Mast cells in the human dura: effects of age and dural bleeding.
Mast cells in the human dura: effects of age and dural bleeding.
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人类硬脑膜中的肥大细胞：年龄和硬脑膜出血的影响。
DOI：
10.1007/s00381-013-2275-5
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Karst,WouterA
中科院分区：
文献类型：
--
作者：
Greeley,ChristopherS;Karst,WouterA
尊敬的编辑：我们怀着极大的兴趣阅读了Varatharaj及其同事关于人类硬脑膜中存在肥大细胞的手稿[2]。作者们继续努力，试图使这个仍然不透明和复杂的领域-硬膜下出血(SDH)收集的时机-清晰，这一点应该受到赞扬。他们研究的中心特征是硬脑膜中存在肥大细胞。值得注意的是，正如作者指出的那样，几十年来，免疫活性细胞和血管生成因子已被确定为硬膜下出血修复反应的一部分。Varatharaj和他的同事指出，Sarkar和他的同事[1]在2002年证明了嗜酸性粒细胞和慢性SDH的存在。Sarkar和他的同事报告了Yamashima和他的同事早在1985年就发现了这一发现。Varatharaj及其同事的最新贡献[2]--评估死后硬脑膜样本中的肥大细胞密度--相当令人信服，但鉴于已知硬膜下出血中存在嗜酸性粒细胞，一些结论不能得到所提供的数据的支持。本研究旨在测定人硬脑膜中肥大细胞的密度。作者还想描述新的和旧的SDH之间肥大细胞密度的变化。调查人员的部分意图似乎是评估肥大细胞可能具有的与硬膜下收集的年龄相关的“概况”。从方法部分仍不清楚的是，肥大细胞密度的评估是否是由对临床信息视而不见的评估者完成的。如果在肥大细胞密度的评估中没有盲点，那么研究者的偏见就有很大的机会。Varatharaj和他的同事[2]指出，肥大细胞的密度与SDH的年龄几乎在统计上相关，尽管目前还不清楚进行了什么统计分析。如图4所示，平均肥大细胞密度的标准误差范围相对较大。鉴于样本量较小，缺乏统计学意义也就不足为奇了。尽管缺乏统计学意义，肥大细胞密度和SDH年龄之间的关系将证实Yamashima和他的同事的发现。在评估50名受试者(10-87岁)的硬脑膜样本时，Yamashima及其同事指出，嗜酸性粒细胞的密度与SDH的年龄有关，而不是受试者的年龄。此外，他们还注意到淋巴细胞、组织细胞和肥大细胞根据SDH的年龄有不同的分布。这些作者得出结论，嗜酸性粒细胞是损伤后更广泛的细胞炎症反应的一部分，并有助于与“慢性”SDH相关的愈合和血管生成。我们认为，Varatharaj和他的同事的发现与这些发现非常一致，肥大细胞密度与受试者年龄的任何明显关联都被SDH的年龄和小样本量混淆。为了帮助解决这一明显的差异，我们建议进行一些澄清。首先，以表格的形式介绍受试者的年龄和SDH收藏的年龄将是有帮助的。我们预计肥大细胞随年龄增长的明显趋势与“老年”SDH在年轻受试者中的过度表达有关。此外，还不清楚为什么使用200个月(16岁零8个月)作为年龄界限。对于读者来说，让年龄以更标准化的方式表示会很有帮助
Dear Editor: We read with great interest the manuscript by Varatharaj and colleagues [2] regarding the presence of mast cells in the human dura. The authors should be applauded for their continued efforts to try to bring clarity to an area which remains opaque and complex—timing of subdural hemorrhage (SDH) collections. The central feature of their study is the presence of mast cells in the dura. It is important to note that, as the authors indicate, immunologically active cells and angiogenic factors have been identified as part of the reparative reaction to subdural hemorrhage for decades. Varatharaj and colleagues note that Sarkar and colleague [1] have demonstrated in 2002 the presence of eosinophils and chronic SDH. Sarkar and colleagues report on the finding that have been discovered by Yamashima and colleagues [3] demonstrating this finding as early as 1985. The most recent contribution by Varatharaj and colleagues [2], evaluating mast cell density within postmortem dural samples, is quite compelling, but given what is already known about the presence of eosinophils in subdural hemorrhage, some of the conclusions are unsupported by the data presented. The current study was aimed to determine the density of the mast cell population in the dura mater of humans. The authors also wanted to describe changes in the density of the mast cells between fresh and old SDH. It appears that the intention of the investigators, in part, is to assess a “profile” that mast cells may have, as related to the age of the subdural collection.What remains unclear from the methods section is if the assessment of the mast cell density was done by an assessor blinded to clinical information. If there were no blinding in the assessment of mast cell density, then there is significant opportunity for investigator bias. Varatharaj and colleagues [2] note that the density of mast cells was nearly statistically related to the age of the SDH, although it remains unclear what statistical analysis was being performed. The standard error ranges of the average mast cell density, as shown in Fig. 4, are relatively large. Given the small sample size, the absence of a statistical significance is not surprising. Despite the lack of statistical significance, a relation between the mast cell density and the age of the SDH would confirm the findings of Yamashima and colleagues. In evaluating the dural membrane samples of 50 subjects (10–87 years), Yamashima and colleagues noted that the density of eosinophils was related to the age of the SDH as opposed to the age of the subject. In addition, they noted lymphocytes, histiocytes, and mast cells in various distributions according to age of the SDH. These authors concluded that eosinopshils were part of a broader cellular inflammatory response to injury and contributed to the healing as well as the angiogenesis associated with “chronic” SDH. We would contend that the findings of Varatharaj and colleagues is quite consistent with these findings, and that any apparent association of mast cell density to age of the subject is confounded by the age of the SDH and small sample size. To help resolve the apparent discrepancy, we suggest some clarifications. First, it would be helpful for the authors to present the ages of the subjects and the ages of the SDH collection in tabular form. We would anticipate that the apparent trend of mast cells to the age of the subject is related to the overrepresentation of “old” SDH in younger subjects. Additionally, it is unclear why 200 months (16 years and 8 months) was used as the age cutoff. It would be helpful to the reader to have the ages represented in a more standardized