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I.はじめに
早朝空腹時に,朦朧状態ないしは昏睡をきたし,食事摂取または高張ブドウ糖液の静注により,ただちに覚醒する場合には,低血糖性昏睡,ことに,ランゲルハンス氏島(以下ラ氏島と略す)の機能亢進による過インシユリン症が疑われる。低血糖性昏睡をきたす原因には,種々の疾患(第2表)が考えられるが1),やはり,ラ氏島腺腫または増殖によるものが最も多く2),わが国でも,かなりの報告3)がみられる。しかし,著者らはラ氏島腺腫を疑いながらも,剖検して,膵臓には異常なく,原発性肝癌による低血糖性昏睡と考えられる1例を経験したのでその臨床および脳病理所見の概略を述べ,考察を加えたい。
The 66 year old man could not awake without a sugary diet every morning, since one month before admission to the hospital. The comatose state was improved by dietary measures or glucose administra-tion. The fasting blood sugar was found to be 20mg per 100cc (Fig.1). Laboratory findings suggested adisturbance of liver function (TABLE 1). On 62 th day after admissitn, death occurred in highly fever-ish and comatose condition.
Pathological findings:The liver weighed 2200 g and almost consisted of multiple hepatocarcinomas, while the pacreas revealed no obvious changes except an abscence the tail (Fig. 2, 3). Carcinoma cells showed a typical trabecular nature and contained abundant glycogen granules (Fig. 4).
The brain weighed 1330 grams and macroscopically presented no marked abnormality except the milky opacities of the leptomeninges. Microscopically, there were widespread degenerative changes in the neurons of the cerebral cortex, basal ganglia, cerebellum and olivary nuclei. The cerebral cortex revealed a shrin-granules kage of cell body associated nuclear pyknosis and a pseudolaminar loss of nerve cells, especially on the gyrus-valley. In the hippocampus a selectve degeneration of the end-plate occurred, so-called incrustation of Golgi-network and sclerotic shrinkage (Fig. 7). Purkinje cells, dentatous nerve cells and olivary nerve cells showed markedly a homogenising change which exhibited a disappearance of Nissl's bodies (Fig. 5, 6).
The above-mentioned pathoanatomical findings of the central nervous system, presumably due to the hepatogenic hypoglycemia, extremely resembled to the anoxic one. These changes in hypoglycemic con-dition were discussed with special reference to ano-xic changes of nervous tissue.
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