Hypothyroidism is divided in primary, caused by failure of thyroid function and secondary (central) due to the failure of adequate
thyroid-stimulating hormone (TSH) secretion from the pituitary gland or
thyrotrophin-releasing
hormone (TRH) from the hypothalamus.
Secondary hypothyroidism can be differentiated in pituitary and hypothalamic by the use of TRH test. In some cases, failure of
hormone action in peripheral tissues can be recognized.
Primary hypothyroidism may be clinical, where free T(4) (FT(4)) is decreased and TSH is increased or subclinical where FT(4) is normal and TSH is increased. In
secondary hypothyroidism FT(4) is decreased and TSH is normal or decreased.
Primary hypothyroidism is most commonly caused by chronic
autoimmune thyroiditis, less common causes being radioiodine treatment and
thyroidectomy.
Salt iodination, which is performed routinely in many countries, may increase the incidence of overt
hypothyroidism. The incidence of clinical
hypothyroidism is 0.5-1.9% in women and <1% in men and of subclinical 3-13.6% in women and 0.7-5.7% in men. It is important to differentiate between clinical and subclinical
hypothyroidism as in clinical symptoms are serious, even
coma may occur, while in subclinical symptoms are less and may even be absent. Subclinical
hypothyroidism may be transformed to clinical and as recent research has shown it may have various consequences, such as
hyperlipidemia and increased risk for the development of
cardiovascular disease, even
heart failure, somatic and neuromuscular symptoms, reproductive and other consequences. The administration of novel
tyrosine kinase inhibitors for the treatment of neoplastic diseases may induce
hypothyroidism.
Hypothyroidism is treated by the administration of
thyroxine and the prognosis is excellent.