背景:人类免疫缺陷病毒(HIV)和结核病(TB)的共同感染由于这些疾病之间复杂的相互作用而提出了重大挑战。导致代谢紊乱加剧。了解这些代谢谱对于改善诊断和治疗方法至关重要。
目的:本研究旨在表征尿中的酰基肉碱和氨基酸谱,包括5-羟基吲哚乙酸(5-HIAA),使用靶向液相色谱质谱(LC-MS)代谢组学在同时感染HIV和TB的患者中。
方法:尿样,归类为艾滋病毒,TB,艾滋病毒/结核病共同感染,和健康的控制,使用HPLC-MS/MS进行分析。统计分析包括单向ANOVA和Kruskal-Wallis检验,以确定组间酰基肉碱和氨基酸谱的显著差异。
结果:这项研究揭示了显著的代谢改变,特别是在结核病和共感染的群体中。中链酰基肉碱水平升高表明脂肪酸氧化增加,结核病中通常与恶病质有关。改变的氨基酸谱表明蛋白质和葡萄糖代谢中断,表明向糖尿病样代谢状态转变。值得注意的是,结核病被确定为这些变化的主要驱动因素,影响蛋白质周转,并影响合并感染患者的能量代谢。
结论:HIV/TB合并感染的代谢谱突出了TB对代谢途径的深远影响,这可能会加剧共感染的临床复杂性。了解这些代谢紊乱可以指导靶向治疗的发展并改善管理策略。最终提高这些患者的临床结果。需要进一步的研究来验证这些发现,并探索它们在更大,不同的人群。
BACKGROUND: The human immunodeficiency virus (HIV) and tuberculosis (TB) co-infection presents significant challenges due to the complex interplay between these diseases, leading to exacerbated metabolic disturbances. Understanding these metabolic profiles is crucial for improving diagnostic and therapeutic approaches.
OBJECTIVE: This study aimed to characterise the urinary acylcarnitine and amino acid profiles, including 5-hydroxyindoleacetic acid (5-HIAA), in patients co-infected with HIV and TB using targeted liquid chromatography mass spectrometry (LC-MS) metabolomics.
METHODS: Urine samples, categorised into HIV, TB, HIV/TB co-infected, and healthy controls, were analysed using HPLC-MS/MS. Statistical analyses included one-way ANOVA and a Kruskal-Wallis test to determine significant differences in the acylcarnitine and amino acid profiles between groups.
RESULTS: The study revealed significant metabolic alterations, especially in TB and co-infected groups. Elevated levels of medium-chain acylcarnitines indicated increased fatty acid oxidation, commonly associated with cachexia in TB. Altered amino acid profiles suggested disruptions in protein and glucose metabolism, indicating a shift towards diabetes-like metabolic states. Notably, TB was identified as a primary driver of these changes, affecting protein turnover, and impacting energy metabolism in co-infected patients.
CONCLUSIONS: The metabolic profiling of HIV/TB co-infection highlights the profound impact of TB on metabolic pathways, which may exacerbate the clinical complexities of co-infection. Understanding these metabolic disruptions can guide the development of targeted treatments and improve management strategies, ultimately enhancing the clinical outcomes for these patients. Further research is required to validate these findings and explore their implications in larger, diverse populations.