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I.はじめに
慢性アルコール中毒患者の血清CPK異常活性をミオパチーの観点から論じた報告は過去にも見ることができる16,26,27)。しかしアルコール中毒における筋の障害は,神経系(中枢性および末梢性)の障害に比べて,臨床的にははるかに頻度の低いものであり11),いまだ数編の症例報告をみるにすぎない7,12,17,28)。他方Bengzon3),Meltzer20〜24)らによって導びかれた精神病急性期における血清CPK異常活性に関する研究により,慢性アルコール中毒でもCPK異常活性が高頻度に認められることが明らかになりつつある5,23,29)。著者らも躁病,非定型精神病,退行期精神病および精神分裂病におけると同様に,慢性アルコール中毒患者の入院時の血清CPK異常値出現頻度が66.713)〜75.9%14)に達することを指摘してきた。
本論文においては,この慢性アルコール中毒患者の血清CPK異常活性が入院前後における患者の精神症状,特に精神病状態の発現の有無と密接な相関を示すことを報告し,血清トランスアミナーゼ活性の変動とCPK値との関係や,慢性アルコール中毒患者の血清CPK異常活性の発現機序について若干の考察を試みたい。
For the purpose of studying the relationship with the apperance of psychotic state as well as with serum transaminase activity, the serum creatine phosphokinase (CPK) activity was studied at the time of admission to the mental hospital, with all cases hospitalized for chronic alcoholism from April 1975 to January 1976. The results are briefly summarized as follows;
1) Twenty-two cases (78.8%) out of 33 admitted for alcoholism showed an abnormally high level of serum CPK activity on admission.
2) In the majority of the cases with abnormal CPK activity, the CPK level was highest at the time of admission, which decreased gradually, and recovered to about normal level one to two weeks later.
3) There could be observed a significant correlation between the abnormal CPK level and the appearance of psychotic state (delirium, hallucination, amentia and transient attack of convulsion) one month before or/and after admission. Fifteen (71.4%) out of 21 patients showing the CPK level over 101 units at admission showed psychotic state after admission.
4) The change of the serum transaminase activity, especially that of GOT, had a close correlation with the change of CPK activity.
On the basis of these findings, some opinion of the authors was presented in regard to the mechanism for the onset of abnormally high CPK in the sera of chronic alcoholism.
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