Fat-poor renal angiomyolipoma with prominent cystic degeneration: A case report and review of the literature.

BACKGROUND: Angiomyolipoma (AML), the most common benign tumor of the kidney, is usually composed of dysmorphic blood vessels, smooth muscle, and mature adipose tissue. To our knowledge, AML with cystic degeneration has rarely been documented. Cystic degeneration, hemorrhage, and a lack of fat bring great challenges to the diagnosis. CASE SUMMARY: A 60-year-old man with hypertension presented with a 5-year history of cystic mass in his left kidney. He fell 2 mo ago. A preoperative computed tomography (CT) scan showed a mixed-density cystic lesion without macroscopic fat density, the size of which had increased compared with before, probably due to hemorrhage caused by a trauma. Radical nephrectomy was performed. Histopathological studies revealed that the lesion mainly consisted of tortuous, ectatic, and thick-walled blood vessels, mature adipose tissue, and smooth muscle-like spindle cells arranged around the abnormal blood vessels. The tumor cells exhibited positivity for human melanoma black-45, Melan-A, smooth muscle actin, calponin, S-100, and neuron-specific enolase, rather than estrogen receptor, progesterone receptor, CD68, and cytokeratin. The Ki-67 labeling index was less than 5%. The final diagnosis was a fat-poor renal AML (RAML) with prominent cystic degeneration. CONCLUSION: When confronting a large renal cystic mass, RAML should be included in the differential diagnosis.

Combination of hepcidin with neutrophil gelatinase-associated lipocalin for prediction of the development of sepsis-induced acute kidney injury.

BACKGROUND AND AIMS: The early prediction of the development of acute kidney injury (AKI) in critically ill patients with sepsis would facilitate early effective intervention. Recently, interest has focused on the biomarkers for AKI-linked iron metabolism. This study aimed to assess the early predictive values of hepcidin, neutrophil gelatinase-associated lipocalin (NGAL), and their combination for secondary AKI in patients with sepsis. MATERIALS AND METHODS: A prospective cohort study was performed in septic patients. Serum and urine hepcidin, and urine NGAL were analyzed at admission. The primary outcome measure was occurrence of sepsis-induced AKI based on 2011 Kidney Disease: Improving Global Outcomes (KDIGO) criteria during the first week of ICU stay. RESULTS: Of the 90 patients analyzed finally in the study, 44 (48.9%) patients developed AKI. Patients with AKI occurrence were more likely than those without AKI to have higher serum hepcidin and urine NGAL levels at admission (P < 0.01). Higher concentrations of these biomarkers were each independent predictor of the development of AKI in critically septic patients within the first week of their ICU stay. Serum hepcidin and urine NGAL (AUROC 0.787, 95% CI 0.688 to 0.8660 and AUROC 0.729, 95% CI 0.625 to 0.818, respectively) were comparable predictive indicators of AKI occurrence (P = 0.43 for DeLong's test). Combining both biomarkers increased the AUROC to 0.828(95% CI 0.733 to 0.899), and this performance was statistically significantly better than urine NGAL alone (P = 0.03 for DeLong's test). CONCLUSION: Serum hepcidin measured at admission predicts the development of AKI similarly to urine NGAL. However, serum hepcidin adds significant accuracy to this prediction in combination with urine NGAL alone and has a good predictive value in patients with sepsis. Larger studies are needed to validate and explain these findings.

Mortality and serum hepcidin are associated with persistent and transient acute kidney injury in septic patients.

PURPOSE: Acute kidney injury (AKI) is a common complication of sepsis and has high mortality. The 2017 Acute Disease Quality Initiative (AQDI) workgroup proposed new definitions for AKI - transient AKI and persistent AKI; however, very little is known about the effect of transient and persistent septic AKI on short-term mortality among critically ill patients with sepsis. The purpose of this study was to assess the impact of persistent AKI on mortality and to evaluate whether serum hepcidin can predict the occurrence of persistent AKI in critically ill patients with sepsis. MATERIALS AND METHODS: This prospective observational study was performed in a general hospital mixed surgical-medical ICU in Pudong, China. Consecutive adults with sepsis admitted to the ICU with absence of chronic kidney disease, renal transplant, and AKI were included. AKI was defined according to the KDIGO criteria and classified as transient (< 48-hour duration) or persistent (48-hour duration). Blood samples were obtained within 6 hours from when AKI was diagnosed. RESULTS: A total of 90 patients with sepsis or septic shock were included in the analysis. 44 (48.89%) patients developed AKI during ICU stay: 20 (45.45%) had transient and 24 (54.55%) had persistent AKI. Persistent AKI has a higher mortality than transient AKI (66.7 vs. 30.0%, p = 0.002). Persistent AKI and sequential organ failure assessment (SOFA) scores were an independent predictor of 60-day mortality. Patients with persistent AKI had higher concentrations of serum creatinine (SCr) and hepcidin than transient AKI patients when AKI was diagnosed. Logistic regression indicated that serum hepcidin was an independent predictor of persistent AKI in septic patients, with a fairly predictive value (AUC 0.71, 95% CI: 0.47 - 0.87; p = 0.02). CONCLUSION: Persistent AKI was associated with increased 60-day mortality compared with transient AKI in septic patients. The serum hepcidin levels measured when AKI was diagnosed have a fair predictive value to predict the occurrence of persistent AKI in septic patients.

Glycogen storage disease type VI can progress to cirrhosis: ten Chinese patients with GSD VI and a literature review.

Objectives The aim of our study is to systematically describe the genotypic and phenotypic spectrum of Glycogen storage disease type VI (GSD VI), especially in Chinses population.  Methods We retrospectively analyzed ten Chinese children diagnosed as having GSD VI confirmed by next generation sequencing in Children's Hospital of Fudan University and Jinshan Hospital of Fudan University. We described the genotypic and phenotypic spectrum of GSD VI through the clinical and genetic data we collected. Moreover, we conducted a literature review, and we compared the genotypic and phenotypic spectrum of GSD VI between Chinese population and non Chinese population.  Results For the first time, we found that four Chinese patients showed cirrhosis in liver biopsy characterized by the formation of regenerative nodules. In addition, c.772+1G>A and c.1900G>C, p.(Asp634His) were recurrent in three Chinese families and four European families respectively indicating that the genotypic spectrum of PYGL gene may vary among the population. Furthermore, we identified seven novel variants in PYGL gene.  Conclusions Our study enriched the genotypic and phenotypic spectrum of GSD VI, and provided a new clue for management of GSD VI.

Shenfu injection prevents sepsis-induced myocardial injury by inhibiting mitochondrial apoptosis.

ETHNOPHARMACOLOGICAL RELEVANCE: Shenfu injection (SFI) is a well-known Chinese herbal medicine widely used in the treatment of septic shock in China. AIMS: The aims of this study are to investigate the protective effects of SFI on sepsis-induced myocardial injury in mice and to identify the underlying mechanism of action. MATERIALS AND METHODS: Seventy-two male C57/B6J mice (5-6 weeks old) were randomly divided into five groups: control (NC), sham sepsis (sham), sepsis (Lipopolysaccharide- LPS), sepsis treated with a low dose SFI, and sepsis treated with a high dose SFI. Sepsis was induced in mice by intraperitoneal injection of LPS. Myocardial tissue samples were collected from different groups at 6 h, 12 h, and 24 h post-LPS injection. Myocardial injury was examined using hematoxylin-eosin (H&E) and TUNEL staining. Western-blot analysis was performed to determine the protein expression of B-cell lymphoma 2 (Bcl-2), BH3 interacting-domain death agonist (Bid), truncated-Bid (t-Bid) and caspase-9 in all the groups. Moreover, the structural changes in the mitochondria of cardiomyocytes were also observed by transmission electron microscopy. RESULTS: H&E staining revealed structural damage, local necrosis, interstitial edema, inflammatory cell infiltration and vacuolar changes in the myocardial tissue in the sepsis (LPS) group; almost intact myocardial tissue was observed in the high dose SFI group with improvements in interstitial edema and inflammatory cell infiltration. We observed that LPS-induced cardiomyocyte apoptosis was significantly improved with high dose SFI as compared with sepsis (LPS) group (P ˂ 0.05). LPS was found to decrease the protein expression of Bcl-2 and increase the level of Bid, t-Bid and caspase-9. Treatment with SFI significantly increased the Bcl-2 protein expression (P ˂ 0.05) and decreased the protein expression of Bid, t-Bid and caspase-9 as compared with LPS group (P ˂ 0.05). Markedly swollen myocardial mitochondria with partial vacuolation were observed in LPS treated mice while SFI treatment was found to significantly improve the LPS-induced morphological damage of the mitochondria. CONCLUSION: In conclusion, we demonstrate that SFI protects against sepsis-induced myocardial injury in mice through the suppression of myocardial apoptosis. It upregulates the protein expression of Bcl-2 and downregulates the protein expression of Bid, t-Bid and caspase-9, and alleviates sepsis-induced mitochondrial damage.

[Establishment and Clinical Application of Flow Cytometric Immunobead Array in Detecting Plasma von Willebrand Factor Antigen].

OBJECTIVE: To establish a novel flow cytometric immunobead array (FCIA) for detecting plasma von Willebrand factor antigen (vWF:Ag), and to analyze the clinical value of FCIA in predicting the prognosis of patients with ischemic stroke (IS). METHODS: Anti-human vWF monoclonal antibody SZ29 IgG was coated on microspheres overnight, the diluted plasma was added after blocking, then incubated with FITC-conjugated sheep-anti-human vWF IgG polyclonal antibody, and finally detected by flow cytometry. The plasma vWF in 21 case of von Willebrand disease (vWD) and 105 controls (CTL) were detected by FCIA and ELISA, so as to carry out methodological assessment. Plasma vWF:Ag of 61 IS patients was detected by FCIA and the data of prognosis followed-up for 2-year were collected. RESULTS: The linear fitting of FCIA was good (R2=0.99) without significant difference between FCIA and ELISA. The Bland-Altman bias was 1.12% with 95% limits of agreement that spanned from -45.06% to 47.30%, and the slope of the linear regression was 0.97 (r=0.86, P＜0.01). Importantly, the FCIA method was faster than ELISA, and superior to the ELISA in the detection of low levels of vWF:Ag. The levels of vWF:Ag, vWF:GPIbR and vWF:CB in IS patients were significantly higher than those in healthy controls (Z=8.36, 8.71, 6.22, respectively, P＜0.01). CONCLUSION: The FCIA for detecting plasma vWF:Ag is not only an effective supplement to ELISA, but also the efficiency is faster and more sensitive, thus improves the diagnosis of type 3 vWD. Elevated levels of vWF: Ag in IS patients indicate the poor recovery of daily activities and prognosis.

The Effects of Abnormal Body Temperature on the Prognosis of Patients with Septic Shock.

We aimed to use temperature and the area under temperature curve to represent the severity of abnormal body temperature of patients with septic shock and to observe their impact on the prognosis. Five hundred twenty-eight adult patients with septic shock admitted to intensive care unit (ICU) were analyzed. Within the first 24 hours and throughout the period in ICU, the maximum temperature (24hTmax, Tmax), lowest temperature (24hTmin, Tmin), and the temperature range (24hTmax-min, Tmax-min) were aggregated. Patients were divided into the survival group and the death group. Binary logistic regression was used to assess the relationship between body temperature aberrations and survival. The following risk factors of death in 21 days were identified: Tmax (odds ratio [OR] 2.967, 95% confidence interval [CI] 1.626-5.414, p < 0.001), Tmin (OR 0.337, 95% CI 0.143-0.794, p = 0.013), and Tmax-min (OR 3.259, 95% CI 1.847-5.749, p < 0.001). This is an observational study, so one can infer association but not causation. Therefore, we infer that abnormal body temperature is associated with an adverse prognosis in patients with septic shock.

Effect of olprinone on ischemia-reperfusion induced myocardial injury in rats.

AIMS: This study investigated the effect of olprinone on ischemia-reperfusion (I/R) induced cardiac injury, and the underlying mechanism. MAIN METHODS: Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by 24 h reperfusion. After the start of reperfusion, rats were respectively treated with olprinone in three different dosages (0.2, 0.6, 2 mg/kg, intraperitoneal injection, i.p./12 h). Twenty-four hours later, a mean arterial pressure (MAP) heart function analysis system was used to monitor hemodynamic parameters; TTC staining method was used to detect the myocardial infarct size; 24-hour mortality of rats was recorded; western blot was used to detect the protein expressions of Caspase-3, Bax, Bcl-2, Beclin-1 and LC3-II/LC3-I. RESULTS: Cardiac function in I/R group was lower than that in sham group (dp/dt max: 1348.29 ± 266.01 vs. 3333.73 ± 1258.03, -dp/dt max: 1163.23 ± 588.18 vs. 3198.93 ± 1416.00, P < 0.05), which was significantly improved by treatment with high dosage of olprinone (dp/dt max: 1348.29±266.01 vs. 2022.43±493.39, -dp/dt max: 1163.23±588.18 vs. 1784.50±418.92, P < 0.05). The percentage of myocardial infarct size in medium and high dosages of olprinone group was lower than that in I/R group (42.67 ± 2.94, 22.33 ± 3.63 vs. 63.67 ± 5.86, P < 0.05). There was no significant difference in mortality among each group within 24 h. Compared with sham group, the expression of Caspase-3 was significantly up-regulated in I/R group (3.44±0.47-fold of sham, P < 0.05), which was inhibited by medium dosage of olprinone treatment (2.00±0.52-fold of sham, P < 0.05 vs. I/R group); also, expression of Bax was increased compared with sham group (4.06±0.25-fold of sham, P < 0.05), which was markedly inhibited by all dosages of olprinone treatment (low: 2.16±0.61-fold, medium: 2.74±0.66-fold, high 1.65±0.55-fold, P < 0.05 vs. I/R group). Expression of Bcl-2 was increased after I/R (1.17±0.06-fold, P < 0.05), which was further elevated in all dosages of olprinone treatment (low: 1.62 ± 0.13-fold, medium: 1.46 ± 0.13-fold, high: 1.82 ± 0.39-fold, P < 0.05 vs. I/R group). In addition, compared with sham group, the expression of Beclin-1 was up-regulated to 1.44±0.05-fold of sham in I/R group (P < 0.05), which was further increased in low and medium dosages of olprinone group (low: 2.46±0.44-fold, medium: 2.80±0.75-fold, P < 0.05 vs. I/R group). Moreover, expression of LC3-II was elevated in low dosage of olprinone treated group (low: 4.50±0.47-fold, P < 0.05 vs. I/R group). CONCLUSIONS: Olprinone improves the cardiac function in response to myocardial I/R injury by regulation of anti-apoptotic, pro-apoptotic. In addition, autophagic signal pathways may also play a role in olprinone's therapeutic effect.

[Establishment of Flow Cytometric Immunobead Array for Detecting Plasma Von Willebrand Factor Activity and Its Clinical Application in the Prognosis of Ischemic Stroke].

OBJECTIVE: To establish a novel flow cytometric immunobead array (FCIA) for detecting plasma von Willebrand factor activity (vWF:GPIbR) and apply it in ischemic stroke (IS). METHODS: Microspheres coated with anti-human platelet glycoprotein Ibα (GPIbα) monoclonal antibody SZ151 IgG, were incubated with recombinant fragment of GPIbα, then added ristocetin and plasma, finally incubated with FITC-conjugated sheep-anti-human vWF IgG polyclonal antibody, and detected by flow cytometry. vWF antigen (vWF:Ag), vWF:GPIbR, and vWF collagen binding assay (vWF:CB) were also included for evaluating vWF levels in IS patients. RESULTS: The intra-assay coefficient variations (CVs) and inter-assay CVs of FCIA were 7.7% and 13.5%, respectively. The slope of the linear regression was 0.9739 (r=0.855, P<0.001), and the Bland-Altman bias was 9.95%, indicating a good correlation between FCIA and ELISA. The FCIA had better sensitivity, specificity and accuracy as compared with those by ELISA (P<0.05). The levels of vWF:Ag, vWF:GPIbR and vWF:CB in IS patients were significantly higher in comparison with those in healthy controls (H=7.8, 6.4, 6.2, respectively, P<0.01), the level of vWF:GPIbR in IS patients positively correlated with levels of vWF:Ag, high-sensitivity C-reactive protein, Autar score and hospitalization time. CONCLUSION: The FCIA for detecting plasma vWF:GPIbR is more specific and accurate than ELISA. The vWF:GPIbR is involved in the paroxysm of IS, which could be used to evaluate the risk of thrombosis in IS patients.

Protective effects of tanshinone IIA sodium sulfonate on ischemia-reperfusion-induced myocardial injury in rats.

OBJECTIVES: This study investigated the protective effect of tanshinone IIA sodium sulfonate (TSS) on ischemia-reperfusion (I/R) induced cardiac injury, and the underlying mechanism of action. MATERIALS AND METHODS: Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by 24 hours' reperfusion. Half an hour before the left coronary artery ligation, rats were pretreated with TSS in three different dosages (15, 30, 70 mg/kg, IP). Twenty-four hours later, cardiac function was measured and the ratio of infarct size to area at risk (AAR) was calculated. Western blotting examined the expression of the inflammatory mediator high-mobility group box1 (HMGB-1), anti-apoptotic protein Bcl-2, pro-apoptotic mediators such as Bax and Caspase-3, markers of autophagy such as ratio of LC3B/LC3A and Beclin-1 expression. RESULTS: Our results showed that TSS dose-dependently improves cardiac function, accompanied with decrease of HMGB1 level, increase of LC3B/LC3A ratio and increase of Beclin-1 expression. TSS treatment down-regulates Bax and Caspase-3 expression, while up-regulating Bcl-2 levels. CONCLUSION: TSS ameliorates I/R induced myocardial injury and improves cardiac function via reducing inflammation and apoptosis, while enhancing autophagy.

The changes of von willebrand factor/a disintegrin-like and metalloprotease with thrombospondin type I repeats-13 balance in aneurysmal subarachnoid hemorrhage.

The aim of this study was to investigate the role of Von Willebrand Factor/thrombospondin type I repeats-13 (VWF/ADAMTS13) balance in aSAH. Fifty eight patients with aSAH at the First Affiliated hospital of Soochow University, Suzhou, China, between January 2012 and January 2014 were eligible for the study. They were divided into delayed cerebral ischemia group (DCI group) and non-delayed cerebral ischemia group (no DCI group), or cerebral vasospasm group (CVS group) and no spasm group (no CVS group), or good outcome group and poor outcome group. The control group consisted of twenty healthy people. All patients underwent CT, DSA, or (and) CTA diagnosed with intracranial subarachnoid hemorrhage which is caused by aneurysm rupture. Venous blood was drawn in tubes at 3 time points: 1 day after SAH (T1), (4±1) days after SAH (T2), and (9±1) days after SAH (T3) to determine plasma concentrations of ADAMTS13, VWF, P-selectin and IL-6 via enzyme-linked immunosorbent assay (ELISA). Transcranial doppler sonography (TCD) was used to measure mean blood flow velocity of the middle cerebral artery (VMCA). Glasgow Outcome Scale (GOS) was measured before discharge. Among 58 patients, 12 (20.7%) had DCI, 40 (68.9%) had TCD evidence of CVS, and 20 (34.5%) had poor outcome. The concentrations of VWF, P-selectin and IL-6 on T1, T2 and T3 after SAH were significantly higher in DCI, CVS and poor outcome groups compared with those of the control group (P < 0.05). The concentrations of VWF, P-selectin and IL-6 were significantly higher in DCI, CVS and poor outcome groups compared with those of the no DCI, no CVS and good outcome groups. The activity of ADAMTS13 was lower in DCI and poor outcome groups compared with those of the no DCI and good outcome groups (P < 0.05). The activity of ADAMTS13 showed no difference in CVS group and no CVS group (P > 0.05). The results of our study suggest that the increased VWF and decreased ADAMTS13 activity were associated with DCI and poor outcome. The balance of VWF/ADAMTS13 could be used to predict the clinical outcome. The deficiency of ADAMTS13 can not only induce DCI but also accelerate inflammatory reaction. Our results reported in this paper may provide new insights into the possible use of ADAMTS13 as a therapeutic agent in aneurysmal subarachnoid hemorrhage.

Serum albumin and prealbumin predict the poor outcome of traumatic brain injury.

BACKGROUND: Serum albumin and prealbumin are both negative acute-phase reactants, and usually at low levels in stress. We aim to determine their predictive values for poor outcome of traumatic brain injury (TBI). METHODS: A total of 326 patients of TBI were enrolled and followed-up by telephone 6 months after discharge. They were divided into a favorable group (GOS: 3 to 5) and an unfavorable group (GOS: 1 to 2). Serum albumin and prealbumin were measured from vein blood within 24 h after admission. RESULTS: Ninety one (27.9%) patients were with poor outcome (GOS: 1 to 2). The unfavorable group had lower albumin and prealbumin (P<0.001). Albumin and prealbumin were both positively correlated with GCS (r = 0.489, P<0.001; r = 0.222, P<0.001, respectively) and GOS (r = 0.518, P<0.001; r = 0.314, P<0.001, respectively). After adjustment for confounding factors, the odds ratios of albumin and prealbumin were 0.866, 95% CI: 0.829 to 0.904 and 0.990, 95% CI: 0.985 to 0.995, respectively. In subgroup of GCS≤8 (n = 101), the crude and adjusted odds ratios of serum albumin were both statistically significant (P = 0.027, P = 0.033, respectively), while prealbumin were not (P = 0.553, P = 0.576, respectively). The AUC of albumin for predicting poor outcome was 0.762, 95% CI: 0.712 to 0.807, which was significantly higher than that of prealbumin (0.664, 95% CI: 0.610 to 0.715). In analyses of all patients and subgroup of GCS≤8, the AUCs of serum albumin were both significantly higher than those of prealbumin (P = 0.001, P = 0.045, respectively). CONCLUSIONS: Both serum albumin and prealbumin could predict the poor outcome of TBI, but the former is much better, especially, in patients with severe TBI.

Apoptosis and autophagy contribute to gender difference in cardiac ischemia-reperfusion induced injury in rats.

AIMS: Gender difference in cardiac ischemia-reperfusion (IR) induced injury has been reported in animal models. However, a large-scale clinical trial found an increase in cardiovascular incidents in women with hormone replacement therapy. The present study is aimed to explore possible mechanisms of gender difference in cardiac IR induced injury. MAIN METHODS: Male and female Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by reperfusion. The infarct size and apoptotic cell number at 24h after reperfusion were significantly lower in female rats than in male rats. KEY FINDINGS: Male rats expressed higher anti-apoptotic protein Bcl2 levels compared with female rats under physiological conditions. However, levels of Bcl2 were reduced significantly after IR in male rats but not in, female rats. Levels of pro-apoptotic protein, Bax and phospho-p38, showed similar under physiological conditions. In response to IR expression of Bax was markedly reduced in female rats but not in male rats, and expression of phospho-p38 was significantly increased in male rats but not in female rats. In addition, female rats showed marked increase of autophagy marker, ratio of LC3B to LC3A, while male rats significantly decreased the ratio in response to IR. SIGNIFICANCE: Gender difference in IR injury is due to the different regulation of anti-apoptotic protein, pro-apoptotic protein and autophagy protein levels in male rats and levels in female rats. Our results provide better understanding of sex differences in cardiac IR injury.

Expression patterns of plasma von Willebrand factor and serum interleukin-8 in patients with early-stage severe pulmonary contusion.

BACKGROUND: von Willebrand factor (vWF) is only released from endothelial cells and platelets and is an in vivo and in vitro marker of endothelial injury in septic patients with acute lung injury (ALI). Interleukin-8 (IL-8), as a proinflammatory mediator causing recruitment of inflammatory cells, induces an increase in oxidant stress mediators and makes it as a key parameter for localized inflammation. However, it has not been well established whether the level of serum IL-8 is associated with the severity of lung injury and whether it is a prognosis marker for severe lung contusion. This study was to investigate the expression of plasma vWF and IL-8 and their association with the severity and outcomes of severe pulmonary contusion. METHODS: A total of 63 patients were divided into a severe pulmonary contusion with acute respiratory distress syndrome (ARDS) group and a non-ARDS group, or a survivor group and a non-survivor group, or an injury severity score (ISS) <20 group and an ISS ≥20 group. Another 20 healthy volunteers served as controls. The levels of plasma vWF and serum IL-8 were measured by enzyme-linked immunosorbent assay (ELISA) at 1, 3, 5 and 7 days after injury. The expression patterns of the plasma vWF and serum IL-8 were compared between different groups. RESULTS: The concentrations of plasma vWF and serum IL-8 were significantly increased in all severe pulmonary contusion patients at all time points in comparison with the control group. The concentrations of plasma vWF in patients with ARDS increased during the whole study period, but vWF in patients with non-ARDS increased gradually until day 5 and then decreased at day 7. The concentration of serum IL-8 showed a similar expression pattern in both groups, but the expression increased more significantly in the ARDS group than in the non-ARDS group. Interestingly, both plasma vWF and serum IL-8 levels steadily increased in the non-survivor group. Furthermore, the level of plasma vWF was higher in the ISS≥20 group than in the ISS<20 group. The level of serum IL-8 in the ISS≥20 group was consistently high, while that in the ISS<20 group peaked at day 3 and decreased at day 5. In addition, the level of plasma vWF was positively correlated with platelet count, but negatively correlated with oxygen index. The level of serum IL-8 was positively correlated with white blood cell count and ISS score, and inversely correlated with oxygen index. CONCLUSION: The elevated levels of plasma vWF and serum IL-8 in severe pulmonary contusion patients reflect the severity of pulmonary injury and patients outcomes, suggesting that the plasma vWF and serum IL-8 are sensitive markers for clinical evaluation of the severity of pulmonary injury and predication of patient prognosis.