背景:内脏利什曼病(VL),或者kala-azar,是流行地区艾滋病患者的常见共病。尽管有病毒学控制,许多患者仍继续经历VL复发,而是免疫失败.这些患者仍有慢性脾功能亢进症状,例如贫血,白细胞减少症,和血小板减少症,并且由于CD4+计数低而有严重合并感染的风险。因此,在这项研究中,对脾切除的VL和HIV感染患者进行了调查,以了解为什么这些患者的CD4+计数无法恢复,评估脾肿块对脾功能亢进和免疫衰竭的重要性。
方法:从一个回顾性的开放队列中,对13例患者进行了脾切除术作为复发性VL的抢救治疗,调查了11例HIV感染患者。这项研究比较了脾切除术前后患者的全血细胞计数(CBC)以及CD4和CD8细胞计数与脾脏重量的关系。
结果:脾切除术后CBC明显改善,表明脾功能亢进.然而,据我们所知,这是第一项研究表明脾脏质量与CD4细胞计数呈强烈负相关(ρ=-0.71,P=0.015)。
结论:这一发现出乎意料,因为脾脏是最广泛的淋巴组织和T淋巴细胞来源。在回顾了文献和推理之后,我们假设免疫衰竭是继发于最初由生产性HIV感染诱导的脾细胞凋亡引起的CD4+损失,随后,通过脾巨噬细胞寄生虫感染维持的焦亡。
BACKGROUND: Visceral leishmaniasis (VL), or kala-azar, is a common comorbidity in patients with AIDS in endemic areas. Many patients continue to experiences relapses of VL despite virological control, but with immunological failure. These patients remain chronically symptomatic with
hypersplenism, for example with anemia, leukopenia, and thrombocytopenia, and are at risk of severe co-infection due to low CD4+ count. Therefore, in this study, splenectomized patients with VL and HIV infection were investigated to understand why the CD4+ count fails to recover in these patients, evaluating the importance of spleen mass for
hypersplenism and immunological failure.
METHODS: From a retrospective open cohort of 13 patients who had previously undergone splenectomy as salvage therapy for relapsing VL, 11 patients with HIV infection were investigated. This study compared the patients\' complete blood cell count (CBC) and CD4+ and CD8+ cell counts before and after splenectomy with respect to spleen weight.
RESULTS: CBC was substantially improved after splenectomy, indicating
hypersplenism. However, to the best of our knowledge, this is the first study to show that spleen mass is strongly and negatively correlated with CD4+ cell count (ρ = -0.71, P = 0.015).
CONCLUSIONS: This finding was unexpected, as the spleen is the most extensive lymphoid tissue and T-lymphocyte source. After reviewing the literature and reasoning, we hypothesized that the immunological failure was secondary to CD4+ loss initially by apoptosis in the spleen induced by productive HIV infection and, subsequently, by pyroptosis sustained by parasitic infection in spleen macrophages.