Scholarlink

Background and study aim <p>Cirrhosis of the liver occurs in two stages: compensated and decompensated. Increased intestinal permeability and bacterial translocation are the causes of systemic inflammatory response syndrome (SIRs), which may be linked to hepatic decompensation. Serum claudin-3 and hematological indices [mean platelet volume (MPV)/platelet ratio (MPR), red cell distribution width (RDW), red blood cell/lymphocyte ratio (RLR), neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), and red cell/lymphocyte ratio (RLR)] were evaluated in this study as possible indicators of decompensated liver cirrhosis (LC).</p> Patients/materials and methods <p>Twenty healthy people and 80 patients who were admitted to the tropical medicine department of Alexandria Main University Hospital participated in our study. Group I comprised 50 patients with decompensated LC post-chronic hepatitis C virus (HCV) infection, group II included 30 patients with compensated LC related to HCV, and group III included 20 healthy individuals as the control group. Using established protocols, enzyme-linked immunohistochemical assay (ELISA) was used to assess serum claudin-3.</p> Results <p>Comparing patients with decompensated LC to those with compensated LC and the control group, there was a statistically significant increase in serum claudin-3. Patients with decompensated LC had significantly higher NLR, MLR, RPR, and MPR than those with compensated LC (<i>p</i> &lt; 0.05). Serum claudin-3, NLR, MLR, Child–Pugh, and model of end-stage liver disease (MELD) scores showed significant positive relationships (<i>p</i> &lt; 0.05). Linear regression analysis was conducted including claudin-3, RDW, NLR, MPR, PLR, RPR, MLR, and RLR revealed that only the model using combined NLR and claudin-3 was a statistically significant predictor of decompensation. Consequently, the ROC curve analysis for NLR and serum claudin-3 yielded a 90% sensitivity, 62% specificity, a diagnostic accuracy of 68% for NLR at a value of 2.27, while a diagnostic sensitivity of 80%, specificity of 60%, and a 72.5% diagnostic accuracy for claudin-3 at a cut-off value of 16.57&#xa0;ng/L for diagnosing decompensated LC.</p> Conclusions <p>NLR and serum claudin-3 are promising markers for monitoring the progression of LC.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Hematological indicators and serum claudin-3 as valuable indices for severity of HCV-related liver cirrhosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月5日

查看全文
  • Ayman Farid El-Shayeb,
  • Mohamed Sobhy El-Shazly,
  • Akram Abdel Moneim Deghady,
  • Nesreen Mohamed Abdel-Latif,
  • Amany Nabil Abbasy

摘要

Background and study aim

Cirrhosis of the liver occurs in two stages: compensated and decompensated. Increased intestinal permeability and bacterial translocation are the causes of systemic inflammatory response syndrome (SIRs), which may be linked to hepatic decompensation. Serum claudin-3 and hematological indices [mean platelet volume (MPV)/platelet ratio (MPR), red cell distribution width (RDW), red blood cell/lymphocyte ratio (RLR), neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), and red cell/lymphocyte ratio (RLR)] were evaluated in this study as possible indicators of decompensated liver cirrhosis (LC).

Patients/materials and methods

Twenty healthy people and 80 patients who were admitted to the tropical medicine department of Alexandria Main University Hospital participated in our study. Group I comprised 50 patients with decompensated LC post-chronic hepatitis C virus (HCV) infection, group II included 30 patients with compensated LC related to HCV, and group III included 20 healthy individuals as the control group. Using established protocols, enzyme-linked immunohistochemical assay (ELISA) was used to assess serum claudin-3.

Results

Comparing patients with decompensated LC to those with compensated LC and the control group, there was a statistically significant increase in serum claudin-3. Patients with decompensated LC had significantly higher NLR, MLR, RPR, and MPR than those with compensated LC (p < 0.05). Serum claudin-3, NLR, MLR, Child–Pugh, and model of end-stage liver disease (MELD) scores showed significant positive relationships (p < 0.05). Linear regression analysis was conducted including claudin-3, RDW, NLR, MPR, PLR, RPR, MLR, and RLR revealed that only the model using combined NLR and claudin-3 was a statistically significant predictor of decompensation. Consequently, the ROC curve analysis for NLR and serum claudin-3 yielded a 90% sensitivity, 62% specificity, a diagnostic accuracy of 68% for NLR at a value of 2.27, while a diagnostic sensitivity of 80%, specificity of 60%, and a 72.5% diagnostic accuracy for claudin-3 at a cut-off value of 16.57 ng/L for diagnosing decompensated LC.

Conclusions

NLR and serum claudin-3 are promising markers for monitoring the progression of LC.