蛋白喪失性腸症を伴った回腸盲係蹄の1例

A Case of Blind Loop of the Ilenm Associated with Protein-rosing Enteropathy

はじめに

　低蛋白血症の原因として，蛋白喪失性胃腸症は重要なものの1つに挙げられているが，最近10年間に本症に関する知見の進歩は著しいものがある．蛋白喪失性胃腸症はその原因により，胃腸管自体の疾患に起因せず，全身のリンパ系異常の一部分現象とみなされる原発性蛋白喪失性胃腸症あるいは原発性腸リンパ管拡張症と，諸種原因疾患により惹起された腸管のリンパ管異常による続発性蛋白喪失性胃腸症とに大別され，後者には，静脈圧充進を招く心疾患，特に収縮性心膜炎^1)～4)や，諸種原因により起る胸管閉塞など，胃腸管部位におけるリンパの停滞，圧の充進，リンパ管の拡張などを招来する諸疾患^5)～8)がその原因となりうる．消化管部位におけるリンパのうっ滞の結果，血清蛋白が消化管内へ漏出し，血清蛋白の体外への喪失が起るが，その他に胃腸管自体の病変，たとえば炎症，潰瘍，腫瘍など実に多くの諸疾患⁸⁾⁹⁾もまた血清蛋白喪失の原因となり得ることは周知のごとくである．

　筆者らは既往疾患のため開腹手術を受け，その際実施した回腸間瘻孔設置術により盲係蹄が形成され，さらに腸管の癒着，限局性結核性腹膜炎が加わり，盲係蹄部位のリンパの停滞，リンパ管拡張を来たし，蛋白喪失性腸症を呈するに至ったが，手術により盲係蹄を切除し治癒せしめ得た1症例を経験したのでここに報告する．

　A 60-year-old female patient is presented in whom chief complaints were massive edema in the legs and mild diarrhea. On admission, the serum protein was 3.4 gm/dl. Radiological studies of the upper gastrointestinal tract gave no information but those of the small intestine disclosed loop formation and remarkable dilatation of the terminal portion of the ileum. The parenteral administration of a relatively large amount of serum albumin failed to elevate the decreased serum protein levels. From the past history, clinical course ancl radiological findings of the ileum, a diagnosis was made of blind loop associated with protein-losing enteropathy. The blind loop was resected surgically. The patient showed dramatic improvement with striking rapid elevation of serum protein levels from 4.3 gm/dl immediately prior to the operation up to 6.0gm/dl during a postoperative period op 19 days without any supplemental treatment for hypoproteinemia. The serum protein levels estimated on the 38th and 76th day after operation were 7.0 gm/dl and 7.4 gm/dl, respectively. Findings at the operation disclosecl that the blincl loop found in the ileum had been formed by the antecedent ileoileostomy done for intestinal obstruction, and later regional tuberculous peritonitis had developed there. Histological examinations revealed tuberculous changes in the regional mesentery and lymph nodes, and also markedly dilated lymph vessels in the submucosal layer of the affected ileum. The mucosal layer seemed to be almost unchanged. It is concluded that the protein-losing enteropathy observed in this case was induced by regional tuberculous peritonitis which had developed on the blind loop.