Since 1931, sporadic reports have appeared noting an apparent association between
thyroid diseases such as Graves’ disease or Hashimoto’s thyroiditis and idiopathic
thrombocytopenic purpura. Various studies were performed to search for the underlying
mechanisms but still a matter of speculation.
In order to evaluate the thrombocytcpenia and autoantibcdy in Graves’ disease, 24
partients with Graves’ disease were analysed. At the same time platelet counts were
monitored in rats with T3-injections. The results were as follows:
1) Among 24 patients with Graves’ disease, only 2 have experienced easily bleeding,
especially epistaxis. But there were no thrombocytopenia or detectable anti-platelet
antibody in these 2 patients.
2) While 45.5%(10/22) of the patients were anemic, thrcmbocytopenia was noticed in
30% (6/20), and anti-platelet antibody was positive in 21.1% (4/19).
3) The frequency of thrombccytgpenia(44.4%) and positive anti.platelct antibody(44.4%)
was much higher in the patients with anemia than those (18.2%, 0.0%) in patient
without anemia (p<0.001, p<0.025).
4) The frequency of positive anti-platelet antibody was much higher in the patients
with thrombocytopenia(50.0%) than without throinbocytopenia(7.7%, p<0.05).
5) While the hemoglobin value was lower in the patients with positive anti-platelet
anti-body(10.4±0.6gm%) than that (12.5±1.2gm%) in the negative (p<0.01), the
irequency or anemia (100.0%) and thrombocytopenia (75.0%) was much higher in the
patients with positive anti-platelet antibody than those (33.3%, 20.0%) in the patient
with negative anti-platelet antibody(p<0.025, p<0.05).
6) The platelet count and serum T3 level in the experimental animals
were not significantly different between control group and T3-injected
group with & without splenectomy.
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