Vergès B, Giroud-Baleydier F, Olsson O, Vaillant G, Brun J M, Putelat R
Service de médecine II, CHU Dijon.
Rev Med Interne. 1989 Nov-Dec;10(6):565-9. doi: 10.1016/s0248-8663(89)80079-7.
The association between Graves' disease and autoimmune thrombocytopenic purpura is rare and yet more frequent than would be expected from a mere coincidence. The existence of an immunological disorder common to Graves' disease and autoimmune thrombocytopenic purpura and/or a direct responsibility of hyperthyroidism in the genesis of immunological disturbances resulting in autoimmune thrombocytopenic purpura are hypotheses put forward to try and explain why these two pathologies are associated. We report two cases in which the antiplatelet autoimmunity developed independently of the thyroid functional disorder, making it unlikely that hyperthyroidism played a direct role in the occurrence of the immunological disorders responsible for the autoimmune thrombocytopenic purpura. The physiopathology responsible for the Graves' disease-autoimmune thrombocytopenic purpura association remains imperfectly known. The existence of an immunological pathogenetic mechanism underlying both diseases seems to be likely; it probably acts through an antigenic determinant that is common to thyroid cells and platelets.
格雷夫斯病与自身免疫性血小板减少性紫癜之间的关联较为罕见,但比单纯巧合的预期更为常见。格雷夫斯病和自身免疫性血小板减少性紫癜存在共同的免疫紊乱,和/或甲状腺功能亢进在导致自身免疫性血小板减少性紫癜的免疫紊乱发生过程中直接起作用,这些都是为解释这两种病理状况为何相关而提出的假说。我们报告了两例抗血小板自身免疫独立于甲状腺功能障碍而发展的病例,这使得甲状腺功能亢进在导致自身免疫性血小板减少性紫癜的免疫紊乱发生中直接起作用的可能性不大。格雷夫斯病与自身免疫性血小板减少性紫癜关联的病理生理学仍不完全清楚。两种疾病背后存在免疫致病机制似乎是有可能的;它可能通过甲状腺细胞和血小板共有的抗原决定簇起作用。