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The Journal of Society Medicine (JSOCMED)
Published by PT. CoinReads Media Prima
ISSN : -     EISSN : 29645565     DOI : https://doi.org/10.47353/jsocmed.v2i1
Core Subject : Health, Science,
Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience
The Journal of Society Medicine (JSOCMED) | ISSN (e): 2964-5565 is a leading voice in the Indonesia and internationally for medicine and healthcare. Published continuously, JSOCMED features scholarly comment and clinical research. JSOCMED is editorially independent from and its The Editor-in-Chief (EIC) is Prof. dr. Aznan Lelo, PhD, SpFK. JSOCMED offers many attractive features for authors, including free online access to all research articles, online publication ahead of print, and online responses to articles published as Quick Comments. In addition, as befitting a publication of the Journal of Society Medicine, JSOCMED implements best practice in scientific publishing with an open peer review process, declarations of competing interests and funding, full requirements for patient consent and ethical review, and statements of guarantorship, contributorship, and provenance.
Arjuna Subject : Kedokteran - Kedokteran (Lain-Lain)
Articles 5 Documents
 1 
Search results for , issue "vol. 5 no. 3 (2026): march" : 5 Documents clear
Emerging Antimicrobial Resistance in Gram-Negative Pathogens: Protocol for a Pragmatic Cluster-Randomized Controlled Trial Khan , Ahsan Raza; Iqbal , Mehwish
Journal of Society Medicine Vol. 5 No. 3 (2026): March
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Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v5i3.269

Abstract

Introduction: Antimicrobial resistance among Gram-negative pathogens, including extended-spectrum β-lactamase (ESBL)-producing Enterobacterales and carbapenem-resistant Acinetobacter and Pseudomonas, is associated with high mortality and limited therapeutic options. Delayed initiation of effective antimicrobial therapy in bloodstream infections (BSIs) is consistently linked to adverse clinical outcomes. Although rapid diagnostic tests (RDTs) combined with antimicrobial stewardship (AS) improve the timeliness of therapy, high-quality evidence from resource-constrained settings remains limited. This study evaluates a pragmatic strategy integrating rapid diagnostics with stewardship to optimize early targeted therapy. Methods: This multicenter, parallel-group, pragmatic cluster randomized controlled trial includes 20 hospitals randomized to either an intervention bundle or standard care. The intervention comprises PCR-based pathogen and resistance gene identification, EUCAST rapid antimicrobial susceptibility testing (RAST), and a predefined stewardship algorithm for antibiotic optimization. Standard care includes routine culture, MALDI-TOF identification, and CLSI-guided susceptibility testing. Adult patients with confirmed Gram-negative BSIs are enrolled. The primary outcome is the proportion of patients receiving optimal targeted therapy within 24 hours of culture positivity. Secondary outcomes include time to effective therapy, 30-day mortality, hospital length of stay, adverse events, and antibiotic utilization. Analyses will follow an intention-to-treat approach using mixed-effects regression models. Results: As this manuscript presents a study protocol, no clinical outcome data are reported. Patient enrollment and trial implementation are ongoing across participating centers. Conclusion: This rigorously designed pragmatic cluster randomized trial will generate high-quality evidence on whether integrating rapid diagnostics with antimicrobial stewardship improves timely targeted therapy in Gram-negative BSIs, with direct implications for optimizing antimicrobial use and addressing global antimicrobial resistance.
Gut Microbiota as a Critical Modulator of Host Immune Responses in Severe Infections: Mechanistic Insights and Therapeutic Implications Chaiyasit, Anan; Wattanakul , Siriporn; Rattanapong , Kittisak
Journal of Society Medicine Vol. 5 No. 3 (2026): March
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Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v5i3.270

Abstract

Introduction: Severe infections, including sepsis and acute respiratory distress syndrome (ARDS), are the leading causes of morbidity and mortality worldwide, driven by dysregulated host immune responses. Emerging evidence has identified the gut microbiota as a critical regulator of systemic immunity; however, its mechanistic role in severe infection remains unclear. Methods: This narrative review synthesizes evidence from PubMed, Scopus, and Web of Science, focusing on mechanistic, translational, and clinical studies that evaluated microbiota–immune interactions in severe infections. Relevant studies were critically appraised and integrated to generate a mechanistic and clinically meaningful synthesis. Results: The gut microbiota maintains immune homeostasis through metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, which regulate epithelial integrity and T cell differentiation. In critical illness, dysbiosis, characterized by reduced diversity, loss of commensals, and pathogen overgrowth, disrupts these processes, leading to increased intestinal permeability, systemic inflammation, and organ dysfunction. Gut–organ axes, including gut–lung, gut–brain, and gut–kidney pathways, further amplify disease severity. Clinical evidence links dysbiosis to higher mortality and prolonged intensive care unit stays. Microbiota-targeted therapies, including probiotics, fecal microbiota transplantation, and precision interventions, show promise but remain limited by heterogeneity and insufficient high-quality evidence. Conclusion: Gut microbiota is a central modulator of host responses in severe infections, linking intestinal dysregulation and systemic immune dysfunction. Targeting microbiome-related pathways represents a promising strategy for precision critical care, although further mechanistic and clinical studies are required to establish effective therapies, improve patient outcomes in critical illness settings, and advance microbiome-based precision medicine.
Gut Microbiota–Driven Modulation of Host Immune Responses in Severe Infections: Mechanistic Insights and Translational Implications Fatima Bello; Chinedu Okafor
Journal of Society Medicine Vol. 5 No. 3 (2026): March
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Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v5i3.268

Abstract

Introduction: Severe infections, particularly sepsis and ICU-acquired infections, remain leading causes of global morbidity and mortality, primarily driven by dysregulated host immune responses. Increasing evidence positions the gut microbiota as a critical regulator of systemic immunity through bidirectional host–microbiome interactions, functioning not merely as a passive microbial reservoir but also as an active determinant of disease progression and clinical outcomes. Methods: A structured narrative synthesis was conducted using literature retrieved from PubMed, Embase, and Cochrane Library. Priority was given to high-quality randomized controlled trials, large observational cohorts, and mechanistic preclinical studies published within the past 10–15 years. Evidence was systematically appraised using standardized risk-of-bias frameworks, including Cochrane tools, and integrated into a translational model linking microbiome alterations with host immune dynamics. Results: Severe infections were consistently associated with rapid-onset gut dysbiosis, characterized by reduced microbial diversity and expansion of opportunistic pathogens. Five principal mechanistic domains were identified: immune system modulation, disruption of epithelial barrier integrity, altered microbial metabolite signaling, systemic microbial translocation, and antibiotic-induced ecological imbalance. Although observational data demonstrate strong associations between dysbiosis and adverse outcomes, interventional studies targeting the microbiome have reported heterogeneous efficacy, reflecting the underlying biological complexity and current therapeutic limitations. Conclusion: Gut microbiotas represent a dynamic and potentially modifiable regulator of host immune responses during severe infections. Future research should emphasize causal inference, precision microbiome-based interventions, and the integration of multi-omics approaches to develop mechanism-based therapeutic strategies and clinically actionable biomarkers to improve outcomes in critically ill patients.
Risk Factor–Weighted Clinical Probability for Predicting Obstructive Coronary Artery Disease in Patients Presenting with Unstable Angina Batubara , Gio Justisia; Hasan , Refli; Nasution , Ali Nafiah; Hasan, Harris; Lubis, Anggia Chairuddin; Andra, Cut Aryfa
Journal of Society Medicine Vol. 5 No. 3 (2026): March
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v5i3.271

Abstract

Introduction: Determining the optimal invasive strategy for patients with unstable angina remains challenging, often resulting in unnecessary coronary angiography. Existing risk scores, including the GRACE and TIMI scores, were not designed to predict obstructive coronary artery disease. This study evaluated the predictive performance of a risk factor–weighted clinical likelihood model. Methods: This retrospective analytical cohort study included 150 patients with low-to intermediate-risk unstable angina who underwent coronary angiography at a tertiary hospital. Predictive accuracy was assessed using receiver operating characteristic analysis and compared with the Diamond Forrester, Fladseth, guideline-based criteria, GRACE, and TIMI scores. Obstructive disease was defined as significant stenosis or physiologically relevant lesions. Results: The prevalence of obstructive coronary disease was 60%. The model demonstrated superior discrimination, with an area under the curve of 0.885, which exceeded that of the comparator models. At a threshold score, 42.7% of angiographies were safely deferred, with a negative predictive value of 76.6%. Calibration improved after model adjustment. Conclusion: The risk factor–weighted clinical likelihood model provides a robust prediction of obstructive coronary artery disease in patients with unstable angina. This may support objective decision-making and enable a more selective invasive strategy, thereby reducing unnecessary procedures while maintaining diagnostic safety.
Postoperative Pulmonary Hypertension After Complete Tetralogy of Fallot Repair: Mechanistic Determinants and Prognostic Implications for Early Clinical Outcomes Damayanti , Eka; Tavianto, Doddy
Journal of Society Medicine Vol. 5 No. 3 (2026): March
Publisher : CoinReads Media Prima

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.71197/jsocmed.v5i3.272

Abstract

Introduction: Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, with an incidence of approximately three per 10,000 live births. Postoperative pulmonary hypertension following complete repair is a rare but life-threatening complication that may lead to weaning failure from cardiopulmonary bypass. This condition is driven by acute increases in pulmonary vascular resistance and impaired right ventricular–pulmonary arterial coupling. Recognized risk factors include chronic preoperative hypoxia, younger age at surgery, and severe right ventricular dysfunction. Case Description: A three-year-old child with stunted growth and longstanding cyanosis since infancy underwent evaluation, revealing a large malaligned ventricular septal defect, 50% overriding aorta, and severe pulmonary stenosis with a pressure gradient of 85 mmHg. Intraoperative findings confirmed a double-outlet right ventricle with multiple atrial septal defects. Following total correction, the patient was not weaned from cardiopulmonary bypass because of acute right ventricular failure and severe pulmonary hypertension. Atrial septal defect creation for decompression and maximal inotropic support with dobutamine, adrenaline, and milrinone were performed. Despite aggressive management, the patient progressed to refractory cardiogenic shock with an arterial pressure of 25/19 mmHg and died within 24 hours postoperatively. Conclusion: This case underscores the catastrophic impact of postoperative pulmonary hypertensive crises in patients with complex congenital heart disease. The failure of weaning from cardiopulmonary bypass due to acute right ventricular failure represents a critical inflection point associated with extremely high mortality. Early risk stratification, perioperative optimization, and timely consideration of advanced mechanical circulatory support are essential. The integration of targeted pulmonary vasodilator therapy with vigilant hemodynamic monitoring may improve right ventricular adaptation and clinical outcomes in high-risk patients.

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