Analysis of risk factors for early-onset ventilator-associated pneumonia in a neurosurgical intensive care unit.

BACKGROUND: Ventilator-associated pneumonia (VAP) is a severe infection among patients in the neurosurgery intensive care unit (NICU). METHODS: We retrospectively evaluated risk factors for early-onset ventilator-associated pneumonia (EOVAP) from January 2019 to December 2019 at a NICU. A total of 89 NICU patients who were intubated within 48 h of onset and whose mechanical ventilation time was at least 7 days were enrolled. We evaluated EOVAP that occurred within the first 7 days after the onset of mechanical ventilation. The enrolled patients had no history of chronic lung disease and no clinical manifestations of infection before intubation. Clinical data of patients were recorded, and the incidence of and risk factors for EOVAP were analyzed. Patients were also grouped by age (≥ 65 vs. < 65 years) and whether they had received hypothermia treatment or not. RESULTS: Among 89 mechanically ventilated patients (49 men and 40 women; the mean age ± SD was 60.1 ± 14.3 years), 40 patients (44.9%) developed EOVAP within 7 days and 14 patients (15.7%) had a multidrug resistant bacterial infection. Binary logistic regression analysis indicated that older age (≥ 65 years) (odds ratio [OR]:3.53, 95% confidence interval [CI]:1.27-9.79, P = 0.015) and therapeutic hypothermia (OR:3.68, CI:1.10-12.31, p = 0.034) were independent predictors of EOVAP. Levels of peripheral blood leukocytes, neutrophils and platelets were lower in the therapeutic hypothermia group than those who did not receive hypothermia treatment. CONCLUSIONS: This study found that older age (≥ 65 years) and therapeutic hypothermia were independently associated with the risk of EOVAP in NICU patients.

The Role of Human Leukocyte Antigen-DR in Regulatory T Cells in Patients with Virus-Induced Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

BACKGROUND This study assessed the role of different immune phenotypes of T cells in virus-induced acute exacerbation of chronic obstructive pulmonary disease (AECOPD). MATERIAL AND METHODS The study involved 103 participants, including individuals with virus-induced AECOPD (n=32), non-virus-induced AECOPD (n=31), and stable COPD (n=20) and individuals who were healthy smokers (n=20). The immune phenotypes of T cells in peripheral blood were evaluated via flow cytometry analysis, and the differences were analyzed. RESULTS Patients with virus-induced AECOPD (virus group) had a higher COPD assessment test score on admission than those in the group with non-virus-induced AECOPD (nonvirus group; 25.6±3.8 vs 21.9±4.8, P=0.045). A lower CD4⁺ human leukocyte antigen-DR (HLA-DR)+ frequency was found in the peripheral blood of the virus group compared with the nonvirus group (2.2 vs 4.2, P=0.015), and the frequency of CD4⁺ CD25high CD127low HLA-DR⁺ in CD4⁺ in the virus group was lower than in the nonvirus group (1.1 vs 3.6, P=0.011). The CD3⁺, CD4⁺, CD8⁺, CD4⁺ central memory T cell, CD4⁺ effector memory T cell (Tem), CD4⁺ end-stage T cell, and CD8⁺ Tem levels in lymphocytes of peripheral blood were lower in exacerbation groups relative to those in the stable COPD and healthy smoking groups, but similar between exacerbation groups. Similar frequencies and levels of T cells between different stagings of COPD were also identified. CONCLUSIONS The expression of HLA-DR on the cell surface of CD4⁺ regulatory T cells (Tregs) was lower in the peripheral blood of patients with virus-induced AECOPD. The expression of HLA-DR in CD4⁺ Tregs suggested the effect of respiratory viruses on adaptive immunity of patients with AECOPD to some extent.

Remission of hepatotoxicity in chronic pulmonary aspergillosis patients after lowering trough concentration of voriconazole.

BACKGROUND: Chronic pulmonary aspergillosis (CPA) is a rare syndrome that is often accompanied by gradual lung tissue destruction. Voriconazole is usually employed as the first-line agent for CPA treatment. However, some patients can develop hepatotoxicity and often were forced to stop voriconazole treatment. AIM: To record the improving trend of liver function and the therapeutic effects in patients after lowering the trough concentration of voriconazole. METHODS: This study retrospectively analyzed 12 adult CPA patients who developed hepatotoxicity during the voriconazole treatment. In these patients, the oral dose was reduced to 3/4 or 1/2 of the standard dose (4 mg/kg, twice daily), and the lower limit of voriconazole trough concentration was maintained more than 0.5 µg/mL. The trend of remission of liver toxicity after drug reduction in 12 patients was recorded. During the same period, 25 patients who received standard doses served as the control group. Data from the two groups were collected and analyzed for different parameters such as demographic characteristics, underlying pulmonary disorders, laboratory tests, and therapeutic effect. The differences between the two groups were statistically compared. RESULTS: Hepatotoxicity occurred in 12 patients within 28-65 d after oral voriconazole treatment. Hepatotoxicity was mainly manifested by the significantly increased level of gamma-glutamyltransferase and a slight increase of alanine aminotransferase and aspartate aminotransferase. The oral dose of voriconazole was reduced to approximately 3 mg/kg in seven patients and approximately 2 mg/kg in five patients. The average trough concentrations for the 12 patients before and after voriconazole oral dose reduction were 3.17 ± 1.47 µg/mL (1.5-6.0 µg/mL) and 1.70 ± 0.78 µg/mL (0.6-3.3 µg/mL), respectively (P = 0.02). After lowering the trough concentrations, the hepatotoxicity was alleviated in all the patients. However, gamma-glutamyltransferase levels declined slowly. After 4 mo of treatment, 7 of the 12 patients were successfully treated in the low trough concentrations group (41.7%). Similarly, 8 of the 25 patients in the standard treatment dose group (32.0%) were effectively treated. There was no statistical difference between the groups (P = 0.72). CONCLUSION: Reducing the lower limit of the voriconazole trough concentration to 0.5 µg/mL can alleviate the hepatotoxicity and maintained certain clinical efficacy in CPA patients; however, patients should be closely monitored.