Association between Advanced Lung Inflammation Index and 30-Day Mortality in Patients with Acute Respiratory Distress Syndrome.

Background and objectives: The advanced lung inflammation index (ALI) was developed to assess the degree of systemic inflammation and has an association with prognosis in patients with lung malignancy. The prognostic value of ALI has not yet been evaluated in patients with acute respiratory distress syndrome (ARDS). Materials and Methods: Between January 2014 and May 2018, patients with ARDS in the medical intensive care unit (ICU) were reviewed retrospectively. The ALI value was calculated as the (body mass index × serum albumin level)/neutrophil-lymphocyte ratio. The cut-off value for distinguishing low from high ALI was defined according to receiver-operating characteristic curve analysis. Results: A total of 164 patients were analyzed. Their median age was 73 years, and 73% was male. The main cause of ARDS was pneumonia (95.7%, 157/164). ICU and in-hospital mortality rates were 59.8% (98/164) and 64% (105/164), respectively. The 30 day mortality was 60.9% (100/164). The median ALI value in non-survivors was lower than that in survivors at 30 day (3.81 vs. 7.39, p = 0.005). In multivariate analysis, low ALI value (≤5.38) was associated with increased 30 day mortality (odds ratio, 2.944, confidence interval 1.178-7.355, p = 0.021). Conclusions: A low ALI value was associated with increased 30 day mortality in patients with ARDS.

Aged red garlic extract reduces cigarette smoke extract-induced cell death in human bronchial smooth muscle cells by increasing intracellular glutathione levels.

Increasing antioxidant capacity has been proposed as a promising strategy to prevent cigarette smoke-induced lung diseases. This study tested whether garlic extracts prevented cigarette smoke extract (CSE)-induced cell death in human bronchial smooth muscle cells (HBSMCs). Garlic extracts were prepared from fresh raw garlic (FRG), aged black garlic (ABG) and aged red garlic (ARG). Treatment of HBSMCs with 10% CSE induced cell death accompanied by activation of caspase. Of the garlic extracts, treatment with ARG extract reduced CSE-induced cell death. The combination of ARG extract with CSE attenuated the CSE-induced reduction in glutathione (GSH) content, generation of reactive oxygen species (ROS) and induction of heme oxygenase-1 expression compared with CSE treatment without ARG extract. Furthermore, the combination of L-BSO, a GSH synthesis inhibitor, with ARG and CSE extracts failed to increase the intracellular GSH content and cell viability. Taken together, these results demonstrate that ARG extract reduces CSE-induced cell death by increasing GSH content and reducing ROS generation in HBSMCs.

Aged red garlic extract suppresses nitric oxide production in lipopolysaccharide-treated RAW 264.7 macrophages through inhibition of NF-κB.

Lipopolysaccharides (LPS) activate nuclear factor kappa B (NF-κB), a transcription factor that is involved in inflammatory response. The pathways that activate NF-κB can be modulated by phytochemicals derived from garlic. We recently demonstrated that aged red garlic extract (ARGE), a new formulation of garlic, decreases nitric oxide (NO) generation by upregulating of heme oxygenase-1 (HO-1) in RAW 264.7 cells activated by LPS. However, the effects of ARGE on LPS-induced NF-κB activation are unknown. This study was performed to evaluate whether ARGE regulates LPS-induced NO production by modulation of NF-κB activation in macrophages. The inhibition of NF-κB by Bay 11-7085, an inhibitor of NF-κB, decreased LPS-induced NO production. ARGE treatment markedly reduced LPS-induced NO production and NF-κB nuclear translocation. ARGE downregulated expression of inducible nitric oxide synthase (iNOS) and upregulated expression of HO-1, a cytoprotective and anti-inflammatory protein. However, Bay 11-7085 only reduced iNOS expression. The NO production and iNOS expressions upregulated by suppression of HO-1 were suppressed by treatment with ARGE and Bay 11-7085. These results show that ARGE reduces LPS-induced NO production in macrophages through inhibition of NF-κB nuclear translocation and HO-1 activation. Compared to Bay 11-7085, ARGE may enhance anti-inflammatory effects by controlling other anti-inflammatory signals as well as regulation of NF-κB.

A case of hypersensitivity syndrome to both vancomycin and teicoplanin.

Drug hypersensitivity syndrome to both vancomycin and teicoplanin has not been previously reported. We describe here a 50-yr-old male patient with vertebral osteomyelitis and epidural abscess who developed hypersensitivity syndrome to both vancomycin and teicoplanin. Skin rash, fever, eosinophilia, interstitial pneumonitis, and interstitial nephritis developed following the administration of each drug, and resolved after withdrawing the drugs and treating with high dose corticosteroids. The vertebral osteomyelitis was successfully treated with 6-week course of linezolid without further complications. Skin patch tests for vancomycin and teicoplanin was done 2 months after the recovery; a weak positive result for vancomycin (10% aq.,+at D2 and +at D4 with erythema and vesicles; ICDRG scale), and a doubtful result for teicoplanin (4% aq.-at D2 and+/-at D4 with macular erythema; ICDRG scale). We present this case to alert clinicians to the hypersensitivity syndrome that can result from vancomycin and teicoplanin, with possible cross-reactivity, which could potentially be life-threatening.