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Systemic Lupus Erythematosus(SLE)は多彩な臨床症状を示す白己免疫疾患である1).系統的な全身の結合組織の炎症疾患であり,当然血管病変と極めて緊密な関係にあり,さまざまな消化管病変についても,血管病変との関連において検討されていることが多い.ここではSLEの経過中に,いわゆるischemic colitisを起こし,大量の下血をきたし,右半結腸切除術を行った症例の切除漂本を病理組織学的に詳細に検討し,血管病変,なかんずく血管炎との関連について文献的な考察を加えた.
A 48 years old women with SLE complained of abdominal pain, nausea and vomiting with fever, and then developed massive rectal bleeding. She has been treated with steroid (predonisolon 20 mg daily per os) for about 16 years. As rectal bleeding failed to respond to medical treatment, she underwent emergency laparotomy, which showed massive hemorrhagic ascites. The wall of the cecum and the ascending colon was thickened by inflammation. Regional lymph nodes were also slightly swollen. So, the right side colon, involving all the affected intestine, with the terminal ileum was resected, with end-to-end anastomosis.
Macroscopically there were segmental irregular shaped shallow multiple ulcers at the cecum and the ascending colon, and the surrounding mucosa showed severe congestion. About the degree of the lesion, there seemed not so significant difference between the mucosa of the site such as antimesenteric side and the other. The mucosal layer was thickened remarkably by necrosis with hemorrhage and edema. Histologically marked fibrosis was seen in the submucosa, subserosa and almost all the outer longitudinal proper muscle layer, but the change of the circular muscle layer was slight. And Auerbach's plexus was also degenerated. Partially the muscularis mucosa was diminished by the ulceration, and hemorrhagic slough containing fibrin and cellular debris coated the ulcers. Submucosal capillaries and lymphatics were dilatated, and some vessels of the submucosa, the proper muscle layer and the subserosa showed remarkable changes such as fibrinoid degeneration of the arterioles and the small veins (one of the forms of so-called necrotizing angitis-Zeek) and the venous thrombosis with inflammatory cellular infiltration. In these changes, there were such figures similiar to those of the so-called Kußmaul-Maier type periarteritis nodosa. There also seem, however, intact vessels within them. This case suggests that ischemic colitis associated with SLE may be attributed to so-called vasculitis. The old organized venous thrombosis, though histologically it is impossible now to define whether the vasculitis had some relations with such old changes, preceded insidiously. And then active vasculitis progressed and made marked congestion and inflammation in the mucosa and submucosa, resulting in the ulceration. Fresh multiple venous thrombosis also followed and made the lesion worse. This patient has had no further gastrointestinal complaints for three years after this operation.
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