僵直性脊椎炎滑膜炎之病理學研究

Pathologic Studies of Synovitis in Ankylosing Spondylitis

先前之研究，包括血清免疫球蛋白A增加、血尿及IgA之腎病變、及血中免疫複合體增加等，顯示免疫學之異常可能是導致僵直性脊椎炎發生之主因。但周圍關節炎與薦腸骨關節炎真正發生之機轉，尚未明，本實驗將以12例證實為此病患者之滑膜組織作螢光、電子顯微鏡及免疫過氧化氫酶方法檢查，以瞭解其致病機轉。實驗結實顯示，有5例其滑膜上皮細胞有中等度以上之增加。電子顯微鏡下，小血管之基底膜出現增厚，滑膜上皮細胞內吞噬有顆粒之物質。螢光檢查之10例，僅1例之滑膜有補體在血管周圍沉積。過氧化氫酶檢查，顯示滑膜組織內之漿細胞有4例含IgG，有3例含IgA。上述，僵直性脊椎炎滑膜組織電子顯微鏡及光學顯微鏡－－過氧化氫酶的檢查發現，顯示滑膜炎之發生仍可能經由免疫機轉所造成。

In order to understand whether the immunological mechanism play a role to develop the synovitis in ankylosing spondylitis (AS), we performed synovial biopsies on 12 patients and specimens sent for light microscopic, immunofluorescent microscopic, electron microscopic, and light microscopic immunoperoxidase examinations. Moderate to marked synovial hyperplasia was seen in our 5 cases and large amount of lymphocytes and plasma cells around blood vessels in 2 cases. On electron microscope, there were some microvascular changes and granular material phagocytic vacuoles of synovial lining cells. The synovial immunofluorescent study in 10 cases only demonstrated 1 had C3 deposition on vessel. However, IgG and IgA- bearing plasma cells were clearly shown in 4 and 3 of all 10 cases respectively during immunoperoxidase study. The electron microscopic and light microscopic immunopcroxidase findings on AS synovia suggest immune mechanism may be implicated as a cause of synovitis.