皮肤病与性病
皮膚病與性病
피부병여성병
JOURNAL OF DERMATOLOGY AND VENEROLOGY
2014年
3期
137-139
,共3页
李重熙%白劲松%刘俊%田波%杨吟%黄瑛
李重熙%白勁鬆%劉俊%田波%楊吟%黃瑛
리중희%백경송%류준%전파%양음%황영
艾滋病%HAART疗法%基因型耐药突变
艾滋病%HAART療法%基因型耐藥突變
애자병%HAART요법%기인형내약돌변
AIDS%HAART%Genotype drug-resistance mutation
目的:分析昆明地区抗病毒治疗失败艾滋病患者的耐药突变特征及相关影响因素。方法对2012年间在我院进行艾滋病抗病毒治疗满半年以上,病毒量检测大于1000拷贝/ml并成功扩增样本的63例患者,进行血清的基因型耐药检测,对所得到的HIV-1耐药基因突变情况与患者的性别、感染途径、治疗前CD+4 T淋区细胞的计数,抗病毒治疗时间等因素,进行统计学分析。结果其检测出耐药突变33例,占52.3%(33/63)。其中32例对核苷类及非核苷类药物耐药(50%),1例对蛋白抑制剂耐药(1.5%),7例对所有核苷类及非核苷类逆转录酶抑制剂耐药,1例对所有核苷类,非核苷类逆转录酶抑制剂及蛋白酶抑制剂耐药,6例出现对蛋白酶抑制剂的其他耐药突变。治疗前CD4+T淋巴细胞计数<200个/μl患者的耐药发生率大于CD4+T淋巴细胞计数>200个/μl的患者,其差异有统计学意义(P=0.000)。治疗时间<12个月的患者耐药发生率低于治疗>12月的患者,其差异有统计学意义(P=0.01)。结论昆明地区抗病毒治疗后产生耐药的艾滋病患者中有20%同时出现对核苷类及非核苷类逆转录酶抑制剂的耐药,这部分患者将面临三线药物的使用问题,应该考虑启用三线药物。早治疗和治疗后的耐药监测是治疗成功的关键。
目的:分析昆明地區抗病毒治療失敗艾滋病患者的耐藥突變特徵及相關影響因素。方法對2012年間在我院進行艾滋病抗病毒治療滿半年以上,病毒量檢測大于1000拷貝/ml併成功擴增樣本的63例患者,進行血清的基因型耐藥檢測,對所得到的HIV-1耐藥基因突變情況與患者的性彆、感染途徑、治療前CD+4 T淋區細胞的計數,抗病毒治療時間等因素,進行統計學分析。結果其檢測齣耐藥突變33例,佔52.3%(33/63)。其中32例對覈苷類及非覈苷類藥物耐藥(50%),1例對蛋白抑製劑耐藥(1.5%),7例對所有覈苷類及非覈苷類逆轉錄酶抑製劑耐藥,1例對所有覈苷類,非覈苷類逆轉錄酶抑製劑及蛋白酶抑製劑耐藥,6例齣現對蛋白酶抑製劑的其他耐藥突變。治療前CD4+T淋巴細胞計數<200箇/μl患者的耐藥髮生率大于CD4+T淋巴細胞計數>200箇/μl的患者,其差異有統計學意義(P=0.000)。治療時間<12箇月的患者耐藥髮生率低于治療>12月的患者,其差異有統計學意義(P=0.01)。結論昆明地區抗病毒治療後產生耐藥的艾滋病患者中有20%同時齣現對覈苷類及非覈苷類逆轉錄酶抑製劑的耐藥,這部分患者將麵臨三線藥物的使用問題,應該攷慮啟用三線藥物。早治療和治療後的耐藥鑑測是治療成功的關鍵。
목적:분석곤명지구항병독치료실패애자병환자적내약돌변특정급상관영향인소。방법대2012년간재아원진행애자병항병독치료만반년이상,병독량검측대우1000고패/ml병성공확증양본적63례환자,진행혈청적기인형내약검측,대소득도적HIV-1내약기인돌변정황여환자적성별、감염도경、치료전CD+4 T림구세포적계수,항병독치료시간등인소,진행통계학분석。결과기검측출내약돌변33례,점52.3%(33/63)。기중32례대핵감류급비핵감류약물내약(50%),1례대단백억제제내약(1.5%),7례대소유핵감류급비핵감류역전록매억제제내약,1례대소유핵감류,비핵감류역전록매억제제급단백매억제제내약,6례출현대단백매억제제적기타내약돌변。치료전CD4+T림파세포계수<200개/μl환자적내약발생솔대우CD4+T림파세포계수>200개/μl적환자,기차이유통계학의의(P=0.000)。치료시간<12개월적환자내약발생솔저우치료>12월적환자,기차이유통계학의의(P=0.01)。결론곤명지구항병독치료후산생내약적애자병환자중유20%동시출현대핵감류급비핵감류역전록매억제제적내약,저부분환자장면림삼선약물적사용문제,응해고필계용삼선약물。조치료화치료후적내약감측시치료성공적관건。
objective To analyze the characteristics and related impact factors of mutative drug-resistance among HIV/AIDS received ineffective HAART in Kunming. Methods 63 cases of HIV/AIDS patients with viral load over 1000copy/ml who received HAART more than 6 months were accepted in the experiment. The drug-resistance genes were tested in blood sample. Then the mutative HIV-1 drug-resistance genes, together with patients' gender, route of being infected, CD4+ cell counts before treatment and duration of treatment, were statistically analyzed. Results 33 cases were found drug-resistance mutation in serum, which account for 52. 3% (33/63). 32 cases (account for 50%) are resistant to NRTIs or NNRTIs, 1 case (account for 1. 5%) was resistant to PI, 7 patients were resistant to both NRTI and NNRTI, only 1 patient was resistant to all of the NRTI, NNRTI and PI, 6 patients were found to have other resistant mutations for PI group. The drug-resistance rate of patients with CD4 less than 200 copy/ul before HAART treatment was higher than that of patients with CD4 more than 200 copy/ul (PA=0. 000). The drug-resist-ance rate of patients with HAART duration less than 12 months was lower than that of patient with RT duration more than 12 months ( P=0 . 01 ) . Conclusion 20% of HIV/AIDS patients in Kunming are resisitant to both NRTI or NNRTI after HAART. They should be considered to be applied with antiviral therapy of the third level. Early HAART and drug-resistantce surveillance after treatment are the key points to ensure effective treatment.