新发败血症中的 25- 羟维生素 D 和甲状旁腺激素:危重病人的前瞻性研究

Irene Karampela , Theodora Stratigou , Georgios Antonakos , Dimitris Kounatidis , Natalia G. Vallianou , Dimitrios Tsilingiris , Maria Dalamaga
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引用次数: 0

摘要

维生素 D 不足在危重病人中非常普遍,被认为是感染、败血症和死亡率升高的一个危险因素。我们试图研究新发脓毒症重症患者的血清 25- 羟维生素 D(25(OH)D)和甲状旁腺激素(PTH)是否与病情严重程度和预后有关。我们前瞻性地纳入了 50 例连续重症成人新发败血症病例和 50 例年龄和性别匹配的健康对照组。在所有病例和对照组纳入研究时,以及在病例脓毒症发病一周后,通过电化学发光免疫测定法测定血清中的 PTH 和 25(OH)D。与对照组相比,患者在脓毒症发病时 25(OH)D 降低(7.9 ± 3 vs 24.6 ± 6.7 ng/mL,p < 0.001),而 PTH 相似(中位数(范围):34.5 (5.7-2.7) ng/mL,p < 0.001):34.5 (5.7-218.5) vs 44.2 (14.2-98.1) pg/mL,p = 0.35)。患者入院时和入院一周后的 25(OH)D 没有明显差异(7.9 ± 3 vs 7 ± 4.3 ng/mL,p = 0.19)。所有患者均出现维生素D过低(25(OH)D为20纳克/毫升),而40名患者(80%)在败血症发生时出现维生素D缺乏(25(OH)D为12纳克/毫升),其中包括所有10名(20%)非幸存者,他们在败血症发生后28天内死亡。脓毒症患者(28 人)和脓毒性休克患者(22 人)以及幸存者(40 人)和非幸存者(10 人)在入院时的 25(OH)D 值相似(p > 0.05)。25(OH)D与离子钙呈正相关(r = 0.46,p <;0.001),与PTH呈负相关(p <;0.05),而炎症生物标志物或严重程度评分与25(OH)D没有相关性。脓毒性休克患者和非幸存者的 PTH 分别低于脓毒症患者和幸存者(分别为 42.2 ± 42.9 vs 73.4 ± 61.9 pg/mL,p = 0.04;18.3 ± 10.7 vs 69.9 ± 58.8 pg/mL,p = 0.001)。C反应蛋白与PTH呈负相关(r = -0.44,p = 0.001)。总之,80%的重症患者在脓毒症发病时存在维生素D缺乏症,而非存活者的PTH低于存活者。有必要进行更多更大规模的多中心研究,以阐明维生素 D 和 PTH 对败血症发病机制及其结果的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
25-hydroxyvitamin D and parathyroid hormone in new onset sepsis: A prospective study in critically ill patients

Hypovitaminosis D is highly prevalent in critically ill patients, and it has been suggested to be a risk factor for infections, sepsis and higher mortality. We sought to investigate whether serum 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone (PTH) in critically ill patients with new onset sepsis are associated with severity and outcome. We prospectively included 50 consecutive critically ill adult cases with new onset sepsis and 50 healthy controls matched for age and sex. PTH and 25(OH)D were determined in serum via electrochemiluminescence immunoassays at inclusion in the study in all cases and controls, and one week after sepsis onset in cases. Patients had reduced 25(OH)D compared to controls at sepsis onset (7.9 ± 3 vs 24.6 ± 6.7 ng/mL, p < 0.001), whilst PTH was similar (median (range): 34.5 (5.7–218.5) vs 44.2 (14.2–98.1) pg/mL, p = 0.35). In patients, 25(OH)D upon enrollment and one week after did not differ significantly (7.9 ± 3 vs 7 ± 4.3 ng/mL, p = 0.19). All patients presented with hypovitaminosis D (25(OH)D < 20 ng/mL), while 40 patients (80 %) had vitamin D deficiency (25(OH)D < 12 ng/mL) at sepsis onset, including all ten (20 %) nonsurvivors, who died within 28 days from sepsis onset. Patients with sepsis (N = 28) and septic shock (N = 22) as well as survivors (N = 40) and nonsurvivors (N = 10) had similar 25(OH)D at enrollment (p > 0.05). 25(OH)D was positively correlated with ionized calcium (r = 0.46, p < 0.001) and negatively with PTH (p < 0.05), while inflammatory biomarkers or the severity scores exhibited no correlation with 25(OH)D. Patients with septic shock and nonsurvivors had lower PTH than patients with sepsis and survivors respectively (42.2 ± 42.9 vs 73.4 ± 61.9 pg/mL, p = 0.04, and 18.3 ± 10.7 vs 69.9 ± 58.8 pg/mL, p = 0.001, respectively). C-reactive protein was negatively associated with PTH (r = −0.44, p = 0.001). In conclusion, vitamin D deficiency was present in 80 % of critically ill patients at sepsis onset, while nonsurvivors exhibited lower PTH than survivors. Additional, larger and multicenter studies are warranted to elucidate the contribution of vitamin D and PTH to the pathogenesis of sepsis and its outcomes.

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来源期刊
Metabolism open
Metabolism open Agricultural and Biological Sciences (General), Endocrinology, Endocrinology, Diabetes and Metabolism
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