Hypothyroidism is defined as the lack of action of thyroid hormones on target tissues. The term autoimmune hypothyroidism identifies situations with insufficient thyroid function caused by an autoimmune destruction of the thyroid gland. The most common form of autoimmune thyroid diseases (AITDs) is chronic or lymphocytic autoimmune thyroiditis (Hashimoto’s thyroiditis). Prevalence of autoimmune hypothyroidism is high. In its initial stage, chronic autoimmune thyroiditis is characterized by the presence of hallmarks of thyroid autoimmunity and normal thyroid function. As a consequence of the autoimmune attack to the gland, hypothyroidism may develop, usually slowly and insidiously, through a subclinical phase (normal thyroid hormone and slightly elevated thyroid-stimulating hormone [TSH] levels) and an eventual phase of overt insufficiency (low thyroid hormones and frankly elevated TSH levels). Etiology and pathogenesis of chronic autoimmune thyroiditis and mechanisms leading to the hypothyroid phase remain elusive. However, some predisposing genetic factors and some triggering environmental factors have been identified. The role of antigen-presenting cells, of T- and B-cell response, and of effector mechanisms in the immunopathogenesis of chronic autoimmune hypothyroidism has been extensively investigated. Clinical presentation and consequences of autoimmune hypothyroidism vary according to patient’s age and duration and severity of hypothyroidism. The picture is peculiar in the elderly, and the effects are particularly negative in fetuses and newborns. Circulating thyroid autoantibodies and a hypoecogenic pattern at thyroid ultrasound are the two hallmarks of chronic autoimmune diseases. Treatment of hypothyroidism is based on the administration of synthetic levo-thyroxine (l-T4), whereas the usefulness of combined treatment with liothyronine (l-T3) is uncertain and difficult to manage. Opinions about treatment of subclinical hypothyroidims diverge largely, but it should be supported, or at least not discouraged. Because of the awareness about negative consequences of maternal hypothyroidismon the fetus development, screening or intensive case finding for chronic autoimmune hypothyroidism in women of childbearing aging is unanimously recommended.

Autoimmune hypothyroidism

LATROFA, FRANCESCO;PINCHERA, ALDO
2007-01-01

Abstract

Hypothyroidism is defined as the lack of action of thyroid hormones on target tissues. The term autoimmune hypothyroidism identifies situations with insufficient thyroid function caused by an autoimmune destruction of the thyroid gland. The most common form of autoimmune thyroid diseases (AITDs) is chronic or lymphocytic autoimmune thyroiditis (Hashimoto’s thyroiditis). Prevalence of autoimmune hypothyroidism is high. In its initial stage, chronic autoimmune thyroiditis is characterized by the presence of hallmarks of thyroid autoimmunity and normal thyroid function. As a consequence of the autoimmune attack to the gland, hypothyroidism may develop, usually slowly and insidiously, through a subclinical phase (normal thyroid hormone and slightly elevated thyroid-stimulating hormone [TSH] levels) and an eventual phase of overt insufficiency (low thyroid hormones and frankly elevated TSH levels). Etiology and pathogenesis of chronic autoimmune thyroiditis and mechanisms leading to the hypothyroid phase remain elusive. However, some predisposing genetic factors and some triggering environmental factors have been identified. The role of antigen-presenting cells, of T- and B-cell response, and of effector mechanisms in the immunopathogenesis of chronic autoimmune hypothyroidism has been extensively investigated. Clinical presentation and consequences of autoimmune hypothyroidism vary according to patient’s age and duration and severity of hypothyroidism. The picture is peculiar in the elderly, and the effects are particularly negative in fetuses and newborns. Circulating thyroid autoantibodies and a hypoecogenic pattern at thyroid ultrasound are the two hallmarks of chronic autoimmune diseases. Treatment of hypothyroidism is based on the administration of synthetic levo-thyroxine (l-T4), whereas the usefulness of combined treatment with liothyronine (l-T3) is uncertain and difficult to manage. Opinions about treatment of subclinical hypothyroidims diverge largely, but it should be supported, or at least not discouraged. Because of the awareness about negative consequences of maternal hypothyroidismon the fetus development, screening or intensive case finding for chronic autoimmune hypothyroidism in women of childbearing aging is unanimously recommended.
2007
Latrofa, Francesco; Pinchera, Aldo
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/109544
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact