Boyages S C, Halpern J P, Maberly G F, Eastman C J, Chen J, Wang Z H, van der Gaag R D, Drexhage H A
Department of Medicine, Westmead Hospital, Sydney, Australia.
Lancet. 1989 Sep 2;2(8662):529-32. doi: 10.1016/s0140-6736(89)90654-5.
Thyroid atrophy, rather than goitre, is a characteristic feature of myxoedematous cretinism but its cause and nature are unknown. In this study, purified IgG fractions of serum from patients with myxoedematous endemic cretinism inhibited thyrotropin-induced DNA synthesis in guineapig thyroid segments in a sensitive cytochemical bioassay. IgG from patients with euthyroid neurological endemic cretinism or from normal subjects did not inhibit thyroid growth. Furthermore, in myxoedematous subjects, the presence of the thyroid-growth-blocking immunoglobulins showed a positive relation with thyroid atrophy found on ultrasound. These findings provide a pathogenic basis for the variable clinical expression of endemic cretinism.
甲状腺萎缩而非甲状腺肿是黏液水肿性呆小病的特征性表现，但其病因和本质尚不清楚。在本研究中，通过一项灵敏的细胞化学生物测定法，黏液水肿性地方性呆小病患者血清中的纯化IgG组分抑制了豚鼠甲状腺段中促甲状腺素诱导的DNA合成。甲状腺功能正常的神经型地方性呆小病患者或正常受试者的IgG并未抑制甲状腺生长。此外，在黏液水肿患者中，甲状腺生长阻滞性免疫球蛋白的存在与超声检查发现的甲状腺萎缩呈正相关。这些发现为地方性呆小病的不同临床表型提供了致病基础。
