在感染艾滋病毒的个体的测量弱者。体弱患者的识别是第一步改良与弱者拨回
Summary
Frailty syndrome is commonly seen in the aged and reflects multi-system physiological change. However, with reduced functional reserve and resilience frailty is also known to be common in the HIV infected population. This study outlined an easily administered screening test to identify HIV patients with frailty. When significant components of frailty are identified, clinicians will be able to focus on amelioration of the problem and promote reversion to the pre-frail state.
Abstract
一个简单的，经过验证的协议组成的电池测试可用于识别老年患者虚弱综合征。增加储备下降和抗应激综合征的发病率随着年龄的增加。在老年人中，脆弱性可能采取分步进行的非体弱，体弱，体弱丧失功能。我们研究的脆弱在感染艾滋病毒的患者，并发现，约20％是年老体弱的使用油炸型，采用严格的标准开发的老人1,2。在艾滋病毒感染综合征的发生有年轻化。
艾滋病患者进行了检查1）无意减肥; 2）步行速度缓慢; 3）的弱点，作为衡量一个握力计; 4）用尽的抑郁量表的反应;和5）低体力活动，通过评估决定千卡的热量消耗在一个星期的时间。预脆弱存在任何两个五标准，脆弱性是存在的，如果任意三个五个标准为异常。
测试大约需要10-15分钟才能完成，他们可以在例行就诊的医疗助理。测试结果得分参照标准表。了解这五个组件有助于在个别病人的脆弱可以使医师能够解决相关的问题，其中有许多是不体现在日常HIV就诊。
Introduction
该中心疾病控制项目，一半以上的HIV-1感染在美国的个人将超过50岁，到2015年。 HIV-1感染的病人的预期寿命增加导致意外增加与老化相关的疾病，发病率和死亡率的风险增加的艾滋病毒呈阳性的长辈。一个重要的例子就是新近被描述的虚弱综合征，这可能会加速老化HIV-1感染的成人中发挥了重要作用。3-7
弱者已定义的中老年作为生物的储备下降和抗应激综合征，导致生理系统累计跌幅往往进展分步进行的功能随着时间的推移下降。脆弱的临床重要性综合征被认为是一个高风险的状态，预测功能和流动性下降等不良健康结果，hospitalizat离子和死亡。在过去的10年中，许多研究试图评估在不同人群中的脆弱。炒等研究脆弱在男性和女性年龄超过65岁参加在心血管研究它们的定义脆弱女性衰老的研究中得到了验证。9修改它们的定义已被用于在其他研究中，包括HIV-1感染的个体。4-7炸等描述残疾或疾病的情况下，即使是在表明，老年人口的7％，比65岁体弱多病体弱的表型，而年纪比20-26％ 80岁体弱。2弱者可以是一个主要发现，也有辅助诊断为急性事件或合并症，如恶性肿瘤，动脉粥样硬化，感染（HIV），或抑郁症的结果。此外，其他因素可能在艾滋病患者脆弱，例如，静脉吸毒，贫困和精神疾病。
弱者已发现的HIV-1感染的病人更小的年龄比非HIV感染患者4旧版HIV-1感染的个体经常出现更严重的HIV疾病并有较短的存活时间比年轻的人，往往因为他们都不能确诊直到很晚才在疾病过程中。11另一个原因可能是，老年患者有更多的共同病态与HIV-1相互作用的疾病。旧的HIV-1感染的个体被描述为虚弱比年龄匹配控制个人无HIV-1感染。
脆弱的HIV-1感染患者的临床测量非常重要，因为可能是可逆的脆弱性在其早期阶段（ 如干预扭转失调，蛋白质能量营养不良，抑郁症，维生素D缺乏和其他脆弱性相关的条件）储备耗尽之前达到一个临界阈值导致不可逆转的脆弱性和功能下降。
Protocol
Representative Results
Discussion
Previous studies of HIV and frailty: Two retrospective studies by Desquilbet et al. assessed frailty in a cohort of men who have sex with men from the Multicenter AIDS Cohort Studies (MACS). Both studies used a shortened definition of frailty containing fewer criteria than did our study. The first study compared frailty in HIV-1 infected men in the pre-treatment era to a control group of HIV uninfected men.4 There were similar rates of frailty in HIV+ men older than 55 years and HIV- men older than 65 years; frailty was found to occur earlier in HIV-1 infected men. Our study had similar findings of an earlier occurrence of frailty phenotype, but we obtained higher rates of frailty compared with MACS, possibly because our use of the full Fried frailty criteria versus surrogate administrative data, but also because of the different population of patients in our study.
Another study by Desquilbet et al. evaluated CD4 cell count and HIV viral load as predictors of frailty in HIV+ men and found that lower CD4 cell counts and viral loads of more than 50,000 copies of RNA were significantly associated with frailty.5 Also the prevalence of frailty declined in the era of ART. Despite differences in measuring frailty and in population characteristics our study concluded like Desquilbet et al. that a low CD4 cell count is significantly associated with frailty and that patients on long-term ART have less likelihood of developing frailty.1 Premature occurrence of prevalence of frailty, shorter duration of ART, more co-morbidities and lower CD4 count were associated with frailty in both studies, but we did not find a strong association between psychiatric diagnosis and frailty. We found a positive relationship between length of ART and not being frail (Figure 1).
Our findings of frailty in HIV patients: Our initial hypothesis that age was not significantly important when measuring frailty of patients with low CD4 cell counts was confirmed. Frailty is likely more causally related to the inflammatory state and profound immunosuppression found in many patients with low CD4 cell counts. Many of these patients had a history of recently treated opportunistic infections. Because of these observations we propose that an active diagnosis of AIDS (CD4 cell count <200 cells/μl) is a significant co-morbidity itself and significantly predisposes patients to being frail. All of our frail patients had at least one co-morbidity besides HIV itself. Our frail patients <50 years had significantly fewer co-morbidities than the frail population >50 years, though in comparison, the younger people had a lower CD4 cell count.
Our other hypothesis was that frailty may be temporary in younger patients with low CD4 cell counts and may revert when CD4 cell counts improve. We were limited by the low number of patients and this hypothesis could not be proven, but it was a likelyexplanation for the small number of patients in which reversal was demonstrated (Table 1). Longer antiretroviral treatment was found to be protective for frailty (Figure 1). This fact on its own would support the recommendations of starting ART at higher CD4 counts and continuing ART without any treatment breaks. We believe that the main reason by which length of ART treatment was shown to be protective for frailty is that patients on long term treatment are more likely to have better control of co-morbidities as well as HIV and less likely to be frail.
In conclusion we have observed an association between low CD4-cell counts and frailty, which is not affected by age, viral load or the presence of co-morbidities. Effective treatment with ART plays a protective role against frailty, reinforcing the importance of effective ART. Early implementation of ART in the care of HIV patients may protect against frailty. Though not tested in our study, future research should address other interventions known to reverse frailty in the aged including treating deconditioning, protein-energy malnutrition, depression, and vitamin D deficiency.
Disclosures
The authors have nothing to disclose.
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