摘要
本院1992．1～1996．12儿童肝炎住院病例232例，均作出病原学诊断。G-6－PD检测用酶活性测定法，按陈顺存介绍的方法进行。≤1．2Iu／gHb为显著缺乏，1．3～3．2In／gHb为中间值，3．3～7．0IIJ／gHb为正常。232例肝炎患者，83例G－6－PD缺乏，G－6－PD缺乏率35.77％，男性缺乏率44．12％（75／170），女性缺乏率12．90％（8／62）．83例缺乏者中显缺67例，中间值16例，接受两次或两次以上检测者74例，占缺乏总数之89．16％（74／83）。本组对54例肝炎伴G－6－PD缺乏者作了家系调查，85．19％（46／54）符合伴性不显性遗传规律，结论：1．肝炎患者伴随G－6－PD缺乏率高，本组为35．77％。2．肝炎患者伴随G－6－PD缺乏绝大部分是原发性的，理由：G-6－PD缺乏病例中74例检测两次以上，占缺乏病例的89．16％（74／83），检测可靠性大，前后检查基本一致；49例在出院后6月～5年作了随诊，随诊的活性值与住院检查一致；本组89．16％（74／83）符合伴性不显性遗传规律。
The in--patients of children in 1992. 1~1996. 12 were dignosised by pathogenicity, G-6-PD was assayed with enzyme activity, with a way of Chen Shuncuno<1. 2 In/gHb was significuntly deficiency, 1. 3~3. 2 In/gHb was middle number, 3. 3~7. 0 In/gHb was normal number. The 83 patients showed G--6--PD deficiency in the 232 patients. The G--6--PD deficient rate was 35. 37%. The man deficient rate was 44. 12% (75/170), the women deficient rate was 12. 90% (8/62). The 67 patients showed significantly deficienty and the 16 patients were middle number in the 83 patients. G--6--PD was assayed twice or more than twice in the 74 patients, was in 89. 16% (74/83) of total. The 54 patients were checked by family detection. The 85. 19 % (46/54) patients were in accordance with accompany immature non dominance inheritance regularity. Conclusion was that most of viral hepatitis in G--6--PD deficiency were primary, in 98. 67 % (74/75), a few were impermanent.
出处
《中国小儿血液》
1998年第3期116-118,共3页
China Child Blood
