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多发性骨髓瘤患者诊断时血清内皮抑素水平较高,但治疗后的平台期则不然。

High serum level of endostatin in multiple myeloma at diagnosis but not in the plateau phase after treatment.

作者信息

Urbańska-Ryś Halina, Robak Tadeusz

机构信息

Department of Haematology, Medical University of Lodz, Copernicus Memorial Hospital, Poland.

出版信息

Mediators Inflamm. 2003 Aug;12(4):229-35. doi: 10.1080/09629350310001599675.

DOI:10.1080/09629350310001599675
PMID:14514474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1781619/
Abstract

We investigated the serum concentration of endostatin in 84 patients with multiple myeloma (MM) and in 13 healthy controls. The level of measured anti-angiogenic agent was correlated with the phase and stage of the disease, and most importantly with clinical and laboratory parameters depicting the disease activity (haemoglobin, creatinine, albumins, calcium, M-component, C-reactive protein, beta2-microglobulin, lactate dehydrogenase, stage of bone disease) as well as serum levels of pro-angiogenic cytokines such as vascular endothelial growth factor, hepatocyte growth factor, fibroblast growth factor and transforming growth factor-beta. The median serum level of endostatin in MM patients was 58 ng/ml and was statistically significantly higher than in the control group (median, 40 ng/ml; p=0.015). MM patients in phase I (at diagnosis) had higher levels of endostatin (median, 69 ng/ml) than those in phase II (plateau phase after treatment) (median, 49 pg/ml; p=0.044). We did not find any statistical correlation between the level of endostatin and stage of MM according to the Durie and Salmon system. The serum concentration of endostatin in MM patients with a normal level of albumins was significantly higher than in others with hypoalbuminaemia (median, 62 ng/ml versus 39 ng/ml; p=0.033). Also, patients with a normal value of lactate dehydrogenase had a higher concentration of endostatin than those with values >425 U/l (median, 70 ng/ml versus 39 ng/ml; p=0.019). We did not show any statistical correlation between the concentration of endostatin and level of haemoglobin, creatinine, calcium, C-reactive protein, beta2-microglobulin and stage of bone disease. We failed to find positive or negative correlations between the level of endostatin and vascular endothelial growth factor, hepatocyte growth factor, fibroblast growth factor and transforming growth factor-beta. The concentration of endostatin did not influence the probability of survival in MM patients in our study. In conclusion, our data indicate that endostatin has a higher level in MM patients than in healthy controls. Highest values were stated in active phases of the disease (at presentation and in progression). Different clinical and laboratory parameters generally do not influence the concentration of endostatin (except albumins and lactate dehydrogenase).

摘要

我们对84例多发性骨髓瘤(MM)患者及13名健康对照者的血清内皮抑素浓度进行了研究。所测抗血管生成因子水平与疾病的分期和阶段相关,最重要的是与描述疾病活动的临床和实验室参数(血红蛋白、肌酐、白蛋白、钙、M蛋白、C反应蛋白、β2微球蛋白、乳酸脱氢酶、骨病分期)以及促血管生成细胞因子如血管内皮生长因子、肝细胞生长因子、成纤维细胞生长因子和转化生长因子-β的血清水平相关。MM患者内皮抑素的血清中位水平为58 ng/ml,在统计学上显著高于对照组(中位值40 ng/ml;p = 0.015)。I期(诊断时)的MM患者内皮抑素水平(中位值69 ng/ml)高于II期(治疗后平台期)患者(中位值49 pg/ml;p = 0.044)。根据Durie和Salmon系统,我们未发现内皮抑素水平与MM分期之间存在任何统计学相关性。白蛋白水平正常的MM患者血清内皮抑素浓度显著高于白蛋白血症患者(中位值62 ng/ml对39 ng/ml;p = 0.033)。此外,乳酸脱氢酶值正常的患者内皮抑素浓度高于值>425 U/l的患者(中位值70 ng/ml对39 ng/ml;p = 0.019)。我们未发现内皮抑素浓度与血红蛋白、肌酐、钙、C反应蛋白、β2微球蛋白水平及骨病分期之间存在任何统计学相关性。我们未发现内皮抑素水平与血管内皮生长因子、肝细胞生长因子、成纤维细胞生长因子和转化生长因子-β之间存在正相关或负相关。在我们的研究中,内皮抑素浓度并未影响MM患者的生存概率。总之,我们的数据表明MM患者体内的内皮抑素水平高于健康对照者。在疾病的活动期(初诊时和进展期)内皮抑素水平最高。不同的临床和实验室参数一般不影响内皮抑素的浓度(白蛋白和乳酸脱氢酶除外)。

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本文引用的文献

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Lupus. 2002;11(6):348-55. doi: 10.1191/0961203302lu199oa.
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B-CLL cells are capable of synthesis and secretion of both pro- and anti-angiogenic molecules.B淋巴细胞慢性淋巴细胞白血病细胞能够合成和分泌促血管生成分子和抗血管生成分子。
Leukemia. 2002 May;16(5):911-9. doi: 10.1038/sj.leu.2402467.
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Clinical significance of plasma endostatin in acute myeloid leukemia/myelodysplastic syndrome.血浆内皮抑素在急性髓系白血病/骨髓增生异常综合征中的临床意义
Cancer. 2002 Jan 1;94(1):14-7. doi: 10.1002/cncr.10200.
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Antiangiogenic therapy in multiple myeloma.多发性骨髓瘤的抗血管生成治疗。
Acta Haematol. 2001;106(4):208-13. doi: 10.1159/000046617.
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Eur J Hum Genet. 2001 Nov;9(11):811-4. doi: 10.1038/sj.ejhg.5200721.
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