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Metabolite Profiles in Inflammatory Diseases

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A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (15 August 2026) | Viewed by 7794

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Editors

Dr. Rodica Pădureanu

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Guest Editor

Department of Internal Medicine, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania
Interests: autoimmune diseases; rheumatoid arthritis; inflammation; oxidative stress; biomarkers

Dr. Ionut Donoiu

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Guest Editor

Department of Cardiology, University of Medicine and Pharmacy Craiova, 200349 Craiova, Romania
Interests: heart failure; cardiomyopathy; myocardial infarction; arrhythmia
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Dear Colleagues,

Cachexia, the disease-related loss of cellular mass, is a sign of the close connection between inflammation and metabolic processes. It was given the name "cachexin" because it was discovered that tumor necrosis factor-alpha (TNFα) was involved in this process. The capacity of inflammatory cytokines to have such significant impacts on cellular and metabolic systems remains instructive, even if TNFα is now more widely recognized as a modulator of inflammatory responses. Chronic inflammation leads to rheumatic cachexia, and systemic inflammation, such as that observed in RA, alters metabolism. Loss of muscle mass and maintenance of fat mass are characteristics of this. Cachexia is traditionally characterized by a low body mass index. Although RA frequently causes muscle atrophy, low BMI is rare because fat mass is maintained or even increased. Rheumatoid cachexia, which affects 10–20% of RA patients with managed illness and 38% of people with active RA, is more common than the traditional low BMI cachexia, which affects 1–13% of RA patients.

It is believed that proinflammatory cytokines, including TNFα, IL1, and IL6, are the cause of the muscle loss that happens in rheumatoid cachexia. Through the ubiquitin-proteasome pathway, TNF stimulates proteolysis. Additionally, there is some evidence that cytokines may inhibit anabolic resistance, which is the increase in muscle protein synthesis that occurs in response to feeding. The degree of muscular atrophy in rheumatoid cachexia is correlated with the disease activity of RA.

This special issue provides an opportunity for researchers to share cutting-edge findings. We welcome high-quality original research and reviews.

Dr. Rodica Pădureanu
Dr. Ionut Donoiu
Guest Editors

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Keywords

gut
inflammation
markers
metabolomics
multiple sclerosis
rheumatoid arthritis
lung disease
osteoarthritis

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Published Papers (6 papers)

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Research

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11 pages, 1510 KB

Open AccessArticle

Predicting Prolonged Length of Stay in Acute Pancreatitis: Comparison of the CRP-to-Albumin Ratio with Other Inflammatory and Immunoutritional Indices

by Ümit Karatepe and Berçem Afşar Karatepe

Metabolites 2026, 16(5), 320; https://doi.org/10.3390/metabo16050320 - 11 May 2026

Viewed by 1046

Abstract

Objective: Due to the varied clinical manifestations of acute pancreatitis (AP), prompt identification of patients predisposed to extended hospitalization is essential for efficient resource allocation. This study assessed the predictive efficacy of inflammatory and immunonutritional ratios—namely, C-reactive protein/albumin ratio (CAR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and hemoglobin, albumin, lymphocyte, and platelet score (HALP)—in predicting hospitalizations lasting more than 7 days. Methods: A retrospective cohort analysis was performed on 306 patients treated at a tertiary center from June 2020 to June 2025. We used Mann–Whitney U tests, ROC analysis, and multivariate logistic regression models to evaluate the relationship between admission laboratory-derived ratios and length of stay. Results: In total, 27.5% (n = 84) of the cohort experienced prolonged hospitalization. Individual markers exhibited moderate discrimination; however, procalcitonin and CAR displayed high negative predictive values (>85%), demonstrating clinical utility in excluding prolonged hospital stays. Multivariate analysis revealed advanced age (p < 0.001) and increased CAR (p < 0.001) as the most significant independent predictors. On the other hand, the HALP score was much lower in the group that stayed longer, but it was not an independent predictor in the multivariate model. Conclusions: Older age and a higher CAR are both independent factors that can predict longer hospital stays in AP. The high negative predictive value of CAR is important because it represents a reliable way to exclude prolonged hospitalization. Low CAR levels at admission may help clinicians identify patients eligible for early discharge, thereby optimizing bed management. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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17 pages, 1862 KB

Open AccessArticle

Oxidative Stress and Cirrhosis Severity: A Retrospective Cohort Analysis of Predictive and Interactive Effects with Inflammation

by Vlad Pădureanu, Lidia Boldeanu, Denisa Floriana Vasilica Pîrșcoveanu, Dalia Dop, Ramona Cioboată, Anca Bobîrcă and Virginia Maria Rădulescu

Metabolites 2025, 15(11), 711; https://doi.org/10.3390/metabo15110711 - 30 Oct 2025

Cited by 2 | Viewed by 879

Abstract

Background/Objectives: Oxidative stress is a central mechanism in the pathogenesis of cirrhosis, yet its clinical significance relative to established predictors remains unclear. Methods: We conducted a retrospective cohort study of 90 patients with cirrhosis hospitalized between October 2024 and March 2025. Clinical data, biochemical parameters, systemic inflammatory indices, and oxidative stress markers [malondialdehyde (MDA), 8-epi-prostaglandin F2α (8-epi-PGF2α)] were assessed at admission. Statistical analyses included non-parametric group comparisons, Spearman correlations, logistic regression with interaction terms, ROC analysis with bootstrap confidence intervals, model calibration and discrimination metrics, reclassification indices (NRI, IDI), and decision curve analysis (DCA). Results: Patients with advanced encephalopathy (HE3) had significantly higher MDA levels compared with HE1 (123.4 [107.6–248.4] vs. 131.0 [66.9–301.1] ng/mL; p = 0.021), while 8-epi-PGF2α showed a non-significant but consistent trend. Both oxidative markers correlated with biochemical dysfunction (MDA with INR and albumin; 8-epi-PGF2α with direct bilirubin). ROC analyses demonstrated modest discriminative ability (AUC 0.55–0.60) compared with albumin (AUC 0.74–0.90) and INR (AUC 0.72–0.88). In regression models, albumin remained the strongest independent predictor, whereas oxidative markers did not retain significance. Interaction models suggested that oxidative stress exerted context-dependent effects, particularly in patients with elevated inflammatory indices. Incremental predictive value beyond age and albumin was minimal (ΔAUC ≤ 0.01; NRI + 2–4%). DCA confirmed no added clinical utility. Conclusions: Classical clinical markers, particularly albumin and INR, dominate predictive accuracy in cirrhosis. Oxidative stress markers lack independent predictive power but consistently associate with worsening encephalopathy and liver dysfunction, underscoring their biological relevance and suggesting their role is best understood in conjunction with systemic inflammation. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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13 pages, 1005 KB

Open AccessArticle

Association of Gla-Rich Protein (GRP) with Inflammatory Markers in Critically Ill Patients: A Cross-Sectional Observational Study

by Elif Eygi, Sinem Bayrakçı, Onur Bayrakçı, Nazire Ates Ayhan, Ahmet Atlas, Metin Kilinc and Recep Dokuyucu

Metabolites 2025, 15(9), 611; https://doi.org/10.3390/metabo15090611 - 13 Sep 2025

Cited by 1 | Viewed by 1099

Abstract

Objectives: Gla-rich protein (GRP), a vitamin K-dependent protein, has been increasingly recognized for its dual role in modulating inflammation and inhibiting pathological calcification. Despite its emerging importance in chronic conditions, limited evidence exists regarding its behavior during acute critical illness. This study aimed to investigate the association between GRP, systemic inflammatory markers, oxidative stress (via total thiol oxidation-reduction ratio, TORR), and calcium metabolism in critically ill patients. Materials and Methods: This cross-sectional observational study included 93 critically ill patients admitted to the intensive care unit (ICU) and 60 age- and sex-matched non-critically ill volunteers. Serum GRP levels were measured using ELISA. Other biomarkers including TORR, C-reactive protein (CRP), procalcitonin (PCT), white blood cell count (WBC), immature granulocytes (IGs), and serum calcium were also analyzed. Pearson’s correlation, multivariate linear regression, and ROC analysis were performed to assess the relationships among GRP and biochemical markers, as well as their capacity to differentiate ICU patients from controls. Results: GRP, TORR, CRP, PCT, WBC, IGs, and ferritin levels were significantly elevated in ICU patients compared to the control group, whereas serum calcium levels were markedly reduced (all p < 0.05). GRP levels demonstrated moderate positive correlations with WBC (r = 0.47), neutrophils (r = 0.51), TORR (r = 0.42), CRP (r = 0.30), and IGs (r = 0.46), and a strong negative correlation with calcium (r = −0.63). In multivariate regression, TORR, CRP, WBC, IGs, PCT, and calcium levels showed significant correlations with GRP levels in univariate analysis. ROC analysis revealed that CRP had the highest discriminatory power (AUC = 0.88; 95% CI: 0.82–0.94), followed by TORR (AUC = 0.79; 95% CI: 0.71–0.86), GRP (AUC = 0.76; 95% CI: 0.68–0.84), and IGs (AUC = 0.77; 95% CI: 0.69–0.85), for distinguishing ICU patients from non-critically ill individuals. Conclusions: Our findings demonstrated that GRP is significantly associated with systemic inflammation, oxidative stress, and calcium metabolism disturbances in critically ill patients. The combined evaluation of GRP and TORR may enhance the understanding of inflammatory and oxidative mechanisms in acute critical illness. Although this study did not assess patient outcomes, these biomarkers could serve as promising candidates for future prognostic research in ICU settings. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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19 pages, 1936 KB

Open AccessEditor’s ChoiceReview

The Gut Microbiome in Heart Failure: Pathways to Inflammation and Therapeutic Targets

by Uday Sankar Akash Vankayala, Ali Sohail, Bivin George, Madhu Singh, Omar Khayat, Malek Kreidieh, Alia Hasham and Luis Quiel

Metabolites 2026, 16(6), 431; https://doi.org/10.3390/metabo16060431 - 19 Jun 2026

Cited by 1 | Viewed by 966

Abstract

Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut–heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut–heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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18 pages, 1029 KB

Open AccessReview

Nephrological, Pulmonary, and Dermatological Complications in the Context of MAFLD/NAFLD: A Narrative Review

by Vlad Pădureanu, Dalia Dop, Lucrețiu Radu, Dumitru Rădulescu, Rodica Pădureanu, Denisa Floriana Vasilica Pîrșcoveanu and Daniel Cosmin Caragea

Metabolites 2025, 15(4), 272; https://doi.org/10.3390/metabo15040272 - 14 Apr 2025

Cited by 5 | Viewed by 2424

Abstract

Background: The most common cause of chronic liver disease is now known to be non-alcoholic fatty liver disease (NAFLD), recently redefined as metabolic-associated fatty liver disease (MAFLD). This review aims to synthesize current evidence on the pathophysiology and clinical implications of nephrological, pulmonary, and dermatological manifestations among NAFLD/MAFLD patients. In order to find safe and efficient treatments, NAFLD/MAFLD has emerged as a primary concern for hepatologists worldwide. Methods: We conducted a comprehensive review of the literature from major databases, focusing on studies that evaluated the extrahepatic manifestations of NAFLD/MAFLD. Emphasis was placed on identifying pathophysiological mechanisms and assessing their clinical impact on renal, pulmonary, and dermatological systems. Results: Recent developments in the management of chronic viral hepatitis have lowered the mortality rate associated with chronic liver disease. However, the prevalence of NAFLD/MAFLD continues to rise, making chronic liver disease a significant health concern for the future. An increasing percentage of patients on liver transplant waiting lists now have cirrhosis and hepatocellular carcinoma due to non-alcoholic liver disease. Furthermore, the incidence and prevalence of chronic kidney disease have surged, linking NAFLD/MAFLD to higher morbidity, mortality, and healthcare costs. Conclusions: NAFLD/MAFLD is underdiagnosed and underappreciated, yet its incidence is rapidly increasing, raising concerns about a potential global epidemic. Given its multisystemic impact—extending to renal, pulmonary, and dermatological complications—it is crucial to develop interdisciplinary strategies for early detection and effective management of the disease. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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12 pages, 2940 KB

Open AccessSystematic Review

Probiotics After Metabolic and Bariatric Surgery: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

by Mohammed Y. Ezzi

Metabolites 2026, 16(6), 371; https://doi.org/10.3390/metabo16060371 - 29 May 2026

Viewed by 475

Abstract

Background/Objectives: Patients undergoing metabolic and bariatric surgery (MBS) are at risk of micronutrient deficiencies and gut dysbiosis. Probiotics (such as Lactobacillus, Bifidobacterium) have been proposed as adjunct therapy to optimize postoperative outcomes. This review aimed to evaluate the effect of postoperative probiotic supplementation on anthropometric, metabolic, inflammatory, and micronutrient outcomes in MBS patients. Methods: Nine electronic databases were systematically searched, including PubMed, Web of Science, Cochrane Library, Google Scholar, Popline, Global Health Library, Virtual Health Library, New York Academy of Medicine, and OpenGrey, from inception through October 2024. Only randomized controlled trials (RCTs) were included. The Cochrane Collaboration risk-off-bias tool was used for quality assessment. Meta-analyses were performed using Comprehensive Meta-Analysis software version 2. Fixed-effects or random-effects models based on heterogeneity (I² threshold: 50%) were applied. Mean differences (MD) and 95% confidence intervals (CI) were calculated for all continuous variables. Results: Thirteen RCTs encompassing 666 patients (probiotics group: n = 344; control group: n = 322) were included. Incomplete outcome data represented the most prevalent high-risk domain (23%). Probiotic supplementation was associated with significantly improved serum vitamin D (MD: 25.32 nmol/L, 95% CI: 6.96–43.67, p = 0.007) and vitamin B12 levels (MD: 39.36 pg/mL, 95% CI: 1.88–76.84, p = 0.04). No statistically significant differences were observed in anthropometric outcomes (%EWL, BMI, weight, or waist circumference), lipid profile, glycemic indices, or inflammatory markers (TNF-α, IL-6, CRP). Conclusions: Postoperative probiotic supplementation may significantly improve vitamin D and B12 levels in patients undergoing MBS, suggesting a supportive role in mitigating micronutrient deficiencies. However, these findings should be interpreted with caution due to substantial heterogeneity across studies. Probiotics did not significantly affect weight loss, metabolic parameters, or inflammatory markers. Clinicians may consider probiotics as an adjunct strategy to support micronutrient status in at-risk postoperative patients. Large-scale, strain-specific trials incorporating standardized dietary control and microbiome profiling are warranted. Full article

(This article belongs to the Special Issue Metabolite Profiles in Inflammatory Diseases)

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