いわゆるZollinger-Ellison症候群typeⅠ様の経過をたどった十二指腸潰瘍の1例

A Case of Duodenal Ulcer with a Course Resembling Type Ⅰ of the So-called Zollinger-Ellison Syndrome

　Zollinger-Ellison症候群（以下ZE症候群）とは難治性消化性潰瘍，胃液，酸過分泌ならびにgastrin secreting（non-insulin）islet cell tumourを有する疾病に与えられた症候群である．しかし臨床上ZE症候群を呈しながら腫瘍が膵や十二指腸に認められない場合があり，このような症例ではそのZE症候群の診断が確実であるならば胃全摘後，空腹時血中ガストリン・レベルそして酸分泌はすみやかに低下し正常値に復帰するといわれ，その本態は免疫螢光法にて証明される胃前庭部G細胞の増殖であろうとされている．これはPolakらが1972年に非常に興味深いケースとして報告したいわゆるZE症候群typeⅠであるが，このtypeⅠと思われる症例を最近経験したのでここに報告する．

症例

　患　者：○沢○一　男性　38歳　自由業

　主　訴：心窩部痛

　家族歴：特記すべきものはない．

　既往歴・現病歴：昭和42年9月，主訴，家族のすすめがあったが放置，自覚症は自然に消褪す．43年5月，主訴，体重減少，軟便，近医受診により十二指腸潰瘍の診断を受け治療にて症状寛解しそのまま再び放置す．45年4月，主訴，十二指腸潰瘍増悪を指摘され入院加療，当時膵外分泌能亢進，特に水，HCO^-₃conc．で著明であった．軽快一時退院．47年10月，再人院，この時はじめてImmunoassayにて異常なる高ガストリン血を証明した．胃液，酸過分泌，特に夜間基礎胃液分泌，BAO/MAO比からZE症候群を一応考慮した．膵シンチではspace occupying lesionsは不明，試験開腹をすすめるも嫌忌され軽快退院す．48年11月，突然激痛発作ありて来院，十二指腸潰瘍穿孔による急性腹膜炎の疑いにて入院，緊急手術す．

　A 38-year old man had been suffering from intractable duodenal ulcer since several years before. At first treated simply as benign ulcer, the disease attracted our attention because of hypersecretion in exocrine pancreatic function.

　After hospitalization he grew better and soon he left the hospital for private reasons. On the second admission various examinations led us to suspect Zollinger-Ellison syndrome. The ratio of BAO: MAO was 0.65; overnight gastric secretion: 1700 ml; HCl 110 mEq/1; and fasting serum gastrin levels: 1800～2300 pg/ml. However, scintigram of the pancreas did not reveal any definite space occupying lesion.

　The patient doggedly refused to undergo surgical intervention and again he was at home for a time being. One day he had sudden onset of hematemesis and was hospitalized for the third time. Surgical operation revealed acute peritonitis caused by perforation of an ulcer in the duodenal bulb. No gastrin secreting tumor was demonstrated in the pancreas or duodenum. It was remarkable that after 7 days since total gastrectomy fasting serum gastrin returned to normal level, a fact compatible with the report of Cowley et al. The nature of such a case as this was reportedly ascribed to hyperplasia of antral G cells, but unfortunately we could not confirm it.

　As far as we have been able to find out, no such a case has ever been reported in Japan. We have added some comments on it, comparing it with a typical case of Zollinger-Ellison syndrome reported by us 5 years ago.