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Morris et al., Rochester, MN, studied the prevalence of serum autoantibodies
against the carrier protein in the plasma membrane of thyroid follicular
cells that transports iodide into the cell in 27 patients with Graves'
disease (GD), and 27 patients with autoimmune hypothyroidism (HT). The
authors could perform these studies since the Na+lI-symporter (NaIS) was
recently cloned. They found in 63% of GD patients and 33% of HT patients
antibodies against peptide 498-517 of the extra-membranous portion of the
transport protein and similarly in 56% of Graves' disease patients, and
26% of HT patients antibodies against peptide 560-579, while peptide 262-280
also bound antibodies in 44% of GD and 15% of HT patients. From this study
it is apparent that antibodies against NaIS are very frequent in patients
with thyroid autoimmune disease, maybe even more in GD than in HT patients.
(Comment: Apart from the known antibodies against thyroperoxidase (TPO),
thyreoglobulin (TG), and the TSH receptor (TSHR), now another type of antibody
has been detected by these authors. It would be interesting to know to
what extent these antibodies have destructive and/or functional (inhibition
of iodide uptake by the thyroid) effects in thyroid autoimmune disease.
See Endo et all. Bioch Bioph Res Com 228:199, 1966, who reported inhibition
of iodide uptake by thyrocytes in the presence of NaIS-antibodies.)
Benvenga et al., Messina, Italy, report isolated pure musculo-skeletal
myopathy (M) in 5 male and 5 female patients with mild to severe (TSH 6-349
mU/L) autoimmune hypothyroidism and in 1 male with Graves' disease (FT4
83 pmol/L, TSH <0.01 mU/L). These patients were observed between 1992-1995
and showed no other clinical signs of thyroid disease, as confirmed by
3 independent thyroidologists. In this rare clinical presentation of autoimmune
thyroid disease, muscle biopsy (vastus lateralis) showed a variation in
fiber size due to the presence of many atrophic fibers with or without
central nuclei in all patients. In the hypothyroid patients the EMG was
normal in 4 males and 2 females. M disappeared co mpletely upon treatment
of the disease. (Comment: It is very difficult to understand that no other
clinical signs were present despite severe hypothyroidism or hyperthyroidism.
The presence of myopathy in these conditions, however, is very well known,
and this abnormality seems to be prominent in these patients.)
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