Introduction: While hyperammonemia is traditionally associated with decompensated cirrhosis, emerging evidence suggests that disturbances in nitrogen homeostasis contribute to disease progression in earlier stages of steatohepatitis and fibrosis. L‐ornithine L‐aspartate (LOLA), an established ammonia scavenger, targets key pathophysiological mechanisms shared by metabolic dysfunction‐associated steatotic liver disease (MASLD), including oxidative stress, mitochondrial dysfunction and hepatic stellate cell activation. This systematic review synthesizes current experimental and clinical research to evaluate the potential therapeutic role of LOLA in MASLD. Methods: A systematic search of PubMed, Embase and SCOPUS was conducted up to December 1, 2025, following PRISMA 2020 guidelines. Eligible studies included experimental (in vivo/in vitro) and clinical trials evaluating the effects of LOLA or L‐aspartate on hepatic steatosis, inflammation, or fibrosis in the context of MASLD. Data extraction and quality assessment were performed independently by two reviewers using appropriate tools for animal and human studies. Results: Nineteen studies were included, comprising 10 experimental pre‐clinical models (9 in vivo animal studies and 1 in vitro study) and 9 clinical studies involving approximately 1671 participants. Experimental studies consistently demonstrated that LOLA intervention ameliorates hepatic steatosis, inflammation and collagen deposition. Identified molecular mechanisms included the activation of the LKB1‐AMPK axis, restoration of mitochondrial bioenergetics and modulation of the gut‐liver‐muscle axis. In clinical studies, results from three randomized controlled trials (RCTs) indicated significant improvements in liver enzymes (ALT, AST) and lipid profiles, with reductions in hepatic steatosis. Evidence from six observational and open‐label studies corroborated these biochemical improvements and further demonstrated significant reductions in blood ammonia levels, improved intrahepatic microcirculation and reduced liver stiffness and patient‐reported fatigue. However, clinical evidence remains limited by study heterogeneity and a lack of large‐scale randomized trials using specific MASLD criteria. Conclusions: Preclinical evidence suggests that LOLA exerts pleiotropic hepatoprotective effects in MASLD by targeting hyperammonemia‐induced fibrosis and metabolic dysregulation. While growing clinical data indicate benefits in biochemical normalization, structural improvement and symptom relief, further robust clinical research is required to validate these findings and establish LOLA as a standard therapeutic option for MASLD patients.

Background and Objectives: Pulmonary fibrosis, including idiopathic pulmonary fibrosis (IPF) and secondary pulmonary fibrosis (SPF), is a progressive lung disease that significantly impairs respiratory function. Accurate differentiation between IPF and SPF is crucial for effective management. This study explores the association between pulmonary fibrosis and hepatic conditions, evaluating the utility of various hemogram-derived ratios and hepatic fibrosis scores in distinguishing between IPF and SPF. Materials and Methods: We conducted a retrospective study involving patients diagnosed with IPF or SPF at the “Leon Daniello” Clinical Hospital of Pneumology in Cluj-Napoca, Romania. Pulmonary fibrosis was confirmed via imaging techniques, and hepatic steatosis and fibrosis were assessed using non-invasive scores. We analyzed clinical, laboratory, and pulmonary function data, focusing on hemogram-derived ratios and hepatic scores. Statistical analyses, including ROC curves, were used to evaluate the effectiveness of these biomarkers in differentiating IPF from SPF. Results: We included a total of 38 patients with IPF and 28 patients with SPF. Our findings revealed that IPF patients had a significantly higher FIB-4 score compared to SPF patients, suggesting increased hepatic fibrosis risk in IPF, as well as an increased RDW/PLT ratio. Conversely, SPF patients exhibited elevated PLR, PNR, and SII, reflecting a more pronounced inflammatory profile. PLR and PNR demonstrated the highest discriminatory ability between IPF and SPF, while traditional hepatic fibrosis scores showed limited differentiation capabilities. No significant differences in pulmonary function tests were observed across hepatic fibrosis risk categories. Conclusions: The study highlights the value of biomarkers like PLR and PNR in differentiating between IPF and SPF, offering additional diagnostic insights beyond traditional imaging. Integrating hepatic assessments into the management of pulmonary fibrosis could improve diagnostic accuracy and patient care.