Ultrasound-assisted resection of oral tongue cancer.
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| Title: | Ultrasound-assisted resection of oral tongue cancer. |
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| Authors: | Nilsson, Olof (AUTHOR), Knutsson, Johan (AUTHOR), Landström, Fredrik J. (AUTHOR), Magnuson, Anders (AUTHOR), von Beckerath, Mathias (AUTHOR) |
| Source: | Acta Oto-Laryngologica. Sep-Dec2022, Vol. 142 Issue 9-12, p743-748. 6p. |
| Subjects: | Relative medical risk, Ultrasonic imaging, Confidence intervals, Tongue tumors, Intraoperative care, Head & neck cancer, Tongue, Treatment effectiveness, Odds ratio, Squamous cell carcinoma, Evaluation |
| Abstract (English): | In surgical resection of squamous cell carcinoma of the oral tongue (SCCOT), achieving clear margins is important for prognosis. Insufficient histopathological margins are common, particularly deep margins. The aim of the present study was to determine whether ultrasound (US)-assisted resection could decrease the proportion of insufficient histopathological deep margins in SCCOT. 34 patients with SCCOT undergoing US-assisted resection (study group) were compared to 76 whose resections were performed without US (conventional group). Outcome measures were insufficient deep histopathological resection margins and mean difference in deep margins. Insufficient deep resection margins (<5.0 mm) were seen in 8 of 34 (23.5%) in the study group, compared to 31 of 76 (40.8%) in the conventional group, unadjusted RR 0.58 [95% CI 0.30–1.12; p =.11], adjusted RR 0.82 [95% CI 0.35–1.92; p =.64]. Unadjusted mean difference was 1.4 mm (95% CI 0.1–2.7, p =.04), adjusted mean difference 1.1 mm (95% CI −2.7 to 0.5, p =.19). Intraoperative US can visualize the deep resection margins in T1/T2 SCCOT. US-assisted resection seems to decrease the number of insufficient histopathological deep margins, though the results are not statistically significant. Comparatively good results in the conventional group is one explanation for the lack of significance. NCT04059861 [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): | 背景：过敏性鼻炎 (AR) 是西方化世界的一种常见病症, 被认为比典型的"Th2"炎症在免疫学上更为复杂, 需要新的方法来解释这种复杂性。 目的：在本项研究中, 我们探索了一种基于组织学的新型分析法, 用于分析 16 名在花粉季节之外和期间患有季节性 AR 的患者的循环血液白细胞特征。 材料和方法：用尽量少的离体人工制品纯化白细胞, 将其包埋于琼脂糖石蜡颗粒中, 用于基于免疫组织化学的免疫细胞分析, 并进行了血液白细胞制图。 结果：与淡季基线相比, 在花粉季节收集的样本具有统计学意义上的嗜酸性粒细胞、嗜中性粒细胞、单核细胞和 CD8+ 淋巴细胞的增加。 相反, CD20+ B 淋巴细胞和 CD3+ T 淋巴细胞没有观察到任何变化。 CD4+ T 辅助细胞的亚分类表明, 在花粉季节, Th2 和 Th17 细胞显示平行且显著的扩增, 而 Th1 细胞保持不变。 在花粉季节, 尽管嗜碱性粒细胞的绝对数量没有改变, 但嗜碱性粒细胞标记物 GATA2 和 CPA3有所增加。 结论和意义：本研究介绍了一种新的适用于系统免疫细胞筛选的方法, 并提供了季节性 AR 的复杂且平行的 Th2 和 Th17 免疫特征的进一步证据。 它还提出将 GATA2 和 CPA3 作为持续过敏性炎症的潜在生物标志物。 [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | In surgical resection of squamous cell carcinoma of the oral tongue (SCCOT), achieving clear margins is important for prognosis. Insufficient histopathological margins are common, particularly deep margins. The aim of the present study was to determine whether ultrasound (US)-assisted resection could decrease the proportion of insufficient histopathological deep margins in SCCOT. 34 patients with SCCOT undergoing US-assisted resection (study group) were compared to 76 whose resections were performed without US (conventional group). Outcome measures were insufficient deep histopathological resection margins and mean difference in deep margins. Insufficient deep resection margins (<5.0 mm) were seen in 8 of 34 (23.5%) in the study group, compared to 31 of 76 (40.8%) in the conventional group, unadjusted RR 0.58 [95% CI 0.30–1.12; p =.11], adjusted RR 0.82 [95% CI 0.35–1.92; p =.64]. Unadjusted mean difference was 1.4 mm (95% CI 0.1–2.7, p =.04), adjusted mean difference 1.1 mm (95% CI −2.7 to 0.5, p =.19). Intraoperative US can visualize the deep resection margins in T1/T2 SCCOT. US-assisted resection seems to decrease the number of insufficient histopathological deep margins, though the results are not statistically significant. Comparatively good results in the conventional group is one explanation for the lack of significance. NCT04059861 [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00016489 |
| DOI: | 10.1080/00016489.2022.2153916 |
