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

Abstract 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.

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Publication Details

Journal
Egyptian Liver Journal
Published
2025-03-05
DOI
https://doi.org/10.1186/s43066-025-00408-0
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
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article

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

Ayman F. El-Shayeb, Nesreen Mohamed Abdel-Latif, Akram Deghady, Amany N. Abbasy et al.
Egyptian Liver Journal
Liver Disease Diagnosis and Treatment
article

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

Ayman F. El-Shayeb, Nesreen Mohamed Abdel-Latif, Akram Deghady, Amany N. Abbasy, Mohamed El-Shazly
article en

Abstract

Abstract 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.

Egyptian Liver JournalVol. 15(1)
Alexandria University (EG)
Openalex Percentile: Top 94%
Liver Disease Diagnosis and Treatment
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