论文部分内容阅读
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。
Our hospital 1992.1 ~ 1996.12 232 cases of pediatric hepatitis inpatients, are made etiological diagnosis. G-6-PD test with enzyme activity assay, according to the method described by Chen Shun deposit. ≤1.2Iu / gHb is significantly lacking, 1.3 ~ 3.2In / gHb is the middle value, 3.3 ~ 7.0IIJ / gHb is normal. Of the 232 patients with hepatitis, 83 were deficient in G-6-PD. The rate of G-6-PD deficiency was 35.77%, and the rate of males was 44.12% (75/170). The rate of females was 12.90% (8/62). There were 67 cases with deficiency in 83 cases, median 16 cases, 74 cases with two or more tests, accounting for 89.16% (74/83) of the total lack. This group of 54 cases of hepatitis with G-6-PD deficiency were made in a pedigree, 85.19% (46/54) consistent with heritable inheritance, Conclusion: 1. Hepatitis patients with G-6-PD lack of high rate of 35.77% in this group. 2. The majority of hepatitis patients with G-6-PD deficiency are primary due to the fact that 74 of the G-6-PD deficient cases were detected more than twice, accounting for 89.16% (74/83) of the total lack cases, Reliability, and consistent before and after examination; 49 cases were followed up from June to 5 years after discharge, and the follow-up activity was consistent with hospitalization; 89.16% (74/83) in this group were consistent with no significant Sexual genetic law.