Background: Sepsis, a life-threatening condition characterized by a dysregulated immune response to infection, remains a significant clinical challenge globally. This study aims to enhance the predictive accuracy of existing sepsis severity scores by developing augmented versions of the SOFA and SAPS-III models, termed Pro-SOFA and Pro-SAPS, through the integration of biomarkers procalcitonin (PCT), neutrophil-tolymphocyte ratio (NLR), and C-reactive protein (CRP). Methods: This prospective observational study was conducted in the medical ICU of a tertiary care hospital in southern India from August 2022 to December 2023. A total of 301 adult patients suspected or confirmed to have sepsis were assessed for eligibility, with 171 patients completing the study. Demographic and clinical data were collected; SOFA and SAPS-III scores were calculated and augmented with PCT, NLR, and CRP to develop Pro-SOFA and Pro-SAPS models. The performance of these models was evaluated using Brier scores, AUC, and net reclassification index (NRI). Results: The augmented Pro-SOFA and Pro-SAPS models demonstrated superior predictive accuracy compared to their original counterparts. The Brier scores for Pro-SOFA and Pro-SAPS were 0.181 and 0.165, respectively, indicating better calibration than the original scores. The Pro- SAPS showed significant improvement over the original SAPS-III score (NRI = 0.50, SE = 0.14, p < 0.01). Similarly, Pro-SOFA outperformed the original SOFA (NRI = 0.49, SE = 0.13, p < 0.01). Conclusion and clinical significance: Integrating PCT, CRP, and NLR with SOFA and SAPS-III scores to develop Pro-SOFA and Pro-SAPS significantly improves the predictive accuracy for sepsis mortality and can thus potentially improve sepsis outcomes.
15 March 2025 in Computers in Biology and Medicine
O(on behalf of members of the Mission for Ethics and Science in Healthcare (MESH)
on behalf of members of the Mission for Ethics and Science in Healthcare (MESH)
+2
This uniquely original, crowd‑funded laboratory study compared 18 medical‑pharmaceutical and 16 nutraceutical whey protein powders sold in India by analyzing macronutrients, amino‑acid profiles, sugars, heavy metals, mycotoxins, hormones, pesticides and undeclared additives. Nutraceutical products supplied a mean (± SD) 75.6 ± 7.3 g protein/100 g and showed tight agreement with label claims. Ninety‑four per cent met the ≥ 60 g/100 g threshold and exhibited high essential‑amino‑acid densit2y (up to 8.5 g leucine/100 g) with negligible added sugars. By contrast, pharmaceutical powders averaged 29.1 ± 15.4 g protein/100 g; 83% were mis‑labeled beyond ± 5%, and only one product reached the quality benchmark. None exceeded 5 g leucine/100 g, while 44% contained ≥ 2 g sucrose or fructose/100 g, often unlabeled. Heavy‑metal outliers (cadmium, arsenic, copper), aflatoxin, and progesterone appeared more frequently in pharmaceutical brands, and taurine‑based nitrogen spiking was detected in 89% of them versus 12.5% of nutraceuticals. No product contained detectable pesticides or mercury. Overall, nutraceutical powders consistently met compositional expectations, whereas medical‑pharmaceutical formulations delivered lower‑quality protein, higher sugar loads and unreliable labeling, questioning their suitability for therapeutic use.
Background: Transjugular intrahepatic portosystemic shunt (TIPSS) outcomes in patients with moderate-to-severe pre-existing kidney disease (PKD, stages G3a–G4) remain poorly characterized. This study aimed to identify potential predictors of mortality specifically in patients with an eGFR 15–59 mL/min/1.73 m2. Methods: We retrospectively analyzed 68 cirrhosis patients with PKD (eGFR < 60 mL/min/1.73 m2) undergoing a TIPSS between April 2021 and April 2024. Clinical outcomes, renal function changes, and 12-month survival were assessed. Statistical analyses included paired t-tests with false discovery rate adjustment and Kaplan–Meier survival analysis to identify potential predictors of mortality. Results: The cohort (mean age 61.0 ± 8.3 years, 83.8% male, 79.4% with PKD G3a–G3b) showed modest improvement in renal function (creatinine 1.93 to 1.75 mg/dL, p = 0.031), though this biochemical change did not predict survival. Overall mortality was 36.8% (95% CI: 25.4–49.5%) at mean follow-up of 6.7 months. Traditional severity scores (MELD, Child–Turcotte–Pugh) showed no significant association with survival (p > 0.05 for all comparisons). In exploratory analyses, mortality was significantly higher in patients with the following: (1) uncontrolled diabetes before a TIPSS (55.2% vs. 25.9%; RR 2.35, 95% CI: 1.08–5.15, p = 0.032); (2) post-TIPSS infection (70.0% vs. 31.0%; HR 5.44, 95% CI: 1.54–19.23, p = 0.009); and (3) post-procedural cardiac events (85.7% vs. 31.1%; p = 0.005). These associations persisted after false-discovery rate adjustment but require prospective validation given the modest sample size and wide confidence intervals. Conclusions: In this exploratory single-center study of patients with moderate PKD undergoing a TIPSS, we observed associations between mortality and pre-TIPSS poorly controlled diabetes, infections, and cardiac events. These hypothesis-generating findings suggest potential areas for future research. Prospective multi-center studies are needed to validate these associations and determine whether interventions targeting these factors improve outcomes.
Background and Aims: Sepsis drives mortality in cirrhosis, yet the gut antimicrobial resistance (AMR) landscape remains unmapped in high-burden settings like India. This study aimed to integrate shotgun metagenomics with deep immunophenotyping to define the gut–immune–resistome axis and correlate specific microbial and genetic signatures with clinical outcomes in decompensated cirrhosis. Methods: We analysed 78 hospitalized patients with cirrhosis using stool shotgun metagenomics, multiplex cytokine arrays, and flow cytometry. The microbiome and resistome (AMR genes) were mapped and correlated with disease severity, immune function (monocyte HLA-DR, neutrophil CD64), and clinical endpoints including mortality. Results: Disease severity was characterized by a “Gram-negative bloom” (Klebsiella) alongside pathogenic Enterococcus expansion and novel markers: Clostridium sp. C5-48 (severe decompensation) and Sutterella (ascites). A specific, dense resistome predicted adverse outcomes; the quinolone-resistance gene QnrB4 correlated with mortality and immune paralysis, while the carbapenemase OXA-833 gene was linked to gastrointestinal bleeding. Notably, the commensal Ligilactobacillus salivarius was associated with systemic inflammatory cytokines. Conclusions: This study reveals a “pathogenic ecosystem” in Indian decompensated cirrhosis where the resistome is intrinsically linked to host immune failure. The identification of specific prognostic markers (QnrB4, OXA-833) and inflammatory associations with L. salivarius challenges generic probiotic use and underscores the urgent need for precision, resistome-targeted therapies.