本文選題：急性早幼粒細(xì)胞白血病 + 維A酸　； 參考：《吉林大學(xué)》2017年碩士論文

【摘要】：目的:研究單中心360例APL患者的臨床特征及治療效果(近期效果和遠(yuǎn)期效果),分析影響APL治療效果的預(yù)后因素。方法:回顧性分析2009年1月至2016年5月于吉林大學(xué)第一醫(yī)院腫瘤中心就診的360例初治APL患者資料,患者經(jīng)誘導(dǎo)、鞏固、維持治療,于治療后第21~28天行骨穿評價(jià)治療效果,將完成誘導(dǎo)治療的患者納入生存分析。結(jié)果:本研究納入360例患者,其中低危組59例(占16.4%)、中危組204例(占56.7%)、高危組97例(占26.9%),三組患者在血紅蛋白水平(F=0.438,P=0.153)、活化部分凝血活沒時(shí)間APTT(F=0.46,P=0.727)、凝血酶原時(shí)間PT(F=0.95,P=0.608)、纖維蛋白原FBG1.0 g/L所占比例(c2=1.27,P=0.53),無統(tǒng)計(jì)學(xué)意義;而在年齡(F=97.08,P0.001)、FBG水平(F=13.49,P=0.012)、纖維蛋白原1.5 g/L所占比例(c2=9.79,P=0.007)、PML-RARαS型(c2=12.15,P=0.02),差異有統(tǒng)計(jì)學(xué)意義。在初診的360例患者中,3例放棄治療,29例早期死亡,余328例達(dá)CR,無耐藥相關(guān)的治療失敗。早期死亡主要原因?yàn)槟X出血(65.5%),早期死亡與獲得CR的患者臨床特征相比,在初診時(shí)高白細(xì)胞計(jì)數(shù)(P=0.01)、低血小板計(jì)數(shù)(P=0.04)、高危組(P0.001)方面差異有統(tǒng)計(jì)學(xué)意義,而PML-RARα融合基因L、S型、FLT3-TID(+)差異無統(tǒng)計(jì)學(xué)意義。低、中、高三組患者的CR率分別為98.3%、95.1%、80.9%,高危組患者CR率與低、中危組相比差異具有統(tǒng)計(jì)學(xué)意義(c2=21.41,P0.001)。328例獲得CR的患者,27例未行鞏固治療,余301例患者中290例患者在我院接受了2~3個(gè)療程的鞏固治療。分子生物學(xué)完全緩解率為99.2%(264/266)。中位達(dá)分子生物學(xué)轉(zhuǎn)陰的療程數(shù)為2。低、中、高三組患者達(dá)分子生物學(xué)轉(zhuǎn)陰的療程數(shù)分別為2.3±1.9、2.1±0.8和2.2±1.0,差異無統(tǒng)計(jì)學(xué)意義(F=0.094,P=0.516)。高危組應(yīng)用中/大劑量阿糖胞苷的患者32例(47.1%),中位達(dá)分子生物學(xué)轉(zhuǎn)陰的療程數(shù)為2.2±1.1,應(yīng)用其他治療方案分子生物學(xué)轉(zhuǎn)陰的療程數(shù)為2.3±1.0,兩者差異無統(tǒng)計(jì)學(xué)意義(t=0.08,P=0.936)。中位隨訪時(shí)間33個(gè)月(3~91個(gè)月),3年的OS率和RFS率分別為95.4%和91.6%。對可能影響APL預(yù)后的因素如年齡、性別、初診白細(xì)胞計(jì)數(shù)、危險(xiǎn)分層、FLT3-ITD陽性、CD56表達(dá)、PML-RARα融合基因L型、S型等納入單因素分析。對于OS:CD56陽性表達(dá)患者的OS率明顯低于對照組(P=0.024),鞏固治療中不加維A酸組OS率明顯低于加維A酸組(P=0.013),而其他因素對OS的影響差異無統(tǒng)計(jì)學(xué)意義。對于RFS:初診白細(xì)胞數(shù)≥10×109/L的患者明顯低于初診白細(xì)胞10×109/L(P=0.017),危險(xiǎn)分層的高危組RFS率明顯低于低、中危組(P=0.035),CD56陽性表達(dá)患者的RFS率明顯低于對照組(P=0.004),鞏固治療中不加維A酸組RFS率明顯低于加維A酸組(P=0.013),達(dá)分子生物學(xué)緩解的療程數(shù)≥3的患者RFS率明顯低于1療程或2療程(P=0.035),其他因素的影響差異無統(tǒng)計(jì)學(xué)意義。將對OS與RFS預(yù)后有影響的單因素納入多因素分析,結(jié)果顯示,CD56是影響APL患者OS的獨(dú)立危險(xiǎn)因素,初診白細(xì)胞數(shù)、危險(xiǎn)分層、CD56表達(dá)是影響RFS的獨(dú)立危險(xiǎn)因素。結(jié)論:1.本研究的APL患者總體CR率為91.9%,其中低、中、高三組患者的CR率分別為98.3%、95.1%和80.9%(c2=21.41,P0.001)。分子生物學(xué)完全緩解率為99.2%(264/266)。2.患者的早期死亡率為8.1%,高危組患者早期死亡率高達(dá)19.1%,與達(dá)到CR的患者相比,差異有統(tǒng)計(jì)學(xué)意義的為初診時(shí)高白細(xì)胞計(jì)數(shù)(P=0.01)、低血小板數(shù)(P=0.04),危險(xiǎn)分層中高危組(P0.001),而PML-RARα融合基因L、S及FLT3-TID(+)無統(tǒng)計(jì)學(xué)意義。3.生存分析:共286例患者納入生存分析,3年OS率和RFS率分別為95.4%和91.6%。單因素分析:影響OS的因素為CD56表達(dá)、鞏固治療中加或不加維A酸;影響RFS的為初診白細(xì)胞數(shù)、危險(xiǎn)分層、鞏固治療中加或不加維A酸、達(dá)分子生物學(xué)緩解的療程數(shù)。多因素分析:影響OS的預(yù)后因素為CD56表達(dá),影響RFS的預(yù)后因素為初診白細(xì)胞數(shù)、危險(xiǎn)分層、CD56表達(dá)。
[Abstract]:Objective: To study the clinical features and therapeutic effect (short-term effect and long-term effect) of 360 APL patients in a single center, and to analyze the prognostic factors affecting the effect of APL. Methods: a retrospective analysis of the data of 360 cases of primary APL patients in the cancer center of No.1 Hospital of Jilin University from January 2009 to May 2016 was analyzed, and the patients were induced, consolidated and maintained. 21~28 days after treatment, the effect of bone wear evaluation was performed, and the patients completed the induction therapy were included in the survival analysis. Results: This study included 360 patients, including 59 in low risk group (16.4%), 204 in middle risk group (56.7%), 97 in high risk group (26.9%) and three in hemoglobin level (P=0.153), and activated partial coagulation time A PTT (F=0.46, P=0.727), prothrombin time PT (F=0.95, P=0.608), the proportion of fibrinogen FBG1.0 g/L (c2=1.27, P=0.53), no statistical significance, but in age (F=97.08, P0.001), fibrinogen, the proportion of fibrinogen, the difference is statistically significant. Of the 360 patients with primary diagnosis, 3 were given up treatment, 29 died early, 328 were CR, and no drug resistance related treatment failed. The main cause of early death was cerebral hemorrhage (65.5%). Early death was compared with the clinical features of CR, high white cell count (P= 0.01), low platelet count (P=0.04), and high risk group (P0.001) at first diagnosis. Statistical significance, but the PML-RAR alpha fusion gene L, S, FLT3-TID (+) difference was not statistically significant. The CR rate in the lower, middle and high three groups were 98.3%, 95.1%, 80.9% respectively. The rate of CR in the high-risk group was lower than that in the middle risk group, and the difference was statistically significant (c2=21.41, P0.001) in.328 cases received CR, 27 cases were not consolidated, and the remaining 301 patients were 290. The patients received a 2~3 course of consolidation therapy in our hospital. The total remission rate of molecular biology was 99.2% (264/266). The course number of middle molecular biology turned negative for molecular biology was 2. low. The number of treatment courses in the middle and high three groups was 2.3 + 1.9,2.1 + 0.8 and 2.2 + 1 respectively. There was no statistical difference (F=0.094, P=0.516). 32 cases (47.1%) were treated with medium / large dose cytarabine. The number of course of middle molecular biology turned negative was 2.2 + 1.1. The number of treatment courses was 2.3 + 1 with other therapies. The difference was not statistically significant (t=0.08, P=0.936). The median follow-up time was 33 months (3~91 months), and the OS rate and RFS rate of 3 years were 95.4%, respectively. The factors that might affect the prognosis of APL, such as age, sex, initial leukocyte count, risk stratification, FLT3-ITD positive, CD56 expression, PML-RAR alpha fusion gene L, S type, were included in the single factor analysis. The OS rate for OS:CD56 positive patients was significantly lower than that in the control group (P= 0.024), and the OS rate in the unmodified A acid group was significantly lower than that of the Guci in the consolidation therapy. There was no significant difference in the effect of other factors on the effect of A acid group (P=0.013) on OS. For patients with primary leukocyte number more than 10 * 109/L, 10 x 109/L (P=0.017) was significantly lower than that of first diagnosed leukocyte. The RFS rate in high-risk group was significantly lower than that in low risk group (P=0.035). The RFS rate of the positive expression of CD56 was significantly lower than that of the control group (P=0.004). In the treatment, the rate of RFS in the A group was significantly lower than that of the vitamin A group (P=0.013). The RFS rate of the patients with the molecular biological remission of more than 3 was significantly lower than that of the 1 course or 2 course of treatment (P=0.035). There was no significant difference in the influence of other factors. The single factor affecting the prognosis of OS and RFS was included in the multivariate analysis. The results showed that CD56 was the influence of APL. The independent risk factors of patients with OS, primary leukocyte count, risk stratification and CD56 expression are independent risk factors for RFS. Conclusion: the overall CR rate of APL patients in 1. studies was 91.9%, of which the rate of CR was 98.3%, 95.1% and 80.9% (c2=21.41, P0.001) in the lower, middle and high three groups respectively. The total remission rate of the molecular biology was 99.2% (264/266).2. patients. Early mortality was 8.1%, and early mortality in high-risk groups was 19.1%. Compared with CR patients, there were significant differences in high white cell count (P=0.01), low platelet count (P=0.04), high-risk group (P0.001), PML-RAR alpha fusion gene L, S and FLT3-TID (+) without statistically significant.3. survival analysis: a total of 286 cases. The patients were included in the survival analysis. The 3 year OS rate and the RFS rate were respectively 95.4% and 91.6%. single factor analysis. The factors affecting OS were CD56 expression, plus or without adding vitamin A acid; the number of primary leukocytes, the risk stratification, the consolidation of the treatment and the number of treatment courses in the treatment of molecular biological remission. The later factor was CD56 expression, and the prognostic factors of RFS were the number of newly diagnosed white blood cells, risk stratification and CD56 expression.

【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R733.71

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