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Multinodular goitre and neoplastic and autoimmune
goitre are the three main types of non
endemic goitre. Types may overlap in individual
patients.
Epidemiological data demonstrate that development
of a multinodular goitre is highly dependent
on the iodine intake and that TSH stimulation
is of less importance. The basic driving force
during goitrogenesis seems to be the iodostate
which autoregulates the thyroid.
Somehow a more or less irreversibel polyfocal
polyclonal process takes place in the thyroid
gland with replication of highly heterogeneous
follicles. The frequency of growth promoting
mutations is enhanced leading to scattered monoclonal
nodules. An abnormal low iodinating
activity in the sick gland may self-perpetuate the
process.
The main preventive action is a proper level of
population iodine intake and a decrease in the
intake of goitrogens such as tobacco smoke. However
despite these measures, a residual prevalence
of multinodular goitre will remain in which
a genetic etiology may play a role. Preventive
measures may also be helpfull as treatment in the
early stages of the disease, whereas radioiodine
therapy and in some cases surgery is necessary if
treatment is needed in more advanced cases.
A major complication of multinodular goitre is
clinical and subclinical hyperthyroidism which
occur with high prevalence in the elderly in low
iodine intake areas.
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