脂质谱随时间的变化与类固醇治疗有关,但与肉芽肿伴多血管炎(GPA)的炎症状态无关。

M. Marozzi, Teresa Panebianco, A. Vacca, Valeria Dipaola, S. Noviello, Antonio Giovanni Solimando, S. Cicco
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摘要

目的:肉芽肿病合并多血管炎(GPA)是一种小血管炎。血管壁炎症可引起多种血管损伤。血管炎症会加速动脉粥样硬化。这些患者的代谢特征和心血管风险还有待确定。因此,心血管动脉粥样硬化性疾病(ASCVD)可能对患者的预后有风险。目的是在疾病随访期间评估GPA患者的ASCVD风险。方法:回顾性分析37例确诊为GPA (T0)的患者,其中女性22例,年龄51.45±17.15岁。随访1年(T1)和2年(T2)对患者进行评估。所有患者均接受高剂量类固醇治疗,随后一年逐渐减量,同时使用另一种免疫抑制剂。血脂包括总胆固醇、高密度脂蛋白、低密度脂蛋白和甘油三酯。为了评估炎症活性,我们在同一时间点评估红细胞沉降率(ESR)、c反应蛋白(CRP)和中性粒细胞与淋巴细胞比率(NLR)。重复值的方差分析用于评估随时间变化的趋势,Tukey多重比较检验是第二步评估。结果:与基线相比,T1时总胆固醇升高(T1vsT0, p<0.05), T2时总胆固醇升高(T1vsT0, p<0.05)。同样,LDL (T1vsT0, p<0.05)也呈现相同的趋势,而甘油三酯在T1时较基线升高(T1vsT0, p<0.05),但在T2时与T1或T0比较无差异。不同时间点的HDL无差异。c反应蛋白也没有什么不同,尽管已经注意到了其含量的降低。相反,我们发现ESR (T1vsT0, p<0.05)和NLR (T1vsT0, p<0.05)在T2时有降低,而在T1无降低。结论:我们的数据表明,血脂的改变可能与更好地控制炎症无关。相反,第一年随访的增加应该是控制疾病传播所需的类固醇治疗的结果。这些数据可能有助于心血管疾病和脂质代谢的评估,因为这两个参数与血管炎症之间存在联系。需要进一步的研究来更好地评估血管炎对心血管的影响和随之而来的治疗。
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Change over time of lipid profile relates to steroid treatment but not to an inflammatory state in Granulomatosis with poliangioitis polyangiitis (GPA)
Aim: Granulomatosis with polyangiitis (GPA) is a small vessel vasculitis. Inflammation of the vessel wall may induce multiple vascular damages. Atherosclerosis is accelerated during vasa inflammation. Metabolic profile and cardiovascular risk are far to be determined in these patients. Thus, Cardiovascular atherosclerotic disease (ASCVD) may represent a risk for patients' outcomes. The purpose is to evaluate ASCVD risk in GPA over time during disease follow-up. Methods: We retrospectively evaluated 37 patients (22 Females, aged 51.45±17.15) who received a diagnosis of GPA (T0). Patients were evaluated at 1 (T1) and 2 (T2) year follow-up. All patients were treated with high steroid dose followed by a one-year tapering, associated to another immunosuppressant. Lipid profile included total cholesterol, HDL, LDL and Triacylglycerol. To evaluate inflammatory activity, we evaluate erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and neutrophil to lymphocyte ratio (NLR) at the same time points. ANOVA for repeated values was used to evaluate the trend over time and Tukey's multiple comparisons test was a second step evaluation. Results: At T1 there was an increase in total cholesterol compared to baseline (T1vsT0, p<0.05) and T2 (T1vs T2, p<0.05). Similarly, LDL (T1vsT0, p<0.05) presents the same trend, while Triacylglycerol increased in T1 compared to baseline (T1vsT0, p<0.05), but no difference there was in T2 compared to T1 or T0. No difference was found in HDL between the different time points. CRP was no different, despite a reduction being noticed. On the contrary, we found a reduction at T2 but not in T1 in ESR (T1vsT0, p<0.05) and NLR (T1vsT0, p<0.05). Conclusion: Our data suggest that a change in lipid profile may not relate to better control of inflammation. On the contrary, the increase in the first year of follow-up should be a consequence of steroid treatment needed to spread disease control. These data may be helpful in the evaluation of both cardiovascular disease and lipid metabolism due to the connection between the two parameters with vessel inflammation. Further studies are needed to better evaluate the cardiovascular effect of vasculitis and consequent treatment.
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