Liver abscess in the caudate lobe caused by Klebsiella pneumoniae: a rare case report and literature review.

BACKGROUND: K. pneumoniae liver abscess (KPLA) mostly involves the right lobe. We present a case of K. pneumoniae caudate liver abscess with invasive liver abscess syndrome (ILAS) was rarely identified. CASE PRESENTATION: A 53-year-old man with elevated glycated hemoglobin with chills, rigors and a fever of five days. The patient presented with tachycardia and fever. Physical examination revealed tenderness over the right abdomen was elicited. In particular, the inflammatory markers were markedly elevated, and computerized tomography (CT) showed pulmonary abscess, pulmonary embolism and caudate liver abscess. The patient's sequential organ failure assessment (SOFA) score was 10 points. Klebsiella pneumoniae was isolated from sputum, urine and blood. With the suspicion of liver abscesses, ILAS and sepsis. The patient was successfully treated with antibiotics. He returned to close to his premorbid function. CONCLUSION: K. pneumoniae caudate liver abscess was rare. This is the first detailed report of K. pneumoniae caudate liver abscess with invasive liver abscess syndrome. Patients with cryptogenic K. pneumoniae liver abscess are advised to undergo an examination of intestinal barrier function. The study indicates that in patients with K. pneumoniae liver abscess, a caudate liver abscess size of ≤ 9.86 cm² may be characteristic of those suitable for conservative treatment of invasive liver abscess syndrome.

Co-administration of N-acetylcysteine and dexmedetomidine plays a synergistic effect on protection of LPS-induced acute lung injury via correcting Th1/Th2/Th17 cytokines imbalance.

Recently both N-acetylcysteine (NAC) and Dexmedetomidine (DEX) have shown emerging roles in protection of acute lung injury (ALI). However, how their protective roles work and whether they can provide synergistic effects in ALI remain unknown. Here we explored it from the hot research viewpoint of Th1/Th2/Th17 cytokines balance. Lipopolysaccharide (LPS)-induced ALI was established and treated with NAC and/or DEX. Mice were divided into Sham group, ALI group, NAC group, DEX group and NAC+DEX group. Mice were sampled at 6, 12 and 24 hours after the model construction. Histopathology, wet to dry ratio and myeloperoxidase (MPO) activity were assessed in lung tissues. Protein concentration and cell count were assessed in bronchoalveolar lavage fluid (BALF). Th1/Th2/Th17 cytokines were assessed in plasma, BALF and lung homogenate. ALI-induced lung morphological damage, edema and aberrant MPO activity can be attenuated by NAC or DEX and mostly by NAC+DEX. NAC with DEX significantly reduced ALI-induced protein leakage and cell infiltration in BALF. Th1/Th2/Th17 cytokines imbalance aggravated with ALI progression. NAC, DEX and especially NAC+DEX can effectively correct these unbalanced cytokines. Galectin-9 and Tim-3 were transcriptionally up-regulated in ALI. Combination of NAC with DEX obtained a maximum effect on decreasing Galectin-9/Tim-3 expression. In summary, Th1/Th2/Th17 cytokines imbalance is newly found to participate in LPS-induced ALI. NAC or DEX administration can attenuate ALI by rebalancing Th1/Th2/Th17 cytokines. Their protective roles can be enhanced when co-administration, because DEX may relieve the Galectin-9/Tim-3 axis-mediated immune suppression.

Bioinformatics Analysis of Gene Expression Profiles for Risk Prediction in Patients with Septic Shock.

BACKGROUND Septic shock occurs when sepsis is associated with critically low blood pressure, and has a high mortality rate. This study aimed to undertake a bioinformatics analysis of gene expression profiles for risk prediction in septic shock. MATERIAL AND METHODS Two good quality datasets associated with septic shock were downloaded from the Gene Expression Omnibus (GEO) database, GSE64457 and GSE57065. Patients with septic shock had both sepsis and hypotension, and a normal control group was included. The differentially expressed genes (DEGs) were identified using OmicShare tools based on R. Functional enrichment of DEGs was analyzed using DAVID. The protein-protein interaction (PPI) network was established using STRING. Survival curves of key genes were constructed using GraphPad Prism version 7.0. Each putative central gene was analyzed by receiver operating characteristic (ROC) curves using MedCalc statistical software. RESULTS GSE64457 and GSE57065 included 130 RNA samples derived from whole blood from 97 patients with septic shock and 33 healthy volunteers to obtain 975 DEGs, 455 of which were significantly down-regulated and 520 were significantly upregulated (P<0.05). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified significantly enriched DEGs in four signaling pathways, MAPK, TNF, HIF-1, and insulin. Six genes, WDR82, ASH1L, NCOA1, TPR, SF1, and CREBBP in the center of the PPI network were associated with septic shock, according to survival curve and ROC analysis. CONCLUSIONS Bioinformatics analysis of gene expression profiles identified four signaling pathways and six genes, potentially representing molecular mechanisms for the occurrence, progression, and risk prediction in septic shock.