|
The common causes of minimal thyroid failure are the same as for
overt hypothyroidism, i.e. usually autoimmunity (1,8). Serum antithyroid autoantibodies,
either against thyroglobulin (TgAb, Thyroglobulin Antibodies) and/or against peroxidase
(TPOAb, Thyroid Per-Oxidase Antibodies) are usually, but not always, positive. TPOAb
antibodies are more commonly positive than TgAb.
Other cases are associated with previous hyperthyroidism treated by either surgery, radioiodine, or drugs. Surgery and radioiodine may leave a functional thyroid mass just a little below normal, hence the minimal thyroid failure. However, many patients are perfectly euthyroid immediately after treatment, and they develop later subclinical hypothyroidism, that finally may become overt. In such cases, the co-existence of a slowly evolving destructive autoimmune process may tip the balance towards hypothyroidism. The same process may explain hypothyroidism after antithyroid drugs or without any treatment. In some ex-thyrotoxic cases, the initial thyrotropin – receptor stimulating autoantibodies may be replaced by thyrotropin – receptor blocking autoantibodies, and so provoke hypothyroidism. In areas with a moderate or severe iodine deficiency, a large part of the population may be hypothyroid, more frequently to a small or moderate degree, but also as overt cases in severe iodine deficiency.(9–11) Presumably, all known causes of thyroid failure, such as inborn errors of thyroid hormone synthesis, goitrogens, radiation etc could, if present to the right extent, lead to subclinical hypothyroidism. In some cases, however, no evidence of the aetiologic factor responsible can be found by the presently available methods. Subclinical thyroid deficiency in the context of pituitary insufficiency is not discussed here. |
