BackgroundThis study was designed to evaluate the efficacy of exchange transfusion in patients with severe imported falciparum malaria. Twelve patients who met the diagnostic criteria for severe malaria were treated with exchange transfusion 14 times according to a conventional anti-malarial treatment. This study evaluated the efficacy of exchange transfusion for severe imported falciparum malaria.MethodsClinical data of severe imported falciparum malaria patients admitted to the intensive care unit (ICU) of Nantong Third People’s Hospital from January 2007 to December 2016 were investigated in this retrospective study. Patients were divided into the intervention group, which received exchange transfusion, and the control group. This study assessed parasite clearance and outcomes of the two groups, and levels of erythrocytes, haemoglobin, platelets, coagulation, liver function, lactate, C-reactive protein, and procalcitonin, before and after exchange transfusion in the intervention group.ResultsThere was no significant difference in the severity of admitted patients. Exchange transfusion was successfully applied 14 times in the intervention group. Differences in the levels of erythrocytes, haemoglobin and platelets did not reach statistical significance. Exchange transfusion improved coagulation, liver function, lactic acid, C-reactive protein, and procalcitonin. No differences were observed in parasite clearance, ICU and hospital length of stay, in-hospital mortality, and costs of hospitalization between the two groups.ConclusionExchange transfusion as adjunctive therapy for severe malaria was observed to be safe in this setting. Exchange transfusion can improve liver function and coagulation and reduce inflammation, but it failed to improve parasite clearance and the outcomes of severe imported falciparum malaria in this case series.

Mucosal‐associated invariant T (MAIT) cells are important in antibacterial immune responses; however, during sepsis, they are few in number and exhibit highly activated phenotypes. The relationship between MAIT cells in peripheral blood and the prognosis of sepsis is not well understood. Thus, this study aimed to examine the levels and phenotypes of MAIT cells in early sepsis, evaluate their clinical relevance, and investigate their association with patient prognosis. This prospective observational study enrolled 72 septic patients defined according to the Sepsis 3.0 criteria and 21 healthy controls matched for age and sex. Their peripheral blood samples were used to assay the expression of immune activation (CD69 and HLA‐DR) and immune checkpoint (PD‐1 and PD‐L1) markers on MAIT cells. The systemic inflammatory response syndrome, acute physiology and chronic health evaluation (APACHE) II, and sequential organ failure assessment scores were recorded. Subsequently, the association between MAIT cell characteristics and clinical indicators was assessed using Spearman's rank correlation analysis, and binary logistic regression analysis with a forward stepwise approach assessed independent risk factors for 28‐day mortality. We noted a decrease in the percentage of MAIT cells in the patients' peripheral blood, which exhibited an activated phenotype. Besides, HLA‐DR+ MAIT cell percentage and the APACHE II score were independently associated with the 28‐day mortality and, in combination, were the best indicators of mortality. Thus, the percentage of HLA‐DR+ MAIT cells in early sepsis serves as a novel prognostic biomarker for predicting mortality and improves the predictive capacity of the APACHE II score.

Rationale:Extensive thrombosis in the portal venous system caused by hypereosinophilic syndrome (HES) is rare, and there is no consensus on anticoagulant and thrombolytic treatments for arteriovenous thrombosis caused by HES.Patient concerns:The clinical data of a patient with extensive thrombosis in his portal venous system (superior mesenteric, splenic, hepatic, and portal veins), renal artery thrombosis, and mesenteric thrombosis caused by HES with secondary gastrointestinal bleeding and intestinal necrosis were retrospectively analyzed. Before admission, his eosinophil count increased to 7.47 × 109/L, and HES had been confirmed via bone marrow cytology. The patient experienced fever, cough, abdominal pain, massive hematemesis, and hematochezia that developed in succession. Abdominal computed tomography showed portal vein and superior mesenteric vein thromboses.Diagnosis:Hypereosinophilic syndrome; extensive thrombosis in the portal venous system; acute eosinophil-associated pneumonia; gastrointestinal bleeding; intestinal necrosis.Interventions:The patient was first treated with methylprednisolone, plasma exchange/hemofiltration, and single or combined use of unfractionated heparin and argatroban for anticoagulation. He was also administered alteplase and urokinase, successively, for thrombolytic treatment. Once the thromboses finally disappeared, the patient underwent surgery to excise a necrotic intestinal canal.Outcomes:The thromboses disappeared with these treatments, and the patient recovered after the necrotic intestinal canal was excised.Lessons:The clinical manifestations of HES are complex and varied, and this condition can cause severe and extensive arteriovenous thrombosis. Anticoagulation therapy and thrombolysis are necessary interventions, and appear to be safe and effective.

Acute lung injury (ALI) is a life-threatening clinical condition associated with critically ill patients, and the construction of potential microRNA (miRNA) and messenger RNA (mRNA) regulatory networks will help to fully elucidate its underlying molecular mechanisms. First, we screened fifteen upregulated differentially expressed miRNAs (DE-miRNAs) and six downregulated DE-miRNAs from the Gene Expression Omnibus (GEO) database. Then, the predicted target genes of the upregulated and downregulated DE-miRNAs were identified from the miRNet database. Subsequently, differentially expressed mRNAs (DE-mRNAs) were identified from the GEO database and subjected to combined analysis with the predicted DE-miRNA target genes. Eleven target genes of the upregulated DE-miRNAs and one target gene of the downregulated DE-miRNAs were screened out. To further validate the prediction results, we randomly selected a dataset for subsequent analysis and found some accurate potential miRNA-mRNA regulatory axes, including mmu-mir-7b-5p-Gria1, mmu-mir-486a-5p-Shc4 and mmu-mir-486b-5p-Shc4 pairs. Finally, mir-7b and its target gene Gria1 and mir-486b and its target gene Shc4 were further validated in a bleomycin-induced ALI mouse model. We established a potential miRNA-mRNA regulatory network of ALI in mice, which may provide a basis for basic and clinical research on ALI and advance the available treatment options.

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