本研究比较了两组接受同步放化疗(cCHRT)的局部晚期头颈部鳞状细胞癌(LA-HNSCC)患者,特别是一线治疗的患者和以前接受过诱导化疗(iCHT)的患者。关键问题是iCHT在随后的LA-HNSCC治疗过程中是否是一个严重的负担,以及iCHT如何影响对cCHRT的耐受性。在107例LA-HNSCC患者中,54人在cCHRT之前接受了基于顺铂的iCHT。从前一天到完成cCHRT,以每周间隔对患者进行临床监测。收集843个血液样品并分成两个等分试样:用于实验室血液测试和用于核磁共振(NMR)光谱(Bruker400MHz光谱仪)。使用正交偏最小二乘分析(OPLS)和Mann-WhitneyU检验(MWU)分析来自实验室血液测试的NMR代谢物和临床参数。iCHT之后,患者开始cCHRT时血脂显著升高(MWUp值<0.05),甜菜碱,甘氨酸,磷酸胆碱,和网织红细胞计数,以及显著降低NMR炎症标志物,丝氨酸,血细胞比容,嗜中性粒细胞,单核细胞,红细胞,血红蛋白,CRP。在cCHRT期间,白蛋白和心理困扰显着增加,以及血小板的显著减少,N-乙酰半胱氨酸,酪氨酸,和苯丙氨酸,在接受iCHT的患者中。重要的是,所有临床症状(血小板减少除外)和大多数代谢改变(甜菜碱除外,丝氨酸,酪氨酸,葡萄糖,和磷酸胆碱)分解,直到cCHRT完成。总之,iCHT导致血液学毒性,改变的脂质,和一碳代谢,以及下调的炎症,如在开始和cCHRT期间观察到的。然而,这些并发症是暂时的,他们中的大多数在治疗结束时解决了。这表明cCHRT之前的iCHT不会造成重大负担,应被视为LA-HNSCC的安全治疗选择。
The present study compares two groups of locally advanced patients with head and neck squamous cell carcinoma (LA-HNSCC) undergoing concurrent chemoradiotherapy (cCHRT), specifically those for whom it is a first-line treatment and those who have previously received induction chemotherapy (iCHT). The crucial question is whether iCHT is a serious burden during subsequent treatment for LA-HNSCC and how iCHT affects the tolerance to cCHRT. Of the 107 LA-HNSCC patients, 54 received cisplatin-based iCHT prior to cCHRT. The patients were clinically monitored at weekly intervals from the day before until the completion of the cCHRT. The 843 blood samples were collected and divided into two aliquots: for laboratory blood tests and for nuclear magnetic resonance (NMR) spectroscopy (a Bruker 400 MHz spectrometer). The NMR metabolites and the clinical parameters from the laboratory blood tests were analyzed using orthogonal partial least squares analysis (OPLS) and the Mann-Whitney U test (MWU). After iCHT, the patients begin cCHRT with significantly (MWU p-value < 0.05) elevated blood serum lipids, betaine, glycine, phosphocholine, and reticulocyte count, as well as significantly lowered NMR inflammatory markers, serine, hematocrit, neutrophile, monocyte, red blood cells, hemoglobin, and CRP. During cCHRT, a significant increase in albumin and psychological distress was observed, as well as a significant decrease in platelet, N-acetyl-cysteine, tyrosine, and phenylalanine, in patients who received iCHT. Importantly, all clinical symptoms (except the decreased platelets) and most metabolic alterations (except for betaine, serine, tyrosine, glucose, and phosphocholine) resolve until the completion of cCHRT. In conclusion, iCHT results in hematological toxicity, altered lipids, and one-carbon metabolism, as well as downregulated inflammation, as observed at the beginning and during cCHRT. However, these complications are temporary, and most of them resolve at the end of the treatment. This suggests that iCHT prior to cCHRT does not pose a significant burden and should be considered as a safe treatment option for LA-HNSCC.