Symptoms of hypothyroidism

Primary hypothyroidism, represented mainly by its "idiopathic" form, is more often observed in women aged 40-60. In recent decades, there has been an increase in all autoimmune diseases, including hypothyroidism. In this regard, the age range has significantly expanded (the disease is observed in children, adolescents, and the elderly), and gender has become blurred. Hypothyroidism in elderly patients has acquired special significance in terms of both diagnosis and treatment, in which a number of common non-specific symptoms can be mistakenly attributed to natural age-related involution or organ pathology.

Symptoms of severe hypothyroidism are very polymorphic, and patients present a lot of complaints: lethargy, slowness, rapid fatigue and decreased performance, daytime sleepiness and sleep disturbances at night, memory impairment, dry skin, swelling of the face and limbs, brittle and striated nails, hair loss, weight gain, paresthesia, often heavy or scanty menstruation, sometimes amenorrhea. Many note persistent pain in the lower back, but this symptom disappears as a result of effective thyroid therapy, does not attract the attention of doctors and is usually regarded as a manifestation of osteochondrosis.

The severity and speed of development of hypothyroidism symptoms depend on the cause of the disease, the degree of thyroid insufficiency and individual characteristics of the patient. Total thyroidectomy leads to rapid development of hypothyroidism. However, even after subtotal surgery, hypothyroidism develops in the first year or later in 5-30% of those operated on. The presence of antithyroid antibodies may be one of its causes.

The initial manifestations of the disease are characterized by scanty and non-specific symptoms (weakness, rapid fatigue, decreased performance, heart pain, etc.), and patients can be unsuccessfully observed for a long time for "cerebral sclerosis", "pyelonephritis", "anemia", "angina", "depression", "osteochondrosis", etc. In severe hypothyroidism, the appearance of patients is very characteristic: periorbital edema, pale, puffy and mask-like face. Edematous and enlarged facial features sometimes resemble acromegaloid. Patients are shivering and wrap themselves in warm clothes even at high ambient temperatures, since low basal metabolism, impaired thermoregulation with a predominance of heat loss over heat production reduce tolerance to cold. Slowing of peripheral blood flow, often accompanying anemia and specific edema make the skin pale, stiff, cold to the touch. Along with this, in some patients (women), against the background of general pallor, a bright, limited blush appears on the cheeks. The skin is dry, flaky, with areas of keratinization, especially on the feet, anterior surface of the shins, knees, elbows.

Swelling of the vocal cords and tongue results in slow, slurred speech, and the timbre of the voice becomes lower and coarser. The tongue increases in volume, and its lateral surfaces show marks and dents from teeth. Enlargement of the tongue and vocal cords causes episodes of sleep apnea. Hearing is often reduced due to swelling of the middle ear. Hair becomes brittle and dry, thinning on the head, in the armpits, pubis, and outer third of the eyebrows. Secretion of the sebaceous and sweat glands decreases, and yellowing of the skin is often observed, most often in the form of spots on the palmar surface of the hands due to excess circulating beta-carotene, which is slowly transformed into vitamin A in the liver. In this regard, chronic hepatitis is sometimes erroneously diagnosed. Myalgia, decreased muscle strength, and increased muscle fatigue are observed, especially in the proximal groups. Muscle pain, cramps and slow relaxation are the most common manifestations of hypothyroid myopathy, and its severity is proportional to the severity of hypothyroidism. Muscle mass increases, the muscles become dense, stiff, well-contoured. So-called pseudohypertrophy of muscles occurs.

Bone lesions are not typical for hypothyroidism in adults. Moderate osteoporosis develops only with a long and severe course. A decrease in the content of minerals in bone tissue may occur after total thyroidectomy, apparently due to calcitonin deficiency. In adolescence and in patients with hypothyroidism since childhood, but poorly treated, there may be a defect in epiphyseal ossification, a lag in the "bone" age from the chronological one, a slowdown in linear growth and shortening of the limbs. Arthralgia, arthropathies, synovitis and arthrosis are often observed. Cardiovascular disorders are very diverse. Myocardial damage with the subsequent development of hypothyroid heart appears already in the early stages of the disease. Patients are bothered by shortness of breath, which intensifies even with minor physical exertion, discomfort and pain in the heart and behind the sternum. Unlike true angina, they are often not associated with physical exertion and are not always relieved by nitroglycerin, but this difference cannot be a reliable differential diagnostic criterion. Specific changes in the myocardium (edema, swelling, muscle degeneration, etc.) weaken its contractility, causing a decrease in stroke volume, cardiac output in general, a decrease in the volume of circulating blood and an increase in circulation time. Damage to the myocardium, pericardium and tonogenic dilation of the cavities increase the volume of the heart, which is clinically characterized by percussion and radiological signs of expansion of its boundaries. Cardiac pulsation weakens, the sonority of tones is muffled.

Bradycardia with a small and soft pulse is a typical symptom of hypothyroidism. It is observed in 30-60% of cases. In a significant proportion of patients, the pulse rate is within the normal range, and approximately 10% have tachycardia. Low metabolic balance of oxygen in organs and tissues and, in this regard, the relative preservation of the arteriovenous difference in oxygen content limit the mechanisms of cardiovascular insufficiency. Inadequate therapeutic doses of thyroid hormones, which increase oxygen utilization, can provoke it, especially in elderly patients. Rhythm disturbances are very rare, but can appear in connection with thyroid therapy. Blood pressure can be low, normal and elevated. Arterial hypertension, according to various authors, is noted in 10-50% of patients. It can decrease and even disappear under the influence of effective thyroid therapy.

Extensive statistical studies have shown that age-related gradual increase in blood pressure is more pronounced in hypothyroid patients than in individuals with normal thyroid function. In this regard, hypothyroidism can be considered a risk factor for the development of hypertension. This is also evidenced by the syndrome of postthyrotoxic hypertension, which occurs after surgery for DTG. However, the traditional idea of the atherogenic effect of hypothyroidism, accelerating the development of atherosclerosis, hypertension and ischemic heart disease, is considered ambiguously today.

In observations by endocrinologists, hypertension was detected in 14 of 47 patients (29%). The average age of patients was 46-52 years. Most of them had been unsuccessfully treated for hypertension in therapeutic and cardiology hospitals. Hypertension in some patients was very high (220/140 mm Hg). As hypothyroid symptoms decreased as a result of successful therapy, hypertension decreased or normalized in most patients. It is noteworthy that the hypotensive effect of thyroid therapy is revealed rather quickly from the moment of its initiation and long before the onset of complete compensation of thyroid insufficiency. The latter excludes a connection between hypothyroid hypertension and deep structural changes in the myocardium and vessels. However, in elderly people with natural development of atherosclerosis, the hypotensive effect is small and unstable. Severe hypertension, masking and “pushing back” hypothyroid symptoms, is one of the common reasons for untimely diagnosis of hypothyroidism and prescription of thyroid drugs.

In the process of adequate thyroid therapy in people of different ages with and without hypertension, chest pains, which have long been regarded as angina, often disappear. Apparently, in hypothyroidism, two clinically difficult to distinguish types of pain are observed: truly coronary (especially in elderly people), which can intensify and become more frequent even with very careful thyroid therapy, and metabolic, which disappear during treatment.

One of the characteristic symptoms in 30-80% of patients is the presence of fluid in the pericardium. The volume of pericardial effusion may be small (15-20 ml) and significant (100-150 ml). The fluid accumulates slowly and gradually, and such a formidable symptom as cardiac tamponade is extremely rare. Pericarditis may be combined with other manifestations of hypothyroid polyserositis - hydrothorax, ascites, characteristic of autoimmune damage with severe autoaggression. With severe polyserositis, other symptoms of hypothyroidism may not be so obvious. There are observations documented by effective treatment, when effusion into the serous membranes was the only manifestation of hypothyroidism. It is believed that there is a certain parallelism between the severity of hypothyroidism, the level of increased creatine phosphokinase in the blood and the presence of pericardial effusion. The most sensitive and reliable method for detecting pericardial fluid is echocardiography, which also allows recording its decrease observed after several months and sometimes years of adequate treatment. Metabolic processes in the myocardium, pericardial symptoms, especially in the presence of effusion, and hypoxia form a complex of ECG changes, mainly of a non-specific nature. Low-voltage electrocardiogram is observed in approximately one third of patients. Frequently noted deformation of the terminal part of the gastric complex (reduction, biphasicity and inversion of the T wave) have no diagnostic value, since they are no less characteristic of coronary atherosclerosis. These changes in combination with pain syndrome, and sometimes with arterial hypertension, lead to overdiagnosis of ischemic heart disease. The best evidence of their metabolic nature is the disappearance of pain and positive ECG dynamics during treatment.

Respiratory system abnormalities are characterized by muscular incoordination, central regulatory disorders, alveolar hypoventilation, hypoxia, hypercapnia, and edema of the respiratory mucosa. Patients are prone to bronchitis and pneumonia, which are characterized by a sluggish, protracted course, sometimes without temperature reactions.

There are a number of gastrointestinal disorders: loss of appetite, nausea, flatulence, constipation. Decreased tone of the intestinal muscles and bile ducts leads to stagnation of bile in the gallbladder and contributes to the formation of stones, the development of megacolon and sometimes intestinal obstruction with the picture of "acute abdomen".

Renal fluid excretion is reduced both by low peripheral hemodynamics and by elevated vasopressin levels; urinary tract atony favors infection. Mild proteinuria, decreased filtration, and decreased renal blood flow may occasionally occur. Severe renal hemodynamic disturbances are usually not present.

Peripheral nervous system disorders are manifested by paresthesia, neuralgia, slowing of tendon reflexes; the speed of impulse passage along the Achilles tendon slows down in hypothyroidism. Symptoms of polyneuropathy can be not only in obvious hypothyroidism, but also in latent hypothyroidism.

All patients have some degree of mental disorders, and sometimes they dominate the clinical symptoms. Typical symptoms include lethargy, apathy, memory impairment, and indifference to the environment; the ability to concentrate, perception, and reaction are reduced. Sleep is distorted, and patients are bothered by drowsiness during the day and insomnia at night. Along with mental indifference, there may be increased irritability and nervousness. If the disease is left untreated for a long time, severe hypothyroid chronic psychosyndrome develops, including psychoses, which are close in structure to endogenous psychoses (schizophrenia-like, manic-depressive psychosis, etc.).

Hypothyroidism may be accompanied by some or other manifestations of ophthalmopathy, but they are much less common than with thyrotoxicosis and do not tend to progress. Periorbital edema, ptosis, and refractive anomalies are usually observed. Changes in the optic nerve and retinal edema are very rare.

Blood disorders to varying degrees are found in 60-70% of patients. Achlorhydria, decreased absorption of iron, vitamin B12 and folic acid in the gastrointestinal tract, and inhibition of metabolic processes in the bone marrow are the basis of "thyrogenic" anemias, which can be hypochromic, normochromic and even hyperchromic. Anemias of autoimmune genesis accompany severe autoimmune forms of hypothyroidism; in this case, there may be dysproteinemia and a decrease in total protein in the blood due to its release from the vascular bed as a result of increased vascular permeability. Patients are prone to hypercoagulation processes due to increased plasma tolerance to heparin and an increase in the level of free fibrinogen.

Fasting blood sugar levels are usually normal or slightly reduced. Even hypoglycemic comas have been described as rare complications. Due to the slow absorption of glucose in the intestine and its utilization, the glycemic curve with load may be flattened. The combination of diabetes mellitus and hypothyroidism is rare, usually with polyendocrine autoimmune lesions. With decompensation of hypothyroidism, the need for insulin in patients with diabetes mellitus may decrease, and in conditions of full replacement therapy, it may increase.

Hypothyroidism is accompanied by an increase in cholesterol synthesis (its level sometimes increases to 12-14 mmol/l) and a decrease in its catabolism; inhibition of metabolism and the rate of chylomicron clearance, an increased growth in the amount of total triglycerides and low-density lipoprotein triglycerides. At the same time, in a number of patients, the lipid spectrum is not significantly disturbed, and the cholesterol content in the blood remains normal.

In recent years, interest in the syndrome of primary hypothyroidism galactorrhea-amenorrhea has revived. The level of diagnostics of this pathology and its differentiation from other syndromes with a primary disorder of central regulation and secretion of prolactin and gonadotropins (Chiari-Frommel syndrome, Forbes-Albright syndrome, etc.), which are largely similar in clinical presentation but fundamentally different in pathogenesis, has increased. The peculiarity of the syndrome has allowed it to be isolated into a clinical form known as Van Wyck-Hennes-Ross syndrome.

In 1960, JJ Van Wyk and M. M. Grambah reported an unusual course of primary hypothyroidism in 3 girls (aged 7, 8, and 12 years), combined with macromastia, galactorrhea, and sexual dysfunction (premature menarche and metrorrhagia in the absence of pubic hair). Noting the normalization of the general condition and regression of symptoms of premature sexual development with a return to the prepubertal state, cessation of galactorrhea, and restoration of the structure and size of the previously enlarged sella turcica as a result of thyroid therapy, the authors proposed a pathogenetic concept of nonspecific hormonal "crossing", which has not lost its significance to this day. They also pointed to a secondary mechanism for the development of pituitary adenoma in long-term untreated myxedema. U. Hennes and F. Ross observed the postpartum course of primary hypothyroidism with lactorrhea and amenorrhea, and sometimes metrorrhagia, but without changes in the sella turcica. Discussing the mechanisms of hormonal "crossing" at the level of the pituitary gland, when a decrease in the peripheral level of thyroid hormones through TRH stimulation increases the release of not only TSH but also prolactin, the authors assumed that, along with the stimulation effect, there is suppression of both prolactin-inhibiting factor (PIF) and LH-releasing factor. The latter disrupts the secretion of gonadotropins and sex hormones. Unconventional connections may also be involved in the "crossing", for example, hyperpigmentation due to excess melanin-stimulating hormone and metrorrhagia as a result of excess gonadotropins.

Van Wyck-Hennes-Ross syndrome (the listing of the authors in this order corresponds to the chronology) is a combination of primary hypothyroidism, galactorrhea, amenorrhea or other menstrual cycle disorders with or without pituitary adenoma. The syndrome includes the juvenile Van Wyck variant (which has some age-related features, when some maturation parameters are ahead of age, and some are absent) and the postpartum Hennes-Ross variant. The "crossing" syndrome indicates the absence of narrow specialization of both the hypothalamic and pituitary mechanisms of negative feedback. The pituitary gland can sharply increase the reserve of not only TSH, but also prolactin (PRL), as well as STH, which is most demonstratively revealed in the thyroliberin test. Apparently, this syndrome develops in patients with primary hypothyroidism when a decrease in the level of peripheral thyroid hormones puts the entire lactogenic system (TRH, TSH, PRL) in a state of extreme tension. The same mechanism of combined central hyperactivity of thyrotrophs and lactotrophs through their hyperplasia and adenomatous transformation stimulates secondary pituitary adenoma more often than in the general group of patients with primary hypothyroidism. In long-untreated patients, pituitary adenoma may acquire features of autonomy and not respond to either TRH or the level of peripheral hormones. Radiologically and with the help of computer scanning, pituitary adenomas are detected, in some cases extending beyond the sella turcica. Defects of the visual fields, mainly central (compression of the chiasm), are often observed. Correction of visual field defects, and sometimes regression of some radiological symptoms of pituitary adenoma occurs after several months or years of thyroid therapy. Pregnancy and especially childbirth with their natural physiological hyperprolactinemia and suppression of gonadotropin cyclicity provoke the disease. After childbirth, pathological galactorrhea caused by hypothyroidism, which could have been latent for a long time, and physiological, postpartum galactorrhea are summed up. Such a situation leads to the manifestation of hypothyroidism, and on the other hand, masks the true nature of the disease, complicating timely diagnosis. The postpartum course and hypothyroid symptoms simulate panhypopituitarism, but the very fact of lactorea and hyperprolactinemia excludes it.

There are no significant clinical differences between the expressed forms of primary and secondary hypothyroidism. However, the presence of basal, unstimulated secretion of thyroid hormones in the thyroid gland somewhat softens the clinical manifestations of secondary hypothyroidism. The classic form of secondary thyroid insufficiency is hypothyroidism in patients with postpartum panhypopituitarism (Sheehan syndrome). Thyroid insufficiency in various hypothalamic-pituitary diseases (pituitary dwarfism, acromegaly, adiposogenital dystrophy) is combined with impaired growth, sexual development, pathology of lipid metabolism, diabetes insipidus.

The most severe, often fatal complication of hypothyroidism is hypothyroid coma. This complication usually occurs in elderly women with undiagnosed or long-term untreated, as well as poorly treated hypothyroidism. Provoking factors: cooling, especially in combination with physical inactivity, cardiovascular insufficiency, myocardial infarction, acute infections, psychoemotional and muscular overload, various diseases and conditions that contribute to hypothermia, namely gastrointestinal and other bleeding, intoxication (alcohol, anesthesia, anesthetics, barbiturates, opiates, tranquilizers, etc.). The most important clinical landmarks: dry, pale-icteric, cold skin, sometimes with hemorrhagic rashes, bradycardia, hypotension, rapid breathing, oliguria, decreased and even disappearance of tendon reflexes. Hypothyroid polyserositis with fluid accumulation in the pericardium, pleura and abdominal cavity, accompanying the most severe forms of hypothyroidism, in combination with true cardiovascular failure, rarely observed in hypothyroidism and more often in coma, create certain differential diagnostic difficulties. Laboratory studies reveal hypoxia, hypercapnia, hypoglycemia, hyponatremia, acidosis (including due to increased lactic acid levels), high cholesterol and lipid spectrum disorders, increased hematocrit and blood viscosity. Low levels of thyroid hormones (T3, T4) in the blood and high TSH may be of decisive importance for diagnosis _, but _urgent performance of these studies is not always possible.

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