Hodak E, Shamai-Lubovitz O, David M, Hazaz B, Lahav M, Sandbank M
Department of Dermatology, Beilinson Medical Center, Petah Tiqva, Israel.
J Am Acad Dermatol. 1991 Aug;25(2 Pt 2):415-8. doi: 10.1016/0190-9622(91)70218-q.
Although the underlying pathologic mechanisms of primary anetoderma have not yet been identified, data suggest the participation of an immunologic mechanism in some cases. In a woman with clinical and histopathologic features of primary anetoderma (Jadassohn-Pellizzari type) of 30 years' duration, laboratory investigation disclosed positive antinuclear factor, hypocomplementemia, hypergammaglobulinemia, granular deposits of immunoreactants along the dermoepidermal junction, and fibrillar deposits in the papillary dermis. In addition, she was found to have autoimmune hemolysis and circulating lupus anticoagulant associated with recurrent deep-vein thrombosis and a history of Graves' disease (starting 5 years after onset of primary anetoderma). To our knowledge, none of the latter three autoimmune conditions has been previously associated with primary anetoderma.
虽然原发性皮肤松弛症的潜在病理机制尚未明确,但数据表明在某些情况下存在免疫机制参与。一名患有持续30年的原发性皮肤松弛症(雅达松-佩利扎里型)临床和组织病理学特征的女性,实验室检查发现抗核因子阳性、补体低下、高球蛋白血症、免疫反应物在真皮表皮交界处呈颗粒状沉积,以及在乳头真皮中有纤维状沉积。此外,她还患有自身免疫性溶血和循环狼疮抗凝物,伴有复发性深静脉血栓形成,并有格雷夫斯病病史(在原发性皮肤松弛症发病5年后开始)。据我们所知,后三种自身免疫性疾病此前均未与原发性皮肤松弛症相关联。