The complex relationship between CD4 count, HIV viral load, trimethoprim-sulfamethoxazole prophylaxis, and skin-and-soft-tissue infection risk in patients with HIV: insights from a causal diagram and simulation study.
The complex relationship between CD4 count, HIV viral load, trimethoprim-sulfamethoxazole prophylaxis, and skin-and-soft-tissue infection risk in patients with HIV: insights from a causal diagram and simulation study.
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HIV 患者的 CD4 计数、HIV 病毒载量、甲氧苄啶-磺胺甲恶唑预防以及皮肤和软组织感染风险之间的复杂关系：因果图和模拟研究的见解。
DOI：
10.1017/s0950268816000789
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发表时间：
2016
影响因子：
4.2
通讯作者：
David,MZ
中科院分区：
文献类型：
--
作者：
Hemmige,V;Lauderdale,DS;David,MZ
由金黄色葡萄球菌，特别是社区相关耐甲氧西林金黄色葡萄球菌（CA-MRSA）引起的皮肤和软组织感染（SSTI）在美国人类免疫缺陷病毒（HIV）感染人群中很常见。关于流行病学和免疫学因素在这种关系中的重要性，研究存在分歧，并且在多变量分析中采用了相互冲突的变量选择策略。流行病学因果推理方法的发展出现在过去十年中，以澄清变量之间的关系，并确定适当的变量，包括和排除多变量分析。在本文中，我们开发了一个因果关系图，以澄清CA-MRSA和HIV之间的联系途径。我们专注于甲氧苄啶-磺胺甲恶唑（TMP-SMX）预防所发挥的作用，规定许多严重免疫功能低下的艾滋病患者和潜在的保护对SSTI，这两个介导和缓和免疫参数和SSTI风险之间的关系。我们证明，使用模拟数据，统计模型可能会产生偏倚的结果，如果他们不考虑如何HIV病毒载量也可能是一个标记遵守TMP-SMX预防。最后，我们提出了一个因果关系模型，包括流行病学以及免疫因素，可以解释艾滋病毒感染人群的初始和复发性SSTI风险增加的风险。
Skin and soft tissue infection (SSTIs) due to Staphylococcus aureus, particularly community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA), are common in human immunodeficiency virus (HIV)-infected populations in the United States. Studies have differed as to the importance of epidemiological and immunological factors in this relationship, and have employed conflicting strategies for variable selection in multivariate analyses. Developments in causal inference methods in epidemiology have emerged in the last decade to clarify relationships between variables and identify appropriate variables to include in and exclude from multivariate analysis. In this paper, we develop a causal diagram to clarify the pathways linking CA-MRSA and HIV. We focus on the role played by trimethoprim-sulfamethoxazole (TMP-SMX) prophylaxis, prescribed to many severely immunocompromised HIV patients and potentially protective against SSTIs, which both mediates and moderates the relationship between immunological parameters and SSTI risk. We demonstrate, using simulated data, that statistical models may yield biased results if they do not account for how HIV viral load may also be a marker of adherence to TMP-SMX prophylaxis. We conclude with a proposed causal model that includes both the epidemiological as well as immunological factors that may explain the increased risk of initial and recurrent SSTI risk in HIV-infected populations.