日本網内系学会会誌
Online ISSN : 1883-6801
Print ISSN : 0386-9725
ISSN-L : 0386-9725
成人T細胞白血病における消化管病変の特徴
宇都宮 與花田 修一
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ジャーナル フリー

1990 年 30 巻 5 号 p. 401-418

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We studied clinical and pathological features of gastrointestinal (GI) lesions in patients with adult T cell leukemia (ATL) by examining 84 ATL patients treated in our department from September 1977 to May 1990, and 134 ATL patients autopsied in Kagoshima prefecture from November 1976 to December 1988.
We found the following results:
1) Abnormal mucosal pattern throughout the GI tract was demonstrated by radiography using barium meal and enema in most of the patients.
2) Endoscopy demonstrated edematous and reddish mucosa in stomach and/or colon in many cases. Multiple ulcer and erosion were frequently found. Usual endoscopy failed to discriminate granular lesions in stomach and colon which were demonstrable by radiography, but spreading methylene blue on the mucosa surface enabled to discriminate the lesions.
3) In biopsied specimens, ATL cells were found to be invaded into mucosal area of stomach in 28 out of 48, and colon in 5 out of 7 patients examined.
4) In autopsied patients, infiltration of ATL cells into the GI tract was found to be evident in 59 out of 134 patients (44.0% of total). Among the 48 patients that GI lesions were examined thoroughly, 24 patients had the cell invasion in the GI tract except for esophagus. ATL cell invasions were found to be in stomach, small intestine, and colon in 13, 16, and 13 out of 48 patients, respectively. In 5 patients, simultaneous invasions into the three lesions were observed.
5) ATL cell invasion was also frequently found around lymph vessels. In small intestine, invasion into lymph follicles and resulting tumor formation was characteristic.
6) HML-1, a monoclonal antibody produced from small intestinal mucosal lymphocytes, reacted with ATL cells from peripheral blood. The reactivity was higher in the cells from the patients having cell invasion in GI tract as compared with patients without the invasion.
7) In immunohistochemical study, HML-1 reacted with invaded ATL cells in lymph nodes, skin, stomach and tonsil.
In conclusion, GI lesions were observed in most of ATL patients. Characteristic views demonstrated by radiography and endoscopy were present.
Pathologically, ATL cell invasions were evident in mucosal area and around lymph vessels. ATL cells from peripheral blood and several organs reacted with a novel monoclonal antibody HML-1.

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