Tropical Medicine and Infectious Disease, Journal Year: 2025, Volume and Issue: 10(2), P. 39 - 39
Published: Jan. 29, 2025
Background: Severe yellow fever (YF) can result in acute liver failure (ALF) and high mortality. The role of therapeutic plasma exchange (TPE) managing YF-ALF remains unclear. This study evaluated the impact TPE strategies severe YF. Methods: observational case-series three groups patients classified according to treatment: G1 (standard intensive care support [ICS]), G2 (ICS + high-volume-TPE [HV-TPE]), G3 TPE). HV-TPE was performed during 3 consecutive days with extra sessions one plasma-volume, if necessary, whereas consisted volume/session twice daily, additional fresh frozen infusion. Hemostatic agents, including tranexamic acid, platelets, cryoprecipitate, were administered as needed. de-escalated based on clinical laboratory parameters. primary outcome Results: Sixty-six included (G1: 41, G2: 11, G3: 14). Groups had similar baseline characteristics. Mortality significantly lower (14%) compared (82%) (85%) (p < 0.001). Additionally, showed a higher frequency undetectable YF viral load. Conclusions: Intensive is feasible effective intervention for YF, achieving an 84% reduction limitations our results are small sample size, single-center study. Further studies warranted elucidate TPE’s management.
Language: Английский
Citations
1Infezioni in Medicina, Journal Year: 2024, Volume and Issue: 4(32)
Published: Dec. 1, 2024
Yellow fever poses a substantial global health concern as one of the re-emerging diseases with pandemic potential in scenario worldwide distribution some vectors (such
Language: Английский
Citations
4Published: Jan. 1, 2025
Language: Английский
Citations
0bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown
Published: March 5, 2025
ABSTRACT Yellow fever (YF) is classically conceptualized as a hepatotropic disease; indeed, the liver primary site of yellow virus (YFV) replication. However, circumstantial evidence suggests that extra-hepatic disease may be important for ∼30% YF cases progress to severe “intoxication” phase disease. Using Syrian hamster-adapted (HA)-YFV, we worked backwards from observations in humans examine early events precipitate intoxication YF. HA-YFV caused ∼80% infected animals characterized by lethargy and weight loss progressed widespread petechiae death day 6. Clinical chemistry, coagulation testing, histology, immunohistochemistry, in-situ hybridization were consistent with cascade hepatocyte-specific replication causing damage defect clotting factor synthesis. Despite lack replication, pathology was observed intestines pancreas. Histopathological analysis over time-course infection revealed an ischemic pattern these tissues, culminating fibrinoid/coagulative necrosis organs. Further investigation showed ischemia-induced erosion gut epithelial barrier serves entry point luminal bacteria spread systemically via portal system. Thus, sepsis-like syndrome translocation damaged gastrointestinal tract. Evaluation human previously overlooked features confirmed this overarching mechanism: identified vein parenchyma fatal along elevations plasma markers bacteremia bacteria-driven inflammatory response. Importantly, blood concentrations marker intestinal fatty acid binding protein (I-FABP) significantly elevated relative non-fatal cases, suggesting I-FABP measurements could useful prognosis treatment decision making. Our findings tie together several recent historically unexplained surrounding highly-lethal humans: high AST/ALT ratio, “black vomit,” pancreatitis, paradoxical neutrophilia. A better appreciation drivers mesenteric ischemia, preemption bacterial sepsis, improve outcomes
Language: Английский
Citations
0Frontiers in Microbiology, Journal Year: 2024, Volume and Issue: 15
Published: Oct. 8, 2024
Since December 2019, coronavirus disease 2019 (COVID-19) has been spreading worldwide with devastating immediate or long-term effects on people’s health. Although the lungs are primary organ affected by COVID-19, individuals infected SARS-CoV-2 also develop systemic lesions involving multiple organs throughout body, such as cardiovascular system. Emerging evidence reveals that COVID-19 could generate myocardial fibrosis, termed “COVID-19-associated fibrosis.” It can result from activation of fibroblasts via renin-angiotensin-aldosterone system (RAAS), transforming growth factor-β1 (TGF-β1), microRNAs, and other pathways, occur in cellular interactions SARS-CoV-2, immunocytes, endothelial cells. Nonetheless, to gain a more profound insight into natural progression COVID-19-related additional investigations necessary. This review delves underlying mechanisms contributing COVID-19-associated fibrosis while examining antifibrotic potential current treatments, thereby offering guidance for future clinical trials these medications. Ultimately, we propose research directions post-COVID-19 era, artificial intelligence (AI) telemedicine. We recommend relevant tests be added follow-up patients detect promptly.
Language: Английский
Citations
2Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: unknown, P. 156888 - 156888
Published: Oct. 1, 2024
Language: Английский
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2EBioMedicine, Journal Year: 2024, Volume and Issue: 109, P. 105409 - 105409
Published: Oct. 24, 2024
Language: Английский
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2Current Emergency and Hospital Medicine Reports, Journal Year: 2024, Volume and Issue: 12(2), P. 53 - 59
Published: April 22, 2024
Language: Английский
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0Vaccine, Journal Year: 2024, Volume and Issue: 43, P. 126423 - 126423
Published: Nov. 21, 2024
Language: Английский
Citations
0Published: Nov. 30, 2023
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0