AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |
Back to Blog
Increased blood viscosity8/5/2023 ![]() ![]() ![]() Nevertheless, substantial number of HCC patients are negative for these tumor markers. However, minimal development has been achieved in terms of HCC biomarkers although alpha-fetoprotein (AFP) and proteins induced by vitamin K antagonist-II (PIVKA-II) have been used for diagnosis and predicting clinical outcomes. Innovative advances have been made in the treatment of HCCs, mainly due to the recent development of systemic agents besides sorafenib, such as lenvatinib, regorafenib, cabozantinib, and ramucirumab as well as combination regimens (e.g., atezolizumab plus bevacizumab). Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and a representative cause of cancer-related death. Proteins induced by vitamin K antagonist-II PVTT, Modified Union for International Cancer Control OR, The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist.Īrea under the receiver operating characteristic CI, Mary’s Hospital, The Catholic University of Korea (to J.W.H.). This study was also supported by the Research Fund of Seoul St. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the manuscript and its Supporting information files.įunding: This research was supported by Young Medical Scientist Research Grant through the Daewoong Foundation (DY20201P) (to J.W.H.). Received: AugAccepted: NovemPublished: December 2, 2021Ĭopyright: © 2021 Han et al. PLoS ONE 16(12):Įditor: Tatsuo Kanda, Nihon University School of Medicine, JAPAN Our study is the first in which high WBV is associated with the distant metastases and survival in patients with HCC, but future prospective, large cohort studies are necessary to validate the results.Ĭitation: Han JW, Sung PS, Jang JW, Choi JY, Yoon SK (2021) Whole blood viscosity is associated with extrahepatic metastases and survival in patients with hepatocellular carcinoma. In 33 nivolumab-treated patients, high diastolic WBV before the treatment was also tended to be associated with overall and progression-free survival. High diastolic WBV also predicted poor survival in patients with low alpha-fetoprotein (AFP) and proteins induced by vitamin K antagonist-II (PIVKA-II) levels. Patients with high diastolic WBV had poor survival, and multivariate Cox regression analyses showed high diastolic WBV was an independent risk factor for poor survival with the Child-Pugh B7 and PVTT. Notably, patients who developed extrahepatic metastases during the observation period among patients without metastases at diagnosis had higher diastolic WBV initially. Multivariate logistic regression showed that high diastolic WBV > 16 cP was an independent factor associated with metastases. Systolic WBV and diastolic WBV were significantly increased in patients with metastases compared with patients without metastases. Portal vein tumor thrombosis (PVTT), tumor size, number of tumors, and systolic/diastolic WBV were factors associated with extrahepatic metastases. Extrahepatic metastases were observed in 15 treatment-naïve patients (11.3%) at diagnosis. Systolic and diastolic WBV was measured using an automated scanning capillary tube viscometer at diagnosis or before the nivolumab treatment. This pilot study included a discovery cohort of 148 treatment-naïve HCC patients with preserved liver function, and a validation cohort of 33 treatment-experienced HCC patients with nivolumab. ![]() However, relevance of WBV in hepatocellular carcinoma (HCC) remains unclear. Whole blood viscosity (WBV) is increased in cancer patients and associated with the advanced stage with systemic metastases. ![]()
0 Comments
Read More
Leave a Reply. |