AUTOIMMUNE THYROID-DISEASES

AITD (autoimmune thyroid disease) comprise atrophic thyroiditis (AT), hypertrophic Hashimoto's thyroiditis (HT), and immunogenic hyperthyroidism (Graves' disease, GD). Combinations with other types of autoimmune disorders frequently occur and are called polyglandular autoimmune syndrome. Familial disposition may be documented by genetic markers: GD and AT are associated with HLA-B8 and DR3 respectively, while HT associates with DR5. Pathogenesis of the forementioned 3 AITD may be explained on the one hand by an immunological balance and on the other hand by a predominance of either stimulating or destructive/blocking immune processes. In diagnosing AITD the determination of antibodies against thyroglobulin or thyroidal peroxidase have been in use for quite some times. Antibodies directed against TSH receptors (TRAb) are determined by means of a radioligand assay which will not distinguish between stimulating or blocking antibodies, so that clinical symptoms and thyroid function parameters are essential in evaluating hyper- oder hypothyroid function. TRAb are transferred via the placenta and should therefore be determined in patients with AITD within the 3rd trimester of pregnancy. The prevalence of AITD is far higher in iodine rich countries and is 4 times more frequent in women, with a general age peak between the 5th and 6th decade. The rarer AT mostly presents as primary myxoedema and is discovered less frequently during the exploration of an unclear hypercholesterolemia. In HT we differentiate between the chronic fibrous and the juvenile oxiphilic variant. In the former fibrosis is predominant with plasmacellular infiltration producing extremely high titers of antibodies enabling diagnosis without fine needle biopsy (FNB). In the latter, the oxiphilic variant, titers of antibodies are mostly low or even missing so that a reliable diagnosis will require a FNB. However, two thirds of adolescent goitres are caused by HT. In HT a mostly slow development of a firm goitre without compression of the surrounding tissues and without lymph node involvement is characteristic. The insidious transition to hypothyroidism shows 4 laboratory phases. Moreover, in early stages iodisation disturbances and pathologic iodoproteins may be observed. In the course of HT occasionally an unexpected reversal to ''hashitoxicosis'' may be seen, whereas a frequent change is precipitation of hypothyroidism induced by high iodine intake. Long-lasting iodine excess should consequently be avoided. In therapy an overt hypothyroidism requires a permanent T4 substitution. Only in juvenile HT spontaneous remissions are observed which allow a tentative discontinuation of T4 medication after 6 months. In subclinical hypothyroidism in the elderly a T4 medication is advisable, since hypothyroidism develops in 5% of patients p.a. Moreover, hypothyroid symptoms are very often misinterpreted as early aging and may be thus cured by T4 administration. On the other hand long-term effects upon heart and lipid metabolism are to be avoided by early diagnosis and treatment of subclinical hypothyroidism. The average T4 dosis administered daily amounts to 1.6 mug/kg which should lead to a lowered but not suppressed TSH level. A modulation of immune processes by means of a T4 long-term medication has still to be established.