Background: This study investigated perioperative clinical risk factors for early post-transplant bacteremia in patients undergoing living donor liver transplantation (LDLT). Additionally, postoperative outcomes were compared between patients with and without early post-transplant bacteremia. Methods: Clinical data of 610 adult patients who underwent elective LDLT between January 2009 and December 2018 at Seoul St. Mary's Hospital were retrospectively collected. The exclusion criteria included overt signs of infection within 1 month before surgery. A total of 596 adult patients were enrolled in this study. Based on the occurrence of a systemic bacterial infection after surgery, patients were classified into non-infected and infected groups. Results: The incidence of bacteremia at 1 month after LDLT was 9.7% (57 patients) and Enterococcus faecium (31.6%) was the most commonly cultured bacterium in the blood samples. Univariate analysis showed that preoperative psoas muscle index (PMI), model for end-stage disease score, utility of continuous renal replacement therapy (CRRT), ascites, C-reactive protein to albumin ratio, neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio, and sodium level, as well as intraoperative post-reperfusion syndrome, mean central venous pressure, requirement for packed red blood cells and fresh frozen plasma, hourly fluid infusion and urine output, and short-term postoperative early allograft dysfunction (EAD) were associated with the risk of early post-transplant bacteremia. Multivariate analysis revealed that PMI, the CRRT requirement, the NLR, and EAD were independently associated with the risk of early post-transplant bacteremia (area under the curve: 0.707; 95% confidence interval: 0.667-0.745; p < 0.001). The overall survival rate was better in the non-infected patient group. Among patients with bacteremia, anti-bacterial treatment was unable to resolve infection in 34 patients, resulting in an increased risk of patient mortality. Among the factors included in the model, EAD was significantly correlated with non-resolving infection. Conclusions: We propose a prognostic model to identify patients at high risk for a bloodstream bacterial infection; furthermore, our findings support the notion that skeletal muscle depletion, CRRT requirement, systemic inflammatory response, and delayed liver graft function are associated with a pathogenic vulnerability in cirrhotic patients who undergo LDLT.
Background: Chemotherapy-induced neuropathic pain is a disabling condition following cancer treatment. Vincristine has more neurotoxicity than other vinca alkaloid agents. This study evaluated the correlation of different doses of nefopam with antiallodynic effects in a mouse vincristine neuropathy model. Methods: A peripheral neuropathic mouse model was made by intraperitoneal injection of vincristine (0.1 mg/kg/day; 5-day-on, 2-day-off schedule over 12 days). After the development of allodynia, mice were injected intraperitoneally with 0.9% normal saline (NS group) or various doses (10, 30, 60 mg/kg) of nefopam (Nefopam group). We examined allodynia using von Frey hairs pre-administration and at 30, 60, 90, 120, 180, 240 mins, and 24 hrs after drug administration. We also measured the neurokinin-1 receptor concentrations in the spinal cord to confirm the antiallodynic effect of nefopam after drug administration. Results: The peripheral neuropathic mouse model showed prominent mechanical allodynia. Intraperitoneal nefopam produced a clear dose-dependent increase in paw withdrawal threshold compared with pre-administration values and versus the NS group. The concentration of neurokinin-1 receptor was significantly decreased in the Nefopam group (P<0.05). Conclusion: Intraperitoneally administered nefopam yielded a dose-dependent attenuation of mechanical allodynia and decreased neurokinin-1 receptor concentration, suggesting that the neurokinin-1 receptor is involved in the antiallodynic effects of nefopam in vincristine neuropathy.
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