乙肝肝硬化并发原发性肝癌危险因素的logistic回归分析

【目的】探讨乙肝肝硬化（hepatitic cirrhosis ，HC）并发原发性肝细胞癌（Hepatocellular carcinoma ，HCC）的危险因素。【方法】选取2011年5月至2016年5月本院收治的133例 HC 并发 HCC 患者作为观察组，选取同期本院收治的 HC 未并发 HCC 患者133例作为对照组（HC 病程≥10年）。收集整理两组患者的临床资料，采用多因素 Logistic 回归分析筛选 HC并发 HCC 的危险因素。【结果】单因素分析结果显示：观察组患者在肝癌家族史（一级亲属）、饮酒史、吸烟史、酒精性脂肪肝、非酒精性脂肪肝、糖尿病史、HBeAg 阳性、HBVDNA ＞104 copies／mL 及未抗病毒治疗等方面的构成比明显高于对照组，差异具有统计学意义（ P ＜0．05）。多因素 Logistic 回归分析结果显示，HC 并发 HCC 的独立危险因素有：肝癌家族史（一级亲属）（OR ＝4．173，95％ CI 1．673～9．602，P ＝0．000）；饮酒指数3～7（OR ＝3．282，95％ CI 1．265～5．273，P ＝0．001）；饮酒指数8～16（OR ＝4．732，95％ CI 1．644～8．574，P ＝0．000）；吸烟指数8～16（OR ＝4．121，95％ CI 1．543～5．288，P ＝0．000）；酒精性脂肪肝（OR ＝4．763，95％ CI 1．442～7．219，P ＝0．000）；糖尿病史（OR ＝3．982，95％ CI 1．743～6．182，P ＝0．000）；HBeAg 阳性（OR ＝3．172，95％ CI 1．543～5．182，P ＝0．001）；HBVDNA （104～105 copies／mL ）（OR ＝5．874，95％ CI 2．382～9．104，P ＝0．000）；HBVDNA（105～106 copies／mL）（OR ＝7．473，95％ CI 2．874～12．129，P ＝0．000）；HBVDNA （106～107 copies／mL ）（OR ＝10．393，95％ CI 6．182～34．645，P ＝0．000）；HBVDNA （≥107 copies／mL）（OR ＝12．475，95％ CI 6．987～39．543，P ＝0．000）；未抗病毒治疗（OR ＝6．122，95％ CI 2．884～8．138，P ＝0．000）。【结论】HBeAg 阳性、HBVDNA ＞104 copies／mL 、未抗病毒治疗、有长期吸烟饮酒史、糖尿病史、肝癌家族史（一级亲属）的 HC 患者发生 HCC 的危险性较高。

Logistic Regression Analysis of Risk Factors of Hepatitis Cirrhosis(HC)Complicated With Hepatocellular Car-cinoma (HCC)

Objective] To investigate the risk factors of the hepatitis cirrhosis(HC)complicated with hepatocellular carci‐noma (HCC) .[Methods] One hundred and thirty‐three cases of HC complicated HCC patients admitted in our hospital were selected from May 2011 to May 2016 as the observation group ,and another 133 cases of HC non‐complicated HCC patients (HC course more than 10 years) as the control group .The clinical data of two groups were collected and sorted ;the risk fac‐tors of HC complicated with HCC were screened by multi factor Logistic regression analysis .[Results] Single factor analysis showed that the proportion of patients in the observation group was significantly higher than that in the control group in the fields of family history of liver cancer (first degree relatives) ,drinking history ,smoking history ,alcoholic fatty liver ,nonalco‐holic fatty liver ,diabetes history ,HBVDNA > 104 copies/mL and not anti viral treatment ,the difference was statistically sig‐nificant ( P < 0 .05) .The independent risk factors of HC complicated with HCC were :family history of liver cancer (first‐de‐gree relatives) (OR = 4 .173 ,95% CI 1 .673 ~ 9 .602 ,P = 0 .000) ;alcohol drinking index 3 ~ 7(OR = 3 .282 ,95% CI 1 .265 ~5 .273 ,P = 0 .001) ;alcohol drinking index 8 ~ 16(OR = 4 .732 ,95% CI 1 .644 ~ 8 .574 ,P = 0 .000) ;smoking index 8 ~ 16(OR =4 .121 ,95% CI 1 .543 ~ 5 .288 ,P = 0 .000) ;alcoholic fatty liver(OR = 4 .763 ,95% CI 1 .442 ~ 7 .219 ,P = 0 .000) ;diabetes melli‐tus(OR = 3 .982 ,95% CI 1 .743 ~ 6 .182 ,P = 0 .000) ;HBeAg positive(OR = 3 .172 ,95% CI 1 .543 ~ 5 .182 ,P = 0 .001) ;HBVD‐NA(104 ~ 105 copies/mL)(OR = 5 .874 ,95% CI 2 .382 ~ 9 .104 ,P = 0 .000) ;HBVDNA(105 ~ 106 copies/mL)(OR = 7 .473 ,95%CI 2 .874 ~ 12 .129 ,P = 0 .000) ;HBVDNA(106 ~ 107 copies/mL)(OR = 10 .393 ,95% CI 6 .182 ~ 34 .645 ,P = 0 .000) ;HBVDNA ( ≥ 107 copies/ml)(OR = 12 .475 ,95% CI 6 .987 ~ 39 .543 ,P = 0 .000) ;no anti viral treatment(OR = 6 .122 ,95% CI 2 .884 ~ 8 . 138 ,P = 0 .000) .[Conclusion]HBeAg positive ,HBVDNA > 104 copies/ml ,non‐antiviral treatment ,a long history of drink‐ing ,smoking ,diabetes history ,family history of liver cancer (first‐degree relatives) are the high risk factors of HC complicat‐ed with HCC .