The natural history and clinical significance of intermittent viraemia in patients with initial viral suppression to < 400 copies/ml
The natural history and clinical significance of intermittent viraemia in patients with initial viral suppression to < 400 copies/ml
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DOI：
10.1097/00002030-200207260-00009
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发表时间：
2002-07-26
期刊：
影响因子：
3.8
通讯作者：
Gazzard, BG
中科院分区：
文献类型：
--
作者：
Easterbrook, PJ;Ives, N;Gazzard, BG
目的：为了确定间歇性病毒血症（IV）在接受高效抗逆转录病毒治疗（HAART）6个月内达到不可检测的病毒载量（VL）< 400拷贝/ml的患者中的患病率和预后意义。病毒载量反弹≥ 400拷贝的回顾性分析/765例患者在初始VL不可检测后随访大于或等于12个月，比较了226例（29.5%）从HAART开始后1年内维持不可检测VL的患者和122例（15.9%）有一次或多次IV发作的患者。基因型耐药性在IV大于或等于2000拷贝/ml的第一次发作时进行评估。结果：IV患者的持续病毒学反弹率高3倍[风险比（HR），3.15; 95%可信区间（CI），1.72-5.77; P < 0.001]。对于有和没有IV的患者，HAART开始后24和36个月的Kaplan-Meier估计值为19.3%（95% CI，8.9-21.5）与7.7%（95% CI，4.5-13.0）和31.6%（95% CI，21.8-44.2）与12.9%（95% CI，7.5-21.5）（P < 0.001）。在18个月和24个月时，IV组的中位CD 4细胞计数升高显著低于未IV组：138 [四分位距（IQR），58-221] vs 224 X 10（6）个细胞/l（IQR，119-357）（P = 0.0001）和200（IQR，89-294）与260 × 10（6）个细胞/l（IQR，125-384）（P = 0.003）。在16例患者的亚组中，5例（31%）逆转录酶基因和1例蛋白酶基因中发现了基因型耐药突变。一个可能的促成因素/事件被确定为大多数患者与IV，如依从性差（42.6%），并发感染（26.2%）或药物相互作用（6.8%）。结论：患者与IV > 400拷贝/毫升是三倍更有可能经历持续的病毒反弹，并有一个受损的CD 4细胞上升相对于那些谁保持不可检测的VL。这支持采取更加积极主动的强化治疗方法，并需要谨慎对待有组织的治疗中断。(C)2002年利平科特威廉姆斯威尔金斯。
Objectives: To determine the prevalence and prognostic significance of intermittent viraemia (IV) in patients who attained an undetectable viral load (VL) < 400 copies/ml within 6 months on highly active antiretroviral therapy (HAART).Methods: Retrospective analysis of viral load rebound greater than or equal to 400 copies/ml and CD4 cell counts rise for 765 patients followed for greater than or equal to 12 months following initial VL undetectability, comparing the 226 (29.5%) who maintained an undetectable VL for > 1 year from initiation of HAART and 122 (15.9%) who had one or more episodes of IV. Genotypic resistance was evaluated at the time of the first episode of IV greater than or equal to 2000 copies/ml.Results: Patients with IV had a threefold higher rate of sustained virological rebound [hazards ratio (HR), 3.15; 95% confidence interval (CI), 1.72-5.77; P < 0.001]. For patients with and without IV, the Kaplan-Meier estimates at 24 and 36 months after initiation of HAART were 19.3% (95% Cl, 8.9-21.5) versus 7.7% (95% Cl, 4.5-13.0) and 31.6% (95% Cl, 21.8-44.2) versus 12.9% (95% Cl, 7.5-21.5), respectively (P < 0.001). The median CD4 cell count rise at 18 and 24 months was significantly lower in those with IV than in those without: 138 [interquartile range (IQR), 58-221] versus 224 X 10(6) cells/l (IQR, 119-357) (P = 0.0001) and 200 (IQR, 89-294) versus 260 X 10(6) cells/l (IQR, 125-384) (P = 0.003), respectively. In a subgroup of 16 patients, genotypic resistance mutations were found in the reverse transcriptase gene for five (31%) and in the protease gene in one. A probable contributing factor/event was identified for most patients with IV, such as poor adherence (42.6%), intercurrent infection (26.2%) or drug interaction (6.8%).Conclusions: Patients with IV > 400 copies/ml are three times more likely to experience sustained viral rebound and to have an impaired CD4 cell rise relative to those who maintain undetectable VL. This supports the adoption of a more pro-active approach to treatment intensification and the need for caution with structured treatment interruptions. (C) 2002 Lippincott Williams Wilkins.