Importance of endothelial dysfunction biomarkers in patients with Crimean-Congo hemorrhagic fever.

The pathogenesis of the Crimean-Congo hemorrhagic fever (CCHF) and the cause of the hemorrhage are not yet fully understood. However, the endothelium plays a key role in the pathogenesis. The purpose of this study was to investigate endothelial dysfunction markers (asymmetrical dimethyl arginine [ADMA], endothelin 1[ET-1], thrombomodulin [TM], von Willebrand factor [vWf], and intercellular adhesion molecule [ICAM-1]) in serum in patients with CCHF and their associations with hemorrhage. Seventy-three patients with CCHF were included in the study. All patients' endothelial dysfunction markers were studied using routine biochemical and hematological tests. The data obtained were then subjected to statistical analysis. Statistically significant differences were determined between the patients and healthy control groups at time of presentation to hospital in terms of ADMA (P < 0.001), ET-1 (P < 0.001), TM (P = 0.039), vWf (P < 0.001), and ICAM-1 (P < 0.001) levels. Only the differences in TM and vWf were significant between the hemorrhagic and non-hemorrhagic groups (P < 0.05). Both serum ADMA and TM levels were significantly higher in the hemorrhage and non-hemorrhage CCHF groups on the 5th day compared to the 1st day (P < 0.05). Levels of endothelial dysfunction markers in CCHF vary in proportion to the damage occurring in the endothelium. ADMA and TM levels were lower in periods with mild endothelial injury. They were increased in line with severity endothelial injury. They may be an early marker in showing hemorrhage. Elevation in ADMA levels and low nitric oxide levels lead to endothelial injury and hemorrhage. Soluble TM that entered the circulation in line with the increased endothelial injury in hemorrhagic patients has been compromised the coagulation cascade.

The value of ischemia-modified albumin compared with d-dimer in the diagnosis of pulmonary embolism.

STUDY OBJECTIVE: The primary aim of this study was to investigate whether IMA levels are helpful in the diagnosis of pulmonary embolism (PE). The secondary aim was to determine whether IMA was more effective alone or in combination with clinical probability scores in the diagnosis of PE. Thirdly, the sensitivity and specificity of IMA is compared with D-dimer both with and without clinical probability scores in patients with suspected PE. METHODS: Consecutive patients presenting to the emergency department with suspected PE were prospectively recruited, and healthy volunteers were also enrolled as controls. D-dimer and IMA levels were measured for the entire study group. Wells and Geneva scores were calculated and s-CTPA was performed on all suspected PE patients. RESULTS: The study population consisted of 130 patients with suspected PE and 59 healthy controls. Mean IMA levels were 0.362 +/- 0.11 ABSU for Group A, the PE group (n = 75); 0.265 +/- 0.07 ABSU for Group B, the non-PE group (n = 55); and 0.175 +/- 0.05 ABSU for Group C, the healthy control group (p < 0.0001). At a cut-off point of 0.25 ABSU, IMA was 93% sensitive and 75% specific in the diagnosis of PE. PPV was 79.4% and NPV was 78.6%. Mean D-dimer levels were 12.48 +/- 10.88 microg/ml for Group A; 5.36 +/- 7.80 microg/ml for Group B and 0.36 +/- 0.16 microg/ml for Group C (p < 0.0001). The D-dimer cut-off point was 0.81 microg/ml with a sensitivity of 98.9% and a specificity of 62.7%, PPV of 69.4% and NPV of 83.3%. The use of IMA in combination with Wells and Geneva clinical probability scores was determined to have a positive impact on these scores' sensitivity and negative predictive values. CONCLUSION: IMA is a good alternative to D-dimer in PE diagnosis in terms of both cost and efficiency. Used in combination with clinical probability scores, it has a similar positive effect on NPV and sensitivity to that of D-dimer. The PPV of IMA is better than D-dimer, but it is still unable to confirm a diagnosis of PE without additional investigation.