Athyreosis
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
This article from the 1928–1936 Soviet Great Medical Encyclopedia defines athyreosis as the absence of the thyroid gland and the resulting total loss of its function. It details the congenital and acquired forms of the condition, its clinical manifestations—including myxedema, stunted growth, and intellectual impairment—and notes the effectiveness of organotherapy.
Encyclopedia article (1928–1936)
ATHYREOSIS, the absence of the thyroid gland and, consequently, the total loss of its function. Congenital athyreosis is sometimes the result of agenesis of the organ or disturbances in embryonic development; usually, however, like acquired athyreosis, it is caused by toxic-infectious factors (syphilis). Acquired athyreosis arises under the influence of infections and intoxications, as well as local processes in the neck and the gland itself (inflammation, hemorrhage), which cause simple or degenerative atrophy and sclerosis of the organ. Athyreosis after the surgical removal of the entire thyroid gland is currently very rare, since its complete extirpation is performed only in extreme cases (e.g., cancer). The influence of athyreosis on the organism is more severe the earlier in life the loss of thyroid function occurs. However, children with congenital aplasia of the thyroid gland are born without signs of insufficiency of this organ, receiving hormonal influences from the thyroid gland of the maternal organism during intrauterine life. Breastfeeding also delays the development of symptoms of thyroid insufficiency. The symptoms of athyreosis are especially pronounced in cases of congenital athyreosis and extend to all functions of the organism. Their essence consists in the slowing down and suppression of physiological processes due to the loss of the activating, dissimilatory, ion-endocrine influences of the thyroid gland secretion—thyroxine (see). The consequences of athyreosis, whether congenital or acquired in the first months of life, are: dwarfism, short limbs with short, thick fingers, myxedema (see), hyperplasia of adenoid tissue, anemia, early development of arteriosclerosis and myocardial insufficiency, a tendency toward constipation, a decrease in the barrier function of the liver (easy onset of alimentary glycosuria), and a sharp (up to 50%) decrease in basal metabolism. Sexual maturity does not occur, and secondary sexual characteristics are absent (infantilism). Hair is sparse, thick, brittle, and falls out easily; the skin becomes atrophic early on. Renal secretion occurs sluggishly, metabolism is slowed, there is a tendency toward a positive protein balance and the formation of pasty adipose tissue; there is also a slowing of reactions from the nervous system, apathy, suppression of higher nervous activity (idiocy), early appearance of signs of senile decay, and cachexia. The hypertrophy of the pituitary gland observed in athyreosis is generally considered to have a compensatory significance.

Athyreosis arising in later childhood and adolescence halts the normal development of the organism and, without treatment, leads to the same final results as the congenital form.
Athyreosis in adults finds expression in a number of trophic disorders, myxedema, a decrease in (maximum) blood pressure, a decrease in the intensity of metabolism, the extinction of sexual function, general apathy, suppression of higher nervous activity, and ends in cachexia and death from an intercurrent disease (tuberculosis). Opotherapy and organotherapy with thyroid gland preparations produce a brilliant effect. Experimental athyreosis yields results that fully coincide with clinical data.
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“Athyreosis.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/athyreosis/