thyroid function (TSH, T4 sv., At to TPO), echography of the thyroid gland. L-T4 replacement therapy is prescribed according to individual indications.
ICD 10
E02 E03.8
Meaning
Subclinical hypothyroidism (SH, SHT, latent/latent hypothyroidism, minimal thyroid insufficiency) is a decrease in thyroid function, in which normal levels of T3 and T4 are maintained against the background of increased TSH synthesis, and there are no symptoms of hypothyroidism. The population frequency of pathology, depending on gender and age, ranges from 4 to 15%. Often, subclinical hypothyroidism is regarded as a pre-stage of manifest hypothyroidism. The gender structure of patients is dominated by women (W:M – 2:1). SH is a risk factor for the development of cardiovascular diseases, reproductive failures, therefore, increased attention is paid to it in modern endocrinology.
Causes
The etiology of subclinical hypothyroidism is multifactorial. The main mechanisms leading to thyroid insufficiency include destruction of thyroid tissue, disruption of hormone synthesis, toxic suppression of gland function. The immediate causes of latent hypothyroidism are:
- Chronic autoimmune thyroiditis. In most cases, persistent SH develops in the outcome of Hashimoto’s thyroiditis. Antibodies to the enzyme thyroperoxidase attack thyroid cells, causing the death of thyrocytes, a decrease in the number of functioning cells and the secretion of thyroid hormones.
- Deficient states. The cause of both manifest and subclinical hypothyroidism may be iodine deficiency. Iodine deficiency is often aggravated by a lack of protein in food, a deficiency of selenium.
- Intoxication. Chemical toxicants that adversely affect the function of the thyroid gland include components of tobacco smoke (carbon monoxide), chlorine, benzene, manganese. A drug-induced decrease in thyroid hormone activity may be associated with taking lithium, sulfonamides, amiodarone, potassium iodide.
- Other reasons. Possible triggers of subclinical hypothyroidism may be surgical resection of the thyroid gland, radiotherapy, radiation therapy of tumors of the head and neck. Transient hypofunction of the endocrine organ can be caused by subacute, postpartum thyroiditis, severe general diseases.
Risk factors
Women with the following risk factors are more likely to develop subclinical hypothyroidism:
- elderly and senile age;
- obesity;
- smoking, including passive;
- circadian rhythm disorders;
- anxiety disorders, etc.
Pregnancy, stressful situations, intercurrent diseases can provoke the manifestation of SHT.
Pathogenesis
There is an inverse relationship between the value of free thyroxine (T4 sv.) and the thyroid-stimulating hormone of the pituitary gland (TSH), so even a slight decrease in the synthesis of T4 leads to a multiple increase in TSH. The course of autoimmune thyroiditis is accompanied by gradual destruction of glandular tissue, as a result of which the production of thyroid hormones decreases and the level of thyrotropin increases.
High TSH values lead to hyperstimulation of the thyroid gland, due to which T4 production remains within the normal range for a long time, more often at the lower limit of the norm. Target tissues are extremely sensitive even to subclinical hormonal fluctuations, which determines the polysystemic nature of the lesion.
There is a slowdown in all types of metabolism. A decrease in protein metabolism leads to the accumulation of glycosaminoglycans in tissues, which contribute to water retention, the appearance of pasty tissues. Violation of lipid metabolism is manifested by hypercholesterolemia, hypertriglyceridemia. Slowing down the utilization of carbohydrates leads to an increase in insulin levels, a violation of glucose tolerance.
Structural and functional changes develop in various organs: arterial vessels, heart muscle, brain, organ of vision, reproductive system.
Subclinical hypothyroidism symptoms
By definition, latent hypothyroidism is asymptomatic. However, with the most thorough questioning of patients, 25-50% of them have mild or moderate signs of thyroid hypofunction. Many signs of SHT remain underestimated: swelling under the eyes is attributed to insomnia and fatigue, weight gain is attributed to inactivity, and forgetfulness, apathy, lethargy in elderly patients is explained by old age. Therefore, the diagnosis of subclinical hypothyroidism is usually made retrospectively, only after the identification of a characteristic hormonal imbalance.
With SH, there are violations on the part of many systems. The most typical neurological complaints are decreased performance, depressed mood, unreasonable anxiety, sleep disturbance. There is a deterioration of memory and attention, a moderate cognitive decline. Often develops refractory to therapy depression.
To a large extent, the cardiovascular system is sensitive to thyroid hormone deficiency. Patients with subclinical hypothyroidism often suffer from dyslipidemia, arterial hypertension, rhythm and conduction disorders. One of the frequent problems of patients with subclinical hypothyroidism is the metabolic syndrome, which combines increased BMI, insulin resistance and increased blood pressure.
Disorders of the reproductive system include menstrual dysfunction (amenorrhea, menometrorrhagia), endometriosis, infertility. The companions of subclinical hypothyroidism from the gastrointestinal tract are often constipation, GI, dyskinesia of the gastrointestinal tract. Among other disorders, hypochromic anemia, increased intraocular pressure, myalgia, polyarthritis, edematous syndrome occur in hypertension.
Complications
In pregnant women, subclinical hypothyroidism can provoke complications such as miscarriage, preeclampsia, placental abruption, premature birth. Against this background, gestational diabetes and hypertension are statistically more likely to develop. Children born to mothers with SH have a low score on the Apgar score, the worst intelligence indicators.
Subclinical hypothyroidism is a predictor of an increased risk of cardiovascular complications and mortality from them. Thus, patients with SH have a tendency to develop aortic atherosclerosis, atherothrombosis, hypertrophic cardiomyopathy, coronary artery disease, heart failure. Within a few years, the progression of subclinical hypothyroidism to manifest form is possible (at the age of over 65 years, in the presence of TSH > 12 mEd / l, increased titer of At-TPO).
Diagnostics
The main and decisive method of confirming subclinical hypothyroidism is laboratory. All patients need to consult an endocrinologist in order to assess clinical symptoms, interpret the results of tests, and decide on the appropriateness of prescribing replacement therapy. The mandatory diagnostic minimum includes:
- Hormonal studies. Markers of subclinical hypothyroidism are an increase in TSH (>4 IU / l), a normal level of T4 sv. With SH, a high titer of AT-TPO is determined. Hyperprolactinemia may occur.
- Clinical and biochemical blood tests. Dyslipoproteinemia is detected in patients with SH: reduction of HDL, increase in LDL, total cholesterol, triglycerides, increase in the coefficient of atherogenicity. It is characterized by an increase in the level of glycemia, insulin, HOMA-IR. Normo- or hypochromic anemia is often found.
- Echography. According to the ultrasound of the thyroid gland, signs of autoimmune thyroiditis, thyroid nodes are detected. Echocardiography reveals myocardial hypertrophy. During stress tests, there is a decrease in stroke volume, cardiac index, and maximum velocity in the aorta compared to patients without subclinical hypothyroidism.
- Psychodiagnostics. When examined on the Wexler score, a number of patients with SH are diagnosed with a decrease in memory and attention. Other tests and questionnaires demonstrate increased anxiety, a tendency to neurotic reactions, depression.
Differential diagnosis
Subclinical hypothyroidism should be differentiated from other conditions occurring with transient or persistent hypersecretion of thyrotropin:
- neonatal hyperthyroidism;
- hypothyroidism (transient, central, peripheral);
- TSH-secreting pituitary adenoma;
- euthyroid sick syndrome;
- primary hypocorticism (including Schmidt syndrome);
- chronic renal failure.
Subclinical hypothyroidism treatment
The question of the need for SH correction remains debatable. Currently, the expediency of prescribing therapy is determined individually, based on laboratory parameters, age, risk factors, and the manifestation of subclinical hypothyroidism. At the initial detection of elevated TSH levels, it is recommended to repeat the analysis after 3-6 months to exclude transient hypothyroidism. Indications for the appointment of HRT are:
- persistent hyperthyroidism;
- TTG ≥ 10 mEd/L;
- TSH 5-10 mEd/l in the presence of At to TPO, dyslipidemia, HF and other concomitant disorders;
- pregnancy or preparation for pregnancy in women with SH.
Levothyroxine preparations are used as replacement therapy. The target value of TSH is in the range of 0.5-2.0 mEd/l. Therapy is carried out for life under the control of TSH levels.
Prognosis and prevention
Normalization of TSH levels as a result of therapy leads to the restoration of lipid and carbohydrate metabolism, improvement of mental processes, reduction of the risk of cardiovascular disasters. In the absence of treatment, the transition of subclinical hypothyroidism to the manifest stage occurs.
The preventive direction includes the correction of nutrition for sufficient intake of trace elements and protein, limiting the effect of toxicants on the thyroid gland, the exclusion of uncontrolled medication intake. For the timely detection of subclinical hypothyroidism, the American Thyroidological Association recommends that TSH screening be performed every 5 years for women over 35 and men over 50.
