Assessment of Hepatorenal Biomarkers and Functional Compensation in Patients with Hepatocellular Carcinoma in Northwest Libya
DOI:
https://doi.org/10.65405/rg255s55الكلمات المفتاحية:
Hepatocellular Carcinoma (HCC), Alkaline Phosphatase (ALP), Hepatorenal Interdependence, Functional Compensation, Tumor Dynamics.الملخص
Clinical laboratory surveillance of baseline biochemical parameters serves as a pivotal, non-invasive diagnostic avenue to monitor cellular cytotoxicity, assess the physiological progression of malignancy, and detect secondary systemic stress prior to overt clinical manifestation. Objectives: The aim of this study was to investigate pathophysiological and enzymatic changes associated with the clinical course of hepatocellular carcinoma. Specifically, it explored the biochemical interdependence between hepatic degradation and renal clearance pathways, elucidated the phenomenon of subclinical functional compensation, and studied the clinical effects of age and gender on important laboratory profiles such as hepatic enzymes (ALT, AST, ALP, and GGT) and renal clearance indices (creatinine and urea). Methodology: A cross-sectional laboratory-based study was conducted over a four-month period (February to May 2026). Clinical and laboratory datasets were compiled from confirmed HCC cases across major regional oncology centers. Statistical analysis was executed using SPSS, utilizing descriptive indices, independent t-tests, effect size (Cohen's d) calculations, and Pearson’s correlation matrix to detect statistically significant variations and evaluate biochemical interdependencies associated with tumor dynamics. Results: Hepatic enzyme panels demonstrated highly statistically significant elevations, with Alkaline Phosphatase (ALP) exhibiting the most substantial biological effect size in response to micro biliary obstructions and tumor mass dynamics. Crucially, Pearson’s correlation matrix unveiled a potent, statistically significant positive relationship coupling hepatic enzymatic surges (AST and ALT) with increased renal markers (Urea and Creatinine). Conversely, a critical clinical paradox was recorded, wherein a substantial sub cohort of patients maintained routine biomarkers within established reference intervals despite advanced malignancy. Conclusion: This study underscores that the progression of HCC induces selective enzymatic surges, alongside a subclinical metabolic strain on renal clearance that represents the subclinical onset of hepatorenal syndrome. Furthermore, the extensive functional reserve of both the liver and kidneys frequently induces a state of deceptive laboratory stability. Consequently, isolated reliance on baseline laboratory profiles without radiological correlation can result in a misleading clinical interpretation that delays prognosis, highlighting the clinical necessity of multi-parametric diagnostic surveillance. The study recommends the necessity of conducting future research encompassing larger samples and comparisons across different stages of the disease (early, intermediate, and advanced) to identify the "tipping point" at which the functional compensation of vital organs collapses.
التنزيلات
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