Thyroid autoantibodies: a good marker for the study of symptomless autoimmune thyroiditis.

In 3737 subjects without clinically thyroid disorders we evaluated the incidence of thyroid microsomal and thyroglobulin antibodies. These autoantibodies were found in 7% of a normal population, in 9% of patients with various non-autoimmune diseases, and in 11-16% of groups who either had or were at risk for autoimmune diseases: patients with IDDM, vitiligo, alopecia areata, idiopathic hypoparathyroidism, Addison's disease, and first-degree relatives of IDDM patients. Functional thyroid evaluation with TRH test was performed in 197 seropositive subjects and 144 seronegative controls. One-quarter (26%) of the subjects with thyroid autoantibodies showed functional abnormalities on TRH testing, whereas only 2.8% of the 144 seronegative controls showed subclinical hypothyroidism. After an observation period of 12-44 months, 102 persistently seropositive subjects were reassessed and 31% of them showed an impairment in TRH test response.

Acute and chronic effects of dextro-thyroxine on pituitary thyroid axis and on reverse triiodothyronine production in euthyroid subjects.

Serum levels of thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3) and TSH were measured in euthyroid subjects after a single dose of 4 mg D-thyroxine (DT4) or of 0.25 mg L-thyroxine (LT4). The same parameters and TSH response to TRH were also evaluated in 7 dyslipidemic patients before and after one month of treatment with 6 mg DT4. T4 levels increased about 165% at h 4 after DT4 and only 47% after LT4; T3 levels remained unchanged until h 10 both after DT4 and after LT4; rT3 levels increased almost 179% after DT4 and only 32% after LT4. TSH levels decreased about 30% after both DT4 and LT4. In the long term study similar variations of the same parameters were observed: basal TSH levels decreased and TSH response to TRH was inhibited in all patients but one; T4 levels increased 62%, T3 levels increased 35%, while rT3 levels increased 545%. Our results show that: both acute and long-term treatment with DT4 suppress TSH secretion; DT4 both in acute and in long-term administration, is preferentially dealogenated in the alaninic ring with production of rDT3, instead of in the phenolic ring with production of DT3. This may contribute to explain its lower metabolic activity.