Mori A, Hashino S, Kobayashi S, Tanaka J, Yamamoto Y, Asaka M, Imamura M
The Third Department of Internal Medicine, Hokkaido University, School of Medicine, Sapporo, Japan.
Ann Hematol. 2001 Apr;80(4):238-42. doi: 10.1007/s002770000253.
We previously reported a case of bone marrow infarction attributable to acute graft-versus-host disease (GVHD) in a patient with acute lymphoblastic leukemia after unrelated bone marrow transplantation (BMT). Although the bone marrow infarction-induced arthralgia in this patient improved, severe arthralgia appeared again with exacerbation of chronic GVHD, and the arthralgia was strongly correlated with the clinical course of chronic GVHD, i.e., the course of symptoms such as dermal and hepatic GVHD and ocular dryness. Finally, the patient developed avascular necrosis (AVN) in the right femoral head. Serum interleukin (IL)-6 and IL-10 levels were high at the onset of arthralgia but low during remission, and levels of interferon-gamma were undetectable throughout the period of arthralgia. Based on the clinical course and these data, chronic GVHD was thought to have been the major cause of the AVN. Since IL-10 antagonizes various other cytokines that induce GVHD, the increase in IL-10 might have inhibited the development of GVHD.
我们之前报道过1例急性淋巴细胞白血病患者在接受非亲缘骨髓移植(BMT)后发生急性移植物抗宿主病(GVHD)导致骨髓梗死的病例。尽管该患者由骨髓梗死引起的关节痛有所改善,但随着慢性GVHD的加重,严重关节痛再次出现,且该关节痛与慢性GVHD的临床病程密切相关,即与皮肤和肝脏GVHD以及眼干等症状的病程相关。最终,该患者右侧股骨头发生无血管性坏死(AVN)。关节痛发作时血清白细胞介素(IL)-6和IL-10水平较高,但缓解期较低,在整个关节痛期间均未检测到干扰素-γ水平。根据临床病程和这些数据,慢性GVHD被认为是AVN的主要原因。由于IL-10可拮抗其他多种诱导GVHD的细胞因子,IL-10的增加可能抑制了GVHD的发展。