Successful treatment of 1 patient with chlorine-induced ARDS using awake self-prone positioning and nasal high-flow oxygen: A case report.

RATIONALE: Accidents involving chlorinated compounds in the context of cleaning are not uncommon. However, improving the treatment success rate for acute respiratory distress syndrome (ARDS) patients caused by chlorine gas presents significant challenges. PATIENT CONCERNS: A 28-year-old female was admitted to the intensive care unit after accidental inhalation of chlorine gas resulting in ARDS. DIAGNOSES: The patient was diagnosed with ARDS attributed to chlorine gas exposure. INTERVENTIONS: The intervention involved utilizing a combination of awake self-prone positioning (ASPP) and high-flow nasal oxygen therapy for treatment. OUTCOMES: After continuous ASPP and high-flow nasal oxygen therapy, the patient quickly recovered and was transferred out of the intensive care unit on the 6th day without any adverse events. LESSONS: ASPP combined with high-flow nasal oxygen therapy can improve patients' hypoxemia, prevent the need for intubation, avoid rapid deterioration of the condition, reduce treatment complexity, and lower mortality rate.

[Secretory leukocyte peptidase inhibitor inhibits the inflammatory response and apoptosis of lipopolysaccharide-induced human proximal renal tubular cells].

OBJECTIVE: To screen out the potential key genes of sepsis-associated acute kidney injury (AKI), and provide theoretical and experimental evidence for the treatment of sepsis-associated AKI. METHODS: (1) Bioinformatics analysis: two gene expression datasets (GSE30718 and GSE53773) were downloaded for bioinformatics analysis from the Gene Expression Omnibus (GEO). These two datasets recorded mRNA microarray data from kidney biopsies before and after kidney transplantation, and a subset of patients developed AKI after kidney transplantation. Differential analysis was conducted, and the genes with the same differential expression and a higher area under the receiver operator characteristic curve (AUC) in both databases were used as the target gene for subsequent cell experiments. (2) Cell validation experiment: human proximal renal tubular cells HK2 were cultured in vitro, and lipopolysaccharide (LPS) was used for establishing LPS-HK2 cell model (LPS 10 mg/L for 6 hours, LPS model group), and the blank control group was set. Then, small interfering RNA (siRNA) technology was used to knock down the target gene obtained by bioinformatics analysis in LPS-HK2 cells (gene knockdown group), and a gene negative control group was set. The real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-qPCR) technique was used to detect the expression of the target gene in HK2 cells. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory factors in the cell supernatants. Western blotting was used to detect the expressions of key apoptosis proteins. RESULTS: (1) Results of bioinformatics analysis: 325 genes in the two datasets showed the same expression trend, of which 144 were significantly down-regulated and 181 were significantly up-regulated, while the expression difference of secretory leukocyte protease inhibitor (SLPI) in the two datasets was both statistically significant. Further receiver operator characteristic curve (ROC curve) analysis confirmed that the SLPI expression in GSE30718 and GSE53773 datasets had a high diagnostic efficiency for AKI, with AUC of 0.83 and 0.92, respectively. Therefore, SLPI was selected as the target gene for subsequent cell validation experiment. (2) Cell validation experiment: the RT-qPCR analysis showed that the expression of SLPI in LPS-HK2 cells of the LPS model group was significantly higher than that of the blank control group (2-ΔΔCT: 1.80±0.14 vs. 1.00±0.11, P < 0.01), and the change trend was the same with the results of bioinformatics analysis. Furthermore, knockdown SLPI gene analysis showed that the levels of inflammatory factors in LPS-HK2 cells supernatants in the gene knockdown group were significantly higher than those in the negative control group [Interleukin-6 (IL-6, ng/L): 509.58±27.08 vs. 253.87±75.83, IL-1ß (ng/L): 490.99±49.52 vs. 239.67±26.97, tumor necrosis factor-α (TNF-α, ng/L): 755.22±48.66 vs. 502.06±10.92, all P < 0.01]. The above results indicated that SLPI could inhibit the inflammatory response of HK2 cells induced by LPS. The expressions of key apoptosis proteins Bax and caspase-3 in LPS-HK2 cells in the gene knockdown group were significantly higher than those in the negative control group [Bax protein (Bax/GAPDH): 1.38±0.12 vs. 1.00±0.10, caspase-3 protein (caspase-3/GAPDH): 1.44±0.15 vs. 1.00±0.11, both P < 0.05], and Bcl-2 expression was significantly decreased (Bcl-2/GAPDH: 0.83±0.08 vs. 1.00±0.05, P < 0.05), the above results indicated that SLPI could inhibit the apoptosis of cells in the inflammatory response. CONCLUSIONS: SLPI can inhibit the inflammatory response and apoptosis of HK2 cells induced by LPS, which may be involved in the protective mechanism of renal tubular cells in the response to sepsis, and is a potential target for the treatment of sepsis-associated AKI.

[Clinical characteristics analysis of patients with pneumonia infected by Chlamydia psittaci].

OBJECTIVE: To explore the clinical characteristics of pneumonia infected by Chlamydophila psittaci (C. psittaci). METHODS: A retrospective analysis was performed on 3 cases of C. psittaci pneumonia admitted to People's Hospital of Tongling City from July 2019 to January 2020. The patients' contact history, clinical manifestations, laboratory examination, imaging characteristics and evolution, etiology, treatment process and outcome were analyzed, so as to provide experience for the diagnosis and prevention of C. psittaci pneumonia. RESULTS: The 3 patients had been infected through pet or zoonotic exposures. All symptoms included high fever (body temperature > 39 centigrade), cough, sputum, chest tightness and dyspnea. The disease progressed rapidly, with severe acute respiratory distress syndrome (ARDS) and shock as the main manifestations, but the damages to the heart, liver and kidney were mild. Laboratory tests showed that C-reactive protein (CRP, all > 200 mg/L) and neutrophil proportion (Neut%, > 0.90) were significantly increased, while white blood cell count (WBC) and procalcitonin (PCT) were not significantly increased. Chest computed tomography (CT) showed inflammatory infiltration with interstitial changes, either unilateral or bilateral. Chest X-ray showed large areas of inflammatory infiltrations, fan-shaped or wedge-shaped to the edge of pleura. After 7 days of treatment, the bedside computed X-ray (CR) showed absorption of infiltration. After 11-13 days, the CT reexamination indicated lung infection was basically absorbed. Metagenomic next-generation sequencing (mNGS) confirmed the presence of C. psittaci in patients' sputum. It was sensitive to quinolones and tetracyclines. The patients' body temperature dropped to normal after 2-3 days of antibiotics, and all patients were extubated and transferred to normal ward 10 days later. The total course of illness was 20-30 days. CONCLUSIONS: The patients with C. psittaci pneumonia are critically ill, and clinical manifestations of moderate to severe ARDS and shock are common. Early diagnosis depends on mNGS, and reasonable treatment is important for prognosis.