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Thyroid
Disease
Autoimmune Issues
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Wuchter
Wuchter T
Dissertation (German), 2007
"An important exogenous risk factor of
autoimmune thyroiditis is iodine. Epidemiological studies show a
different prevalence of thyroid disease depending on iodine
supply. We observed patients with subclinical hypothyroidism due
to Hashimoto thyroiditis who reached euthyroidism after reduction
of iodine intake in our thyroid outpatient department of the
Vivantes hospital “Krankenhaus am Urban” in Berlin. The inorganic
iodine in serum is the decisive parameter that determines the
iodine supply to the thyroid gland. Therefore we determined the
levels of non-hormone-bound iodine in serum (nhI) in 106
Patients. The nhI is not exactly the same as the inorganic iodine
in serum but it shows a high correlation with the latter. To
examine the influence of renal excretion on the concentrations of
nhI we also determined the renal clearance in 10 patients.
Patients with Hashimoto thyroiditis showed lower concentrations
of nhI than the control group, contrary to the data we expected.
The differences were not significant. The lowest concentrations
of nhI were seen in patients who followed a restricted iodine
intake and had no substitution of Levothyroxin. This implies that
nhI varies due to the iodine intake and not because of a
differing renal excretion. Iodine is eliminated up to 90 % by
renal excretion. The measurement of renal iodine clearance did
not show a lower clearance and higher levels of nhI in patients
with Hashimoto thyroiditis. Renal iodine clearance tended to be
even higher in patients with Hashimoto thyroiditis than in the
control group. However, we found that the renal iodine clearance
correlates significantly with the urine volume per minute
(r=0,65; p=0,043). After elimination of a variable diuresis one
should expect an iodine clearance within a lower range. The
concentration of nhI shows a positive correlation with the
concentration of iodine in urine (r=0,79; p=0,007). Because the
patients do not differ in nhI levels, which determine the iodine
supply to the thyroid gland, we suspect that there is most likely
no difference in the entire extrathyroidal metabolism in patients
with Hashimoto thyroiditis and the control group. Consequently,
we suppose that the mechanism which induces the pathogenesis of
Hashimoto thyroiditis should be found in the intrathroidal iodine
metabolism. The reason for the higher prevalence of autoimmune
thyroiditis seems to be the generally increased iodine intake,
that affects genetically susceptible individuals rather than a
differing extrathyroidal iodine metabolism."
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