Eurasian Journal of Chemical, Medicinal and Petroleum Research

Abstract Introduction: Ventilator-associated pneumonia (VAP) remains a major intensive care unit complication, contributing to prolonged mechanical ventilation, antimicrobial overuse, multidrug resistance, and increased mortality. Despite advances in prevention and conventional antibiotics, treatment failure remains frequent. This study aims to review and highlight novel therapeutic strategies for improving clinical outcomes in patients with VAP.
Material and methods: This systematic review was conducted according to PRISMA guidelines. PubMed, Scopus, Web of Science, EMBASE, Google Scholar, SID, and Magiran were systematically searched using keywords including “ventilator-associated pneumonia,” “VAP,” “novel therapeutic strategies,” “bacteriophage therapy,” “immunotherapy,” “monoclonal antibodies,” “inhaled antibiotics,” and “multidrug-resistant pathogens,” combined with Boolean operators to identify eligible studies on emerging VAP treatments.
Results: Synthesis of six eligible studies (n = 6; RCTs: 33.3%, cohort designs: 33.3%) demonstrated that novel VAP strategies enhanced microbiological clearance and clinical cure against MDR/XDR pathogens. Rapid molecular diagnostics reduced time to targeted therapy, whereas resistance-guided regimens improved treatment adequacy. Overall methodology exhibited low risk of bias across key Cochrane domains (>80% domain adequacy), validating the clinical reliability of these precision-guided and adjunctive therapeutic modalities.
Conclusion: Novel therapeutic strategies, including inhaled antibiotics, bacteriophages, monoclonal antibodies, and rapid diagnostic-guided regimens, offer effective alternatives for managing multidrug-resistant VAP. Integrating these precision-driven and adjunctive modalities optimizes targeted pathogen clearance, mitigates systemic toxicity, and improves clinical management in intensive care settings. Future large-scale clinical trials remain essential to standardize protocols and validate long-term clinical efficacy.

Abstract Introduction: ACVRL1 (ALK1) mutations are critical drivers of pulmonary hypertension, significantly influencing endothelial dysfunction and vascular remodeling. Despite its clinical importance, the precise prognostic impact of ALK1 on disease progression remains insufficiently characterized across diverse populations. This systematic review aims to evaluate the prognostic role of ACVRL1/ALK1 in the development and outcomes of pulmonary hypertension.
Material and methods: This systematic review was conducted according to PRISMA guidelines to evaluate the prognostic role of ACVRL1/ALK1 in pulmonary hypertension. Eligible human studies were systematically identified from international and national databases, screened against predefined inclusion and exclusion criteria, and assessed for methodological quality. Data on study characteristics, sample size, mutation status, hemodynamic parameters, disease progression, survival, and clinical outcomes were extracted using a standardized approach.
Results: Synthesis of 11 studies (n=11; cohort, case-control, and genetic designs) confirms that ACVRL1/ALK1 mutations independently correlate with earlier disease onset and accelerated clinical decline. Carriers exhibited significantly worse hemodynamic profiles (e.g., higher pulmonary arterial pressures) and increased right ventricular strain compared to non-carriers. Qualitative synthesis indicates higher risk stratification scores and diminished survival rates, underscoring ACVRL1 as a pivotal genetic determinant of aggressive pulmonary hypertension phenotypes and poor clinical outcomes.
Conclusion: ACVRL1/ALK1 mutations serve as a critical prognostic biomarker in pulmonary hypertension, identifying a high-risk cohort characterized by early-onset disease and rapid hemodynamic deterioration. Incorporating ACVRL1 genotyping into clinical risk stratification is essential for optimizing surveillance and initiating aggressive, personalized therapeutic interventions. Future prospective multicenter trials are necessary to refine genotype-specific survival estimates and standardize long-term management protocols for this vulnerable patient population.