interleukin-8 and Pulmonary-Embolism

We sought to determine the efficacy and safety of perioperative treatment with methylprednisolone on the development of lung injury after pulmonary thromboendarterectomy.. This was a randomized, prospective, double-blind, placebo-controlled study of 98 adult patients with chronic thromboembolic pulmonary hypertension who were undergoing pulmonary thromboendarterectomy at a single institution. The patients received either placebo (n = 47) or methylprednisolone (n = 51) (30 mg/kg in the cardiopulmonary bypass prime, 500 mg IV bolus following the final circulatory arrest, and 250 mg IV bolus 36 h after surgery). The primary end point was the presence of lung injury as determined by two independent, blinded physicians using prospectively defined criteria. The secondary end points included ventilator-free, ICU-free, and hospital-free days and selected levels of cytokines in the blood and in BAL fluid.. The incidence of lung injury was similar in both treatment groups (45% placebo, 41% steroid; P = .72). There were no statistical differences in the secondary clinical end points between treatment groups. Treatment with methylprednisolone, compared with placebo, was associated with a statistically significant reduction in plasma IL-6 and IL-8, a significant increase in plasma IL-10, and a significant reduction in postoperative IL-1ra and IL-6, but not IL-8 in BAL fluid obtained 1 day after surgery.. Perioperative methylprednisolone does not reduce the incidence of lung injury following pulmonary thromboendarterectomy surgery despite having an antiinflammatory effect on plasma and lavage cytokine levels.

Topics: Bronchoalveolar Lavage Fluid; Dose-Response Relationship, Drug; Double-Blind Method; Endarterectomy; Female; Follow-Up Studies; Glucocorticoids; Humans; Injections, Intravenous; Interleukin-10; Interleukin-6; Interleukin-8; Lung Injury; Male; Methylprednisolone; Middle Aged; Preoperative Care; Prospective Studies; Pulmonary Embolism; Thrombectomy; Treatment Outcome

Background: Inflammatory response and endothelial dysfunction contribute to the progression of chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to assess changes in biomarkers involved in those processes in inoperable CTEPH patients treated with balloon pulmonary angioplasty (BPA). Methods: We enrolled 20 patients with inoperable CTEPH qualified for BPA and a control group. Interleukin 6, 8, 10 (IL-6, IL-8, IL-10), monocyte chemoattractant protein-1 (MCP-1), and C-reactive protein (hsCRP) constituted the markers of systemic inflammation. Endothelin 1 (ET-1) served as a marker of endothelial dysfunction. Selected markers were assessed before the BPA treatment, 24 h after the first BPA, and six months after completion of the BPA treatment. Results: At baseline, the CTEPH patients had increased serum concentrations of IL-6, IL-8 and ET-1. Twenty-four hours after a BPA session, we observed an increase in concentrations of IL-6 (∆ = 3.67 (1.41; 7.16); p < 0.001), of IL-10 (∆ = 0.25 (0; 0.47); p = 0.003), of MCP-1 (∆ = 111 (60.1; 202.8); p = 0.002), and of hsCRP (∆ = 4.81 (3.46; 8.47); p < 0.001). Six months after completion of the BPA treatment, there was a decrease in concentrations of IL-6 (∆ = −1.61 (−3.11; −0.20); p = 0.03), of IL8 (∆ = −3.24 (−7.72; 0.82); p = 0.01), and of ET-1 (∆ = −0.47 (−0.96; 0.05); p = 0.005). Conclusions: Patients with inoperable CTEPH exhibit increased systemic inflammation and endothelial dysfunction, which improves after completion of the BPA treatment. A single BPA session evokes an acute inflammatory response.

Topics: Angioplasty, Balloon; Biomarkers; C-Reactive Protein; Humans; Hypertension, Pulmonary; Inflammation; Interleukin-10; Interleukin-6; Interleukin-8; Pulmonary Artery; Pulmonary Embolism

The global COVID-19 pandemic remains a critical public health threat, as existing vaccines and drugs appear insufficient to halt the rapid transmission. During an outbreak from May to August 2021 in Taiwan, patients with severe COVID-19 were administered NRICM102, which was a traditional Chinese medicine (TCM) formula developed based on its predecessor NRICM101 approved for treating mild cases. This study aimed to explore the mechanism of NRICM102 in ameliorating severe COVID-19-related embolic and fibrotic pulmonary injury. NRICM102 was found to disrupt spike protein/ACE2 interaction, 3CL protease activity, reduce activation of neutrophils, monocytes and expression of cytokines (TNF-α, IL-1β, IL-6, IL-8), chemokines (MCP-1, MIP-1, RANTES) and proinflammatory receptor (TLR4). NRICM102 also inhibited the spread of virus and progression to embolic and fibrotic pulmonary injury through reducing prothrombotic (vWF, PAI-1, NET) and fibrotic (c-Kit, SCF) factors, and reducing alveolar type I (AT1) and type II (AT2) cell apoptosis. NRICM102 may exhibit its protective capability via regulation of TLRs, JAK/STAT, PI3K/AKT, and NET signaling pathways. The study demonstrates the ability of NRICM102 to ameliorate severe COVID-19-related embolic and fibrotic pulmonary injury in vitro and in vivo and elucidates the underlying mechanisms.

Topics: Angiotensin-Converting Enzyme 2; Chemokine CCL5; COVID-19 Drug Treatment; Cytokines; Fibrosis; Humans; Interleukin-6; Interleukin-8; Lung Injury; Pandemics; Phosphatidylinositol 3-Kinases; Plasminogen Activator Inhibitor 1; Proto-Oncogene Proteins c-akt; Pulmonary Embolism; Spike Glycoprotein, Coronavirus; Toll-Like Receptor 4; Tumor Necrosis Factor-alpha; von Willebrand Factor

Patients with malignancy have higher risk of developing venous thromboembolism. The incidence among different groups of cancer patients varies considerably depending on clinical factors, the most important being tumor entity and stage. The study was approved by the local ethics committee on human research, and written informed consent was obtained from all the study participants. After written informed consent was obtained, a precise medical history was taken, with particular attention to questions about the presence of thrombotic risk factors at the onset of VTE. We retrospectively enrolled 50 patients with Venous Thromboembolism (DVT and PTE) having malignancy and 50 healthy controls from January 2020 to December 2020. DVT were diagnosed using peripheral vascular duplex ultrasonography while PTE was confirmed in all cases by computed tomography. Patients having treatment with anticoagulant therapy, recent surgery less than 8 days previously, refusal or inability to give informed consent, and inability for ascending contrast venography or inadequate results of the venographic examination were excluded from the study. Biomarkers have been specifically investigated for their capacity of predicting venous thromboembolism (VTE) during the course of disease. The relationships between inflammation markers e.g., IL-6, IL-8 and CRP as indicators of the inflammatory process and clinical venous thromboembolism need to be investigated. We investigated IL-6, IL-8 and CRP in 50 patients with venous thromboembolism having malignancy and reported that patients having venous thromboembolism have increased levels of IL-6, IL-8 and CRP (p value < 0.05). Our study concluded that in cancer patients, inflammatory biomarkers play significant role in developing venous thromboembolism. This supports the hypothesis that, markers of systemic inflammatory response are involved in development of thromboembolism in patients with malignancy.

Topics: Biomarkers; Humans; Incidence; Interleukin-6; Interleukin-8; Neoplasms; Pulmonary Embolism; Retrospective Studies; Risk Factors; Systemic Inflammatory Response Syndrome; Thrombosis; Venous Thromboembolism

Aprotinin, a nonspecific serine protease inhibitor, has been primarily used as a haemostatic drug in cardiac surgery with cardio-pulmonary bypass (CPB). This study investigated the effect of aprotinin on the post-operative levels of procalcitonin (PCT) and a set of cytokines in patients undergoing pulmonary artery endarterectomy (PEA). We analyzed 60 patients with chronic thromboembolic pulmonary hypertension undergoing PEA. 30 patients (Group A) were treated with aprotinin (2,00,00 IU prior anesthesia, then 2,00,00 IU in CPB prime and 50,00 IU per hour continuously); a further 30 patients (Group B) received tranexamic Acid (1 g before anesthesia, 1 g after full heparin dose and 2 g in CPB prime). PCT, TNFalpha, IL-1beta, IL-6, and IL-8 arterial concentrations were measured from before until 72 hours after surgery. Aprotinin significantly affected early post-PEA plasma PCT. Patients treated with aprotinin (Group A) had lower peak PCT levels compared to patients in Group B (1.52 ng/ml versus 2.18, p=0.024). Postoperative peak values of PCT and IL-6 correlated closely in both groups (r=0.78, r=0.83 respectively). Aprotinin attenuates the post-PEA increase of PCT in the same manner as other pro-inflammatory cytokines. Significant correlation between PCT and IL-6 post-surgery may be indicative of an indirect IL-6-mediated pathway of PCT alteration.

Topics: Aged; Aprotinin; Biomarkers; Calcitonin; Calcitonin Gene-Related Peptide; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Endarterectomy; Female; Hemostatics; Humans; Hypertension, Pulmonary; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Protein Precursors; Pulmonary Embolism; Time Factors; Tranexamic Acid; Treatment Outcome; Tumor Necrosis Factor-alpha; Up-Regulation

To asses the association of acute reactants and interleukin 6 and 8 (IL-6 & IL-8) at diagnosis of venous thromboembolic disease (VTD) and clinical outcome.. 100 patients were diagnosed of VTD by image tests. Acute reactants (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen), D-dimer and IL-6 and IL-8 we measured at the moment of diagnosis. We made a 12 month follow-up of these patients to notice any clinical evolution outcomes (recurrences, bleeding, post-phlebitic syndrome, death).. IL-6 was increased in 9 patients and IL-8 in 3. The risk factors, time to diagnosis and pulmonary embolism rate were similar in both interleukin groups (normal and high levels). Fibrinogen levels were significantly increased in high IL-6 group (585 +/- 179 vs. 485 +/- 154 mgr/dl; p = 0.05). During follow-up there were 5 deaths, 3 recurrences, 11 bleedings and 43 postphlebitic syndromes. Normal ESR level was associated to postphlebitic syndrome (17.8 +/- 14.5 vs. 31.4 +/- 27.4 mm/1st h; p = 0.016). Patients who had high levels of IL-6 had worse survival than these with normal levels (p = 0.015).. IL-6, ESR, and CPR at diagnosis of VTD could be useful to identified patients with higher risks of death and postphlebitic syndrome during the first year after diagnosis.

Topics: Acute-Phase Proteins; Adult; Aged; Aged, 80 and over; Biomarkers; Blood Sedimentation; C-Reactive Protein; Comorbidity; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Follow-Up Studies; Humans; Inflammation; Interleukin-6; Interleukin-8; Male; Middle Aged; Postoperative Complications; Postphlebitic Syndrome; Predictive Value of Tests; Prognosis; Prospective Studies; Pulmonary Embolism; Risk Factors; Thrombophlebitis; Treatment Outcome