中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2008年
5期
561-565
,共5页
方宁%章涛%万卫红%胡锡阶%祁莹%张信江%陈代雄
方寧%章濤%萬衛紅%鬍錫階%祁瑩%張信江%陳代雄
방저%장도%만위홍%호석계%기형%장신강%진대웅
煤%砷中毒%淋巴细胞亚群%免疫,细胞%癌变
煤%砷中毒%淋巴細胞亞群%免疫,細胞%癌變
매%신중독%림파세포아군%면역,세포%암변
Coal%Aarsenic poisoning%Lymphocyte subsets%Cellular immunity%Tumor
目的 探讨燃煤型砷中毒患者免疫功能改变及其规律,为肿瘤风险评估提供依据.方法 70例患者均系贵州省黔西南州燃煤型砷中毒高发区既往经临床及实验室确诊的燃煤型砷中毒病例,其中男性44例,女性26例,年龄24～71岁,平均年龄41岁.按病程及是否癌变分为4组:<10年组,23例;10～19年组,21例;≥20年组,20例;癌变组(病程≥20年),6例.对照组为健康职工和大学生自愿者,26例.采静脉血,流式细胞仪分析各组人群外周血淋巴细胞亚群CD3+(总T细胞)、CD3+D4+(诱导性/辅助性T细胞)、CD3+CD8+(抑制性/细胞毒性T细胞)、CD19+(B淋巴细胞)和CD56+CD16+(自然杀伤细胞,NK)细胞组成比例.并对淋巴细胞膜人类白细胞组织相容性抗原-DR(HLA-DR)、细胞表面抗原(CD)25和CD38分子表达率进行检测.结果 <10年组、10～19年组、≥20年组和癌变组人群外周血CD3+细胞百分率分别为(63.76±9.32)%、(55.63±12.97)%、(51.00 ±12.23)%、(49.83 ±9.89)%,均低于对照组[(68.10±8.62)%],组间比较差异有统计学意义(F=12.862,P<0.05).CD3+CD4+细胞比例上述各组分别为(31.35±6.62)%、(28.38±8.66)%、(24.13±6.46)%、(19.17±4.96)%,明显低于对照组[(34.28±7.32)%],组间比较差异有统计学意义(F=10.455.P<0.05).≥20年组和癌变组CD19+细胞百分率[(9.00±5.32)%、(9.00±3.29)%]低于对照组和<10年组[(11.80±3.43)%、(12.35 ±4.53)%],组间比较差异有统计学意义(P<0.05);其余各组之间两两比较差异均无统计学意义(P>0.05).癌变组淋巴细胞CD25和CD38表达率[(17.96±4.98)%、(41.38±8.54)%]明显高于对照组[(13.10±3.38)%、(28.60±5.51)%].组间两两比较差异有统计学意义(P<0.05);HLA-DR表达率在10～19年组[(18.20±6.25)%]明显高于对照组[(10.72±7.06)%]和<10年组[(11.78±5.13)%],≥20年组[(20.30±8.01)%]与癌变组[(21.82±10.97)%]在同一水平.结论 砷所致机体细胞免疫功能削弱可能是燃煤型砷中毒患者皮肤癌变的重要机制,细胞免疫功能状态可作为燃煤砷中毒患者皮肤癌变的预警信号.
目的 探討燃煤型砷中毒患者免疫功能改變及其規律,為腫瘤風險評估提供依據.方法 70例患者均繫貴州省黔西南州燃煤型砷中毒高髮區既往經臨床及實驗室確診的燃煤型砷中毒病例,其中男性44例,女性26例,年齡24～71歲,平均年齡41歲.按病程及是否癌變分為4組:<10年組,23例;10～19年組,21例;≥20年組,20例;癌變組(病程≥20年),6例.對照組為健康職工和大學生自願者,26例.採靜脈血,流式細胞儀分析各組人群外週血淋巴細胞亞群CD3+(總T細胞)、CD3+D4+(誘導性/輔助性T細胞)、CD3+CD8+(抑製性/細胞毒性T細胞)、CD19+(B淋巴細胞)和CD56+CD16+(自然殺傷細胞,NK)細胞組成比例.併對淋巴細胞膜人類白細胞組織相容性抗原-DR(HLA-DR)、細胞錶麵抗原(CD)25和CD38分子錶達率進行檢測.結果 <10年組、10～19年組、≥20年組和癌變組人群外週血CD3+細胞百分率分彆為(63.76±9.32)%、(55.63±12.97)%、(51.00 ±12.23)%、(49.83 ±9.89)%,均低于對照組[(68.10±8.62)%],組間比較差異有統計學意義(F=12.862,P<0.05).CD3+CD4+細胞比例上述各組分彆為(31.35±6.62)%、(28.38±8.66)%、(24.13±6.46)%、(19.17±4.96)%,明顯低于對照組[(34.28±7.32)%],組間比較差異有統計學意義(F=10.455.P<0.05).≥20年組和癌變組CD19+細胞百分率[(9.00±5.32)%、(9.00±3.29)%]低于對照組和<10年組[(11.80±3.43)%、(12.35 ±4.53)%],組間比較差異有統計學意義(P<0.05);其餘各組之間兩兩比較差異均無統計學意義(P>0.05).癌變組淋巴細胞CD25和CD38錶達率[(17.96±4.98)%、(41.38±8.54)%]明顯高于對照組[(13.10±3.38)%、(28.60±5.51)%].組間兩兩比較差異有統計學意義(P<0.05);HLA-DR錶達率在10～19年組[(18.20±6.25)%]明顯高于對照組[(10.72±7.06)%]和<10年組[(11.78±5.13)%],≥20年組[(20.30±8.01)%]與癌變組[(21.82±10.97)%]在同一水平.結論 砷所緻機體細胞免疫功能削弱可能是燃煤型砷中毒患者皮膚癌變的重要機製,細胞免疫功能狀態可作為燃煤砷中毒患者皮膚癌變的預警信號.
목적 탐토연매형신중독환자면역공능개변급기규률,위종류풍험평고제공의거.방법 70례환자균계귀주성검서남주연매형신중독고발구기왕경림상급실험실학진적연매형신중독병례,기중남성44례,녀성26례,년령24～71세,평균년령41세.안병정급시부암변분위4조:<10년조,23례;10～19년조,21례;≥20년조,20례;암변조(병정≥20년),6례.대조조위건강직공화대학생자원자,26례.채정맥혈,류식세포의분석각조인군외주혈림파세포아군CD3+(총T세포)、CD3+D4+(유도성/보조성T세포)、CD3+CD8+(억제성/세포독성T세포)、CD19+(B림파세포)화CD56+CD16+(자연살상세포,NK)세포조성비례.병대림파세포막인류백세포조직상용성항원-DR(HLA-DR)、세포표면항원(CD)25화CD38분자표체솔진행검측.결과 <10년조、10～19년조、≥20년조화암변조인군외주혈CD3+세포백분솔분별위(63.76±9.32)%、(55.63±12.97)%、(51.00 ±12.23)%、(49.83 ±9.89)%,균저우대조조[(68.10±8.62)%],조간비교차이유통계학의의(F=12.862,P<0.05).CD3+CD4+세포비례상술각조분별위(31.35±6.62)%、(28.38±8.66)%、(24.13±6.46)%、(19.17±4.96)%,명현저우대조조[(34.28±7.32)%],조간비교차이유통계학의의(F=10.455.P<0.05).≥20년조화암변조CD19+세포백분솔[(9.00±5.32)%、(9.00±3.29)%]저우대조조화<10년조[(11.80±3.43)%、(12.35 ±4.53)%],조간비교차이유통계학의의(P<0.05);기여각조지간량량비교차이균무통계학의의(P>0.05).암변조림파세포CD25화CD38표체솔[(17.96±4.98)%、(41.38±8.54)%]명현고우대조조[(13.10±3.38)%、(28.60±5.51)%].조간량량비교차이유통계학의의(P<0.05);HLA-DR표체솔재10～19년조[(18.20±6.25)%]명현고우대조조[(10.72±7.06)%]화<10년조[(11.78±5.13)%],≥20년조[(20.30±8.01)%]여암변조[(21.82±10.97)%]재동일수평.결론 신소치궤체세포면역공능삭약가능시연매형신중독환자피부암변적중요궤제,세포면역공능상태가작위연매신중독환자피부암변적예경신호.
Objective To study the change and rule of immunological function among the patients with coal arsenic poisoning in order to provide a basis for tumor risk evaluation and monitoring.Methods Seventy patients with coal arsenic poisoning aged from 24 to 71 years old(44 men,26 women,averaging 41 years old)were divided into 4 groups including 23 cases having a course less than 10 years,21 case8 lasting for 10～19 years,20 cages for more than 20 years,6 cases of cancer,and 26 healthy normal controls.Flow cytometer(FCM)was used to analyze the frequency of CD3+(total T cell),CD3+CD4+(inducer/helper T cell),CD3+CD8+(suppressor/cytotoxic T cell),CD19+(B lymphocyte),and CD56+CD16+(natural killer cell)lymphocyte subsets in the peripheral blood of the subjects and the expression rates of lymphocytic membrane surface molecules of human leucocvte antigen (HLA)-DR,CD25,CD38 were also determined by FCM.Results The pmportions of CD3+cells in periDheral blood of less than 10 years,10～19 years,more than 20 years and cancer groups were (63.76±9.32)%。(55.63± 12.97)%,(51.00±12.23)%and(49.83±,9.89)%respectively,which were significantly lower than that in control group[(68.10±8.62)%],and there was a significant difference between different groups(F=12.862,P<0.05). In less than 10 years,10～19 years,more than 20 years and cancer groups,the proportion of CD3+CD4+cells cells was (31.35±6.62)%,(28.38±8,66)%,(24.13±6.46)%and(19.17±4.96)%respectively,which wag significantly lowerthan that in control group[(34.28±7.32)%],and significant in a-group difference was found(F=10.455, P<0.05).The percentages of CD19+cells in more than 20 yeats and cancer groups[(9.00±5.32)%,(9.00± 3.29)%]were lower than that in control group and less than 10 years group[(11.80±3.43)%,(12.35±4.53)%] (P<0.05),while no statistical difference was found between other groups.The expression rates of CD25 and CD38 in lymphocytes of cancer group[(17.96 ±4.98)%,(41.38±8.54)%]were obviously higher than those in control group[(13.10±338)%,(28.60±5.51)%]and there were statistical differences between the experimental groups(P<0.05).The expression rate of HLA-DR in 10～19 years groups[(18.20±6.25)%]was significantly higher than that in control group[(10.72±7.06)%]and less than 10 years group[(11.78±5.13)%],while it was the same in more than 20 years and cancer group[(20.30±8.01)%,(21.82±10.97)%].Conclusions Reduction of cellular immune function caused by coal arsenic poisoning may be an important mechanism of skin cancer.CelMar immune function may be used as a warning signal of skin cancerization of patients with coal arsenic poisoning.
