Connolly E S, Fiore A J, Winfree C J, Prestigiacoma C J, Goldman J E, Solomon R A
Department of Neurological Surgery, Columbia University, College of Physicians and Surgeons, New York, New York, USA.
Neurosurgery. 1997 May;40(5):903-8; discussion 908-9. doi: 10.1097/00006123-199705000-00003.
alpha 1-Antitrypsin (AAT) and alpha 2-macroglobulin (AMG) are elastase inhibitors that bind the enzyme and reduce measured levels of free elastase. It was recently demonstrated that some patients with intracranial aneurysms have significantly elevated plasma elastase (PE) levels. Although this elevation is unrelated to plasma AAT, it is unknown whether abnormal AAT phenotypes or reduced AMG levels play a role. Moreover, the pathological significance of this elevation is not understood.
Plasma from 24 patients with aneurysms (ruptured, n = 15; unruptured, n = 9) and 10 age-matched patients who comprised a control group was analyzed for PE and AMG levels by enzyme-linked immunosorbent assay and for AAT phenotype by isoelectric focusing. Sections of superficial temporal temporal artery obtained from these patients at the time of surgery were examined for evidence of elastin degradation by using a van Gieson stain, with scoring on a nine-point quantitative scale.
Patients with aneurysms showed significantly elevated PE levels (119 +/- 28 versus 17 +/- 7 micrograms/ml, P < 0.05), but AMG levels were not decreased. AAT phenotypic abnormalities were observed in 10% (2 of 20) of the patients with aneurysms, but this was not different from the expected population incidence (7%). Elastin degradation scores were significantly higher in patients with aneurysms than in patients control group (4.26 +/- 0.54 versus 1.21 +/- 0.43, P < 0.05). In addition, patients with higher elastase levels (> 80 micrograms/ml) demonstrated 55% higher degradation scores than did those with lower elastase levels (< 80 micrograms/ml).
These data suggest that high PE levels may play a role in systemic arterial elastin degradation seen in patients with intracranial aneurysms. These data also support the contention that elevated elastase levels are not the result of decreased protease inhibitor levels. Although PE levels were significantly higher for the entire group of patients with aneurysms, this assay has relatively low sensitivity for predicting the presence of unruptured aneurysms. Additional study is necessary to determine whether serum elastase levels greater than 80 micrograms/ml, in the setting of other risk factors, are useful in identifying asymptomatic patients for additional screening.
α1-抗胰蛋白酶（AAT）和α2-巨球蛋白（AMG）是弹性蛋白酶抑制剂，它们与该酶结合并降低测得的游离弹性蛋白酶水平。最近有研究表明，一些颅内动脉瘤患者的血浆弹性蛋白酶（PE）水平显著升高。尽管这种升高与血浆AAT无关，但尚不清楚异常的AAT表型或降低的AMG水平是否起作用。此外，这种升高的病理意义尚不清楚。
通过酶联免疫吸附测定法分析24例动脉瘤患者（破裂型，n = 15；未破裂型，n = 9）和10例年龄匹配的作为对照组患者的血浆PE和AMG水平，并通过等电聚焦分析AAT表型。在手术时从这些患者获取的颞浅动脉切片，使用范吉森染色检查弹性蛋白降解的证据，并进行九点定量评分。
动脉瘤患者的PE水平显著升高（119±28对17±7微克/毫升，P < 0.05），但AMG水平未降低。在10%（20例中的2例）的动脉瘤患者中观察到AAT表型异常，但这与预期的人群发病率（7%）无差异。动脉瘤患者的弹性蛋白降解评分显著高于对照组患者（4.26±0.54对1.21±0.43，P < 0.05）。此外，弹性蛋白酶水平较高（> 80微克/毫升）的患者的降解评分比弹性蛋白酶水平较低（< 80微克/毫升）的患者高55%。
这些数据表明，高PE水平可能在颅内动脉瘤患者出现的全身动脉弹性蛋白降解中起作用。这些数据还支持弹性蛋白酶水平升高不是蛋白酶抑制剂水平降低所致的观点。尽管整个动脉瘤患者组的PE水平显著更高，但该检测方法对预测未破裂动脉瘤的存在相对灵敏度较低。需要进一步研究以确定在存在其他危险因素的情况下，血清弹性蛋白酶水平大于80微克/毫升是否有助于识别无症状患者进行额外筛查。
