Serum Myeloperoxidase Levels Research Articles

Determination of Serum Myeloperoxidase (MPO) and lactate dehydrogenase (LDH) as a tumour Marker in Chronic Myeloid Leukaemia (CML).

To evaluate the efficacy of serum myeloperoxidase and lactate dehydrogenase levels as tumour markers in chronic myeloid leukaemia patients after one-year treatment with tyrosine kinase inhibitors. The case-control study was conducted at the College of Medicine, Mustansiriyah University, Baghdad, Iraq, in collaboration with the National Centre of Haematology, Baghdad, from December 2019 to April 2020. The cases comprised chronic myeloid leukaemia patients aged ≥18 years who had completed one-year treatment with tyrosine kinase inhibitor. They were divided into two groups on the basis of major molecular response. Group 1 patients had major molecular response >0.1%, while group 2 patients had major molecular response <0.1%. Group 3 had healthy controls matched for age and gender. Serum myeloperoxidase and lactate dehydrogenase concentrations were measured using enzyme-linked immunosorbent assay. Data was analysed using SPSS 25. Of the 88 subjects, 32(36.4%) were in group A with mean age 44.9±12.6 years, 26(29.5%) were in group B with mean age 48.23±10.6 years, and 30(34%) were in group C with mean age 43.1±9.3 years. There was a significant increase in myeloperoxidase and lactate dehydrogenase levels in patient groups compared group 3 controls (p<0.05). Between the patient groups 1 and 2, the difference was significant for myeloperoxidase (p<0.05), but not for lactate dehydrogenase (p>0.05). There was higher oxidative stress in chronic myeloid leukaemia patients.

Zedoary turmeric oil injection ameliorates lung inflammation via platelet factor 4 and regulates gut microbiota disorder in respiratory syncytial virus-infected young mice

BackgroundRespiratory syncytial virus (RSV)-induced lung inflammation is one of the main causes of hospitalization and easily causes disruption of intestinal homeostasis in infants, thereby resulting in a negative impact on their development. However, the current clinical drugs are not satisfactory. Zedoary turmeric oil injection (ZTOI), a patented traditional Chinese medicine (TCM), has been used for clinical management of inflammatory diseases. However, its in vivo efficacy against RSV-induced lung inflammation and the underlying mechanism remain unclear.PurposeThe present study was designed to confirm the in vivo efficacy of ZTOI against lung inflammation and intestinal disorders in RSV-infected young mice and to explore the potential mechanism.Study design and methodsLung inflammation was induced by RSV, and cytokine antibody arrays were used to clarify the effectiveness of ZTOI in RSV pneumonia. Subsequently, key therapeutic targets of ZTOI against RSV pneumonia were identified through multi-factor detection and further confirmed. The potential therapeutic material basis of ZTOI in target tissues was determined by non-target mass spectrometry. After confirming that the pharmacological substances of ZTOI can reach the intestine, we used 16S rRNA-sequencing technology to study the effect of ZTOI on the intestinal bacteria.ResultsIn the RSV-induced mouse lung inflammation model, ZTOI significantly reduced the levels of serum myeloperoxidase, serum amyloid A, C-reactive protein, and thymic stromal lymphoprotein; inhibited the mRNA expression of IL-10 and IL-6; and decreased pathological changes in the lungs. Immunofluorescence and qPCR experiments showed that ZTOI reduced RSV load in the lungs. According to cytokine antibody arrays, platelet factor 4 (PF4), a weak chemotactic factor mainly synthesized by megakaryocytes, showed a concentration-dependent change in lung tissues affected by ZTOI, which could be the key target for ZTOI to exert anti-inflammatory effects. Additionally, sesquiterpenes were enriched in the lungs and intestines, thereby exerting anti-inflammatory and regulatory effects on gut microbiota.ConclusionZTOI can protect from lung inflammation via PF4 and regulate gut microbiota disorder in RSV-infected young mice by sesquiterpenes, which provides reference for its clinical application in RSV-induced lung diseases.

Serum myeloperoxidase level as A marker of activity in patients with systemic lupus erythematosus with lupus nephritis class III and IV

Serum myeloperoxidase level as A marker of activity in patients with systemic lupus erythematosus with lupus nephritis class III and IV

Insight into antiphospholipid syndrome: the role and clinical utility of neutrophils extracellular traps formation

Antiphospholipid syndrome (APLS) is a systemic immune dysregulation distinguished by repetitive complications and pregnancy loss in the absence of definite etiology. Most research focuses on the laboratory detection and clinical features of APLS, but its precise etiology remains to be deeply explored. NETosis is a newly developed theory in the pathophysiology of APLS which may serve as the missing bridge between coagulation and inflammation reaching the disease progression and severity. We aimed in this study to navigate the prognostic role of NETosis in thrombotic APLS. Our study included 49 newly diagnosed APLS patients (both 1ry and 2ry) who met clinical and laboratory criteria as per the international consensus statement on the update of the classification criteria for definite APLS and were sub-classified according to the occurrence of thrombotic events in thrombotic and non-thrombotic types. In addition, 20 sex and age-matched reactive subjects and 20 sex and age-matched healthy volunteer controls were enrolled. NETosis formation was assessed by measuring serum Myeloperoxidase (MPO) and Histones level using the enzyme-linked immunosorbent assay (ELISA) technique. Both MPO and Histones levels were able to discriminate among APLS cases from normal controls, showing significant cutoffs of > 2.09 ng/ml for MPO and > 1.45 ng/ml for Histones (AUC values were 0.987and 1.000, respectively). These values can be used as predictors for NETosis pathophysiology in APLS patients. Additionally, these markers demonstrated a significant association with several prognostic indicators, including thrombosis, higher PT and INR, and lower hemoglobin (Hb) levels which are supposed to be ameliorated by using NETs inhibitors. In conclusion, we suggest that measuring NETosis markers, MPO, and Histones, in the early course of APLS using proposed cutoff values will facilitate the timely initiation of anti-NETosis therapy and improve the overall prognosis, particularly for patients with thrombotic APLS.

Improvement of high-density lipoprotein atheroprotective properties in patients with systemic lupus erythematosus after belimumab treatment.

Chronic inflammatory diseases, like Systemic Lupus Erythematosus (SLE), carry an increased risk for atherosclerosis and cardiovascular events, accompanied by impairment of atheroprotective properties of high-density lipoprotein (HDL). In SLE, serum BAFF (B cell-activating factor), a cytokine implicated in disease progression, has been correlated with subclinical atherosclerosis. We investigated the impact of treatment with belimumab -an anti-BAFF monoclonal antibody- on HDL atheroprotective properties and composition in SLE patients. Serum samples were collected from 35 SLE patients with active disease despite conventional therapy, before and after 6-month add-on treatment with belimumab, and 26 matched healthy individuals. We measured cholesterol efflux and antioxidant capacities, paraoxonase-1 activity, serum amyloid A1, myeloperoxidase and lipid peroxidation product levels of HDL. LC-MS/MS was performed to analyze the HDL lipidome. Following treatment with belimumab, cholesterol efflux and antioxidant capacities of HDL were significantly increased in SLE patients and restored to levels of controls. HDL-associated paraoxonase-1 activity was also increased, whereas lipid peroxidation products were decreased following treatment. HDL cholesterol efflux and antioxidant capacities correlated negatively with the disease activity. Changes were noted in the HDL lipidome of SLE patients following belimumab treatment, as well as between SLE patients and healthy individuals, and specific changes in lipid species correlated with functional parameters of HDL. HDL of SLE patients with active disease displays impaired atheroprotective properties accompanied by distinct lipidomic signature compared with controls. Belimumab treatment may improve the HDL atheroprotective properties and modify the HDL lipidomic signature in SLE patients, thus potentially mitigating atherosclerosis development.

Lactobacillus reuteri mitigates hepatic ischemia/reperfusion injury by modulating gut microbiota and metabolism through the Nrf2/HO-1 signaling.

This study seeks to investigate the impacts of Lactobacillus reuteri (L. reuteri) on hepatic ischemia-reperfusion (I/R) injury and uncover the mechanisms involved. Mice in the I/R groups were orally administered low and high doses of L.reuteri (L.reuteri-low and L. reuteri-hi; 1 × 1010 CFU/d and 1 × 1011 CFU/d), for 4 weeks prior to surgery. Following this, mice in the model group were treated with an Nrf2 inhibitor (ML-385), palmitoylcarnitine, or a combination of both. After treatment with L. reuteri, mice exhibited reduced levels of serum aminotransferase (ALT), aspartate aminotransferase (AST), and myeloperoxidase (MPO) activity, as well as a lower Suzuki score and apoptosis rate. L. reuteri effectively reversed the I/R-induced decrease in Bcl2 expression, and the significant increases in the levels of Bax, cleaved-Caspase3, p-p65/p65, p-IκB/IκB, p-p38/p38, p-JNK/JNK, and p-ERK/ERK. Furthermore, the administration of L. reuteri markedly reduced the inflammatory response and oxidative stress triggered by I/R. This treatment also facilitated the activation of the Nrf2/HO-1 pathway. L. reuteri effectively counteracted the decrease in levels of beneficial gut microbiota species (such as Blautia, Lachnospiraceae NK4A136, and Muribaculum) and metabolites (including palmitoylcarnitine) induced by I/R. Likewise, the introduction of exogenous palmitoylcarnitine demonstrated a beneficial impact in mitigating hepatic injury induced by I/R. However, when ML-385 was administered prior to palmitoylcarnitine treatment, the previously observed effects were reversed. L. reuteri exerts protective effects against I/R-induced hepatic injury, and its mechanism may be related to the promotion of probiotic enrichment, differential metabolite homeostasis, and the Nrf2/HO-1 pathway, laying the foundation for future clinical applications.

Efficacy of metamizole to prevent kidney injury after renal-ischaemic reperfusion injury in Wistar rats.

Renal ischaemia-reperfusion injury (RIRI) is a common kidney procedure complication due to temporary blood flow interruption, leading to kidney injuries. This study aimed to analyze the effect of metamizole on the levels of interleukin-18 (IL-18), neutrophil-gelatinase-associated lipocalin (NGAL), myeloperoxidase (MPO), and histopathological changes in rats with RIRI. Animal pre-clinical design study was used. Thirty-two male Wistar rats (Rattus norvegicus) were divided into four groups: negative control, positive control, M100, and M200. Blood samples were collected by intracardiac puncture, followed by bilateral nephrectomy and analyzed histopathologically. Significant difference in IL-18 levels between positive control vs negative control (114.1 + 12.07 vs. 94.0 + 11.4; P = 0.019) and positive control vs M100 (114.1 + 12.07 vs. 86.9 + 8.34; P = 0.007). There was no difference in NGAL. M100 group had the lowest serum MPO levels (14.78+2.01), there was a significant difference in MPO levels in all pairwise analyses. There was a difference in cumulative EGTI scores among the study groups [positive 10.5 (8-11) vs. negative 9 (7-10) vs. M100 9 (7-10) vs. M200 9 (7-11); P = 0.021]. Metamizole 100mg/kgBW can reduce IL-18 and MPO levels in RIRI, giving more optimal results without affecting NGAL levels. Metamizole administration can reduce cumulative EGTI scores in RIRI, both at doses of 100mg/kgBW and 200mg/kgBW. This study shows that Metamizole can be used to prevent kidney injury caused by RIRI. IL-18 and MPO can be biomarkers in predicting kidney injury in RIRI.

Dynamic thiol/disulfide homeostasis and myeloperoxidase levels in Gilbert's syndrome with mild hyperbilirubinemia.

This study aimed to compare dynamic thiol/disulfide homeostasis and myeloperoxidase (MPO) levels in patients with Gilbert's syndrome (GS) and healthy controls. Thiol/disulfide homeostasis and MPO levels are both associated with increased progression of atherosclerosis. The study included a total of 130 voluntary participants comprising 65 patients with GS and 65 healthy controls. These patients were selected randomly and dynamic thiol/disulfide homeostasis, MPO, complete blood count results, and biochemistry and lipid parameters were evaluated. Patients with known chronic diseases, medication usage, and acute infections were excluded from the study. Serum total thiol and native thiol levels were measured using the fully automated colorimetric method, while serum MPO levels were measured using the sandwich ELISA method. We found that patients with GS had significantly higher total thiol (352.3±38.6 vs. 317.9±47.9, p<0.001) and native thiol (386.6±42.6 vs. 348.0±51.1, p<0.001) and significantly lower disulfide (15.7±4.0 vs. 17.3±4.0, p=0.022) and MPO (130.7 vs. 166.3, p=0.006). In patients with bilirubin of <1 mg/dL, total thiol and native thiol levels were lower and disulfide, disulfide/native thiol (DNT) and disulfide/total thiol (DTT) ratios, and MPO levels were higher. Patients with bilirubin of <1 mg/dL also had higher total cholesterol. In these patients with GS, the thiol/disulfide balance shifted towards thiols and proinflammatory MPO levels were lower. When bilirubin was <1 mg/dL, disulfide, DNT and DTT ratios, and MPO were higher. Bilirubin levels affected all parameters of thiol/disulfide homeostasis and MPO levels independently of other risk factors. In light of our results, we suggest that mild hyperbilirubinemia in cases of GS has an anti-inflammatory and antioxidant effect and may be protective against atherosclerosis.

TREM1 facilitates the development of gastric cancer through regulating neutrophil extracellular traps-mediated macrophage polarization

Triggering receptor expressed on myeloid cell 1 (TREM1) elevation is associated with the unfavorable prognosis of gastric cancer (GC) patients. This work uncovered the effects and mechanism of TREM1 in GC. IHC staining examined TREM1 expression in GC tissues. TREM1-knockout and TREM1 knock-in mice were generated prior to the construction of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced GC mice model. H&E staining detected the pathological alternations of gastric tissues. IHC staining tested Ki67 expression. Wright-Giemsa staining performed neutrophil counting and flow cytometry analysis measured neutrophil infiltration. ELISA analyzed serum and tissue myeloperoxidase (MPO) levels and serum MPO-DNA levels. Immunofluorescence, Western blotting and related kits detected NETs formation. Immunofluorescence and IHC staining evaluated macrophage polarization. In MNNG-treated GES-1 cells and phorbal myristate acetate (PMA)-treated neutrophils, TREM1 expression was also examined. CCK-8 method and Western blotting assayed cell proliferation. Western blotting and immunofluorescence detected NETs formation. Flow cytometry analysis detected the changes of macrophage typing. TREM1 was overexpressed in tumor tissues, MNNG-treated GES-1 cells and PMA-treated neutrophils. TREM1 deficiency hindered tumor growth, reduced neutrophil infiltration, NETs formation and stimulated M1 macrophage polarization in MNNG-induced GC models. Neutrophil extracellular traps (NETs) degrader DNase-1 countervailed the impacts of TREM1 on MNNG-induced GC models in vivo. Collectively, TREM1 knockdown obstructed NETs-mediated M2 macrophage polarization to hamper GC progression.

Effect of Wu Zhi San supplementation in LPS-induced intestinal inflammation and barrier damage in broilers.

Intestinal inflammation and barrier damage can inhibit the absorption and transportation of nutrients in the small intestine, and lead to various chronic diseases. Wu Zhi San (WZS) is a traditional Chinese formula composed of Schisandrae, Anemarrhenae, Lonicerae, and Glycyrrhizae that was made to cure intestinal inflammation and barrier damage in broilers. To evaluate the protective effect of WZS on intestinal inflammation and barrier damage of broilers under lipopolysaccharide (LPS) stress, a total of 200 one-day-old broilers were randomly divided into five groups, namely, the CON group, LPS group, and three WZS groups (WZS-H, WZS-M, and WZS-L). The groups were designed for stress phase I (days 15, 17, 19, and 21) and stress phase II (days 29, 31, 33, and 35). The protective effect of WZS on the intestinal tract was evaluated by measuring the levels of serum myeloperoxidase (MPO), diamine oxidase (DAO), super oxide dismutase (SOD), and serum D-lactate (D-LA) and the expression of inflammatory factors in jejunum. The results showed that the diet supplemented with WZS could significantly reduce serum MPO, DAO, and D-LA levels and jejunal CD in broilers (p < 0.05), increase serum SOD levels and jejunal VH (p < 0.05), significantly downregulate the expression of NF-κB, TLR4, MyD88, and inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-10), and upregulate Claudin-1, Occludin-1, and ZO-1 in broiler jejunum mucosa (p < 0.05). On the other hand, WZS could significantly reduce the protein expression of NF-κB (p65) in broiler jejunum (p < 0.05). These results indicate that supplementing WZS in the diet can reduce intestinal inflammation and alleviate intestinal barrier damage, and by inhibiting the NF-κB/TLR4/MyD88 signaling pathway, supplementation with WZS intervenes in LPS-induced stress injury in broilers.

Effect of comprehensive nursing based on evidence-based nursing on reducing the incidence of pressure ulcers in patients undergoing posterior orthopedic surgery.

To analyze the effect of comprehensive nursing based on evidence-based nursing during the perioperative period on reducing the incidence of pressure ulcers in patients undergoing posterior orthopedic surgery. Data on 120 patients who underwent orthopedic posterior surgery in our hospital from February 2021 to December 2022 were retrospectively analyzed. The patients were divided into an observation group (n = 60) and a control group (n = 60) based on different nursing methods. Patients in the control group received routine nursing, whereas those in the observation group received comprehensive nursing under the guidance of the concept of evidence-based nursing. The incidence of postoperative pressure ulcer was also recorded. Fasting venous blood (5 mL) was collected from patients before and after surgery and used to measure levels of myeloperoxidase (MPO) and superoxide dismutase (SOD) using enzyme-linked immunosorbent assay. Ulcer tissue samples of patients with pressure ulcers were collected and used to detect the expression of caspase-3 protein, vascular endothelial growth factor (VEGF) mRNA, tumor necrosis factor-α (TNF-α) mRNA, and interleukin-1β (IL-1β) mRNA. The incidence of postoperative pressure ulcers was 8% in the observation group and 23% in the control group (P = .024). The scores of sensory perceptions of the patients in the observation group were significantly lower than those in the control group (P < .001), as were the scores for moisture (P < .001), activity (P = .008), mobility (P < .001), nutrition (P = .003), friction, and shear (P < .001). After surgery, the serum MPO level in the observation group was significantly lower than that in the control group (P < .001), whereas the SOD level in the observation group was significantly higher than that in the control group (P < .001). The expression of TNF-α, IL-1β, VEGF mRNA, and caspase-3 protein in pressure ulcer tissues in the observation group was significantly lower than that in the control group. Comprehensive nursing based on the concept of evidence-based nursing can significantly reduce the incidence of postoperative pressure ulcers following posterior orthopedic surgery.

Predictive role of MMP-9 and MPO in patients with reduced glomerular filtration rate after acute coronary syndrome

Background. Coronary artery disease (CAD) persistently remains the leading cause of mortality globally. Given the severity and impact of this condition, researchers have been meticulously studying the pathogenesis of athe-rosclerosis, a principal cause behind CAD. The pathogenesis stages are complex and multifaceted, including factors such as lipid accumulation, inflammation, and plaque formation. A particular area of active exploration pertains to the influence and role of different biomarkers, including matrix metalloproteinase 9 (MMP-9) and myeloperoxidase (MPO), on these processes. These biomarkers have been associated with the progression and destabilization of athe-rosclerotic plaques, which are central to CAD. However, the use of these biomarkers in the context of comorbidities, such as chronic kidney disease, remains an open area of research, especially in patients after myocardial infarction. Materials and methods. In our study, 96 patients who had acute coronary syndrome and subsequently undergone percutaneous coronary intervention were enrolled. They were stratified into groups (A and B) based on respective glomerular filtration rates. The primary endpoint of the study was all-cause mortality and major adverse cardiovascular and cerebrovascular events. Results. Our analysis revealed that serum levels of MPO in group B were insignificantly higher than those in group A. Conversely, the area under the receiver operating characteristic (ROC) curve for MMP-9 in group A exhibited a significant difference, standing at 0.8 (95% confidence interval 0.609–0.991; p = 0.039). However, the ROC curve for MPO did not yield a significant result in any group. A combined ROC curve was also generated, with the area under this curve showing a significantly higher value of 0.890 (95% confidence interval 0.805–0.975; p &lt; 0.001). Conclusions. We found that plasma levels of the above-mentioned biomarkers do not seem to influence a decrease in glomerular filtration rate. Nonetheless, MMP-9 levels offered significant prognostic information regarding predicted outcomes.

Changes of serum MMP-9, NSE, MPO levels and prognostic influencing factors in patients with intracranial aneurysm undergoing interventional embolization at different treatment timing.

To analyzes the changes in serum levels of matrix metalloproteinase-9 (MMP-9), neuroenolase (NSE), myeloperoxidase (MPO) and prognostic factors in patients with intracranial aneurysm (IA) undergoing interventional embolization at different treatment times. A retrospective analysis was made of 200 IA patients admitted to our department from January 2018 to June 2021 was performed. All patients underwent interventional embolization. According to the timing of surgery, the patients were divided into an early group (n=120, onset to surgery ≤72 h) and a delayed group (n=80, onset to surgery >72 h). The effect of embolization, complications and neurological deficit scale (NDS) scores were compared between the two groups. Serum MMP-9, NSE and MPO levels were compared before and after surgery, and the prognosis of all patients within 2 years after surgery was assessed by the Glasgow outcome scale (GOS) and divided accordingly into the good prognosis group (n=147) and the poor prognosis group (n=53) accordingly, and the prognostic factors influencing the patients were analyzed univariately and multifactorially.

Effect of Thoracic Epidural Anesthesia on Perioperative Neutrophil Extracellular Trapping Markers in Patients Undergoing Anesthesia and Surgery for Colorectal Cancer: A Randomized, Controlled Trial.

Neutrophil extracellular trapping (NETosis) is an immunologic mechanism strongly linked with increased metastatic risk in colorectal cancer. The authors hypothesized that patients who received propofol-epidural anesthesia (PEA) would exhibit decreases in the expression of serum neutrophil myeloperoxidase (MPO) and citrullinated histone H3 (H3Cit) levels compared with patients who received general anesthesia (GA). Colorectal cancer surgery patients were randomly assigned to the PEA (n = 30) or GA (n = 30) group. Serum MPO, H3Cit, and metalloproteinase-9 (MMP-9) levels before surgery and 24 h after surgery were measured, and visual analogue scale (VAS) scores were recorded. The patients who received PEA showed decreases in MPO (28.06 ± 11.23 vs 20.54 ± 7.29 ng/ ml; P = 0.004) and H3Cit [3.22 ± 0.86 vs 2.73 ± 0.94 ng/ ml; P = 0.042) 24 h after surgery compared with the patients subjected to GA. In addition, there was no difference in MMP-9 levels (75.98 ± 26.9 vs 73.45 ± 28.4 ng/ ml; P = 0.726). The visual analogue scale scores 2 h and 24 h after operation were significantly lower in PEA group (P < 0.05). The number of postoperative analgesia pump pressings and sufentanil consumptions within 48 h after surgery were significantly lower in the PEA group (P < 0.001). Propofol-epidural anesthesia reduces the expression of NETosis (MPO and H3Cit) in serum during colorectal cancer surgery. ChiCTR2200066708 ( www.chictr.org.cn ).

Melanoma-derived soluble mediators modulate neutrophil biological properties and the release of neutrophil extracellular traps

Polymorphonuclear neutrophils (PMNs) are the main effector cells in the inflammatory response. The significance of PMN infiltration in the tumor microenvironment remains unclear. Metastatic melanoma is the most lethal skin cancer with an increasing incidence over the last few decades. This study aimed to investigate the role of PMNs and their related mediators in human melanoma. Highly purified human PMNs from healthy donors were stimulated in vitro with conditioned media (CM) derived from the melanoma cell lines SKMEL28 and A375 (melanoma CM), and primary melanocytes as controls. PMN biological properties (chemotaxis, survival, activation, cell tracking, morphology and NET release) were evaluated. We found that the A375 cell line produced soluble factors that promoted PMN chemotaxis, survival, activation and modification of morphological changes and kinetic properties. Furthermore, in both melanoma cell lines CM induced chemotaxis, activation and release of neutrophil extracellular traps (NETs) from PMNs. In contrast, the primary melanocyte CM did not modify the biological behavior of PMNs. In addition, serum levels of myeloperoxidase, matrix metalloprotease-9, CXCL8/IL-8, granulocyte and monocyte colony-stimulating factor and NETs were significantly increased in patients with advanced melanoma compared to healthy controls. Melanoma cell lines produce soluble factors able to “educate” PMNs toward an activated functional state. Patients with metastatic melanoma display increased circulating levels of neutrophil-related mediators and NETs. Further investigations are needed to better understand the role of these “tumor-educated neutrophils” in modifying melanoma cell behavior.

The value of serum Lp-PLA2 combined with MPO in the diagnosis of cerebral infarction caused by large artery atherosclerosis

ObjectiveTo explore the value of serum lipoprotein-associated phospholipase A2（Lp-PLA2）combined with myeloperoxidase（MPO）for the diagnosis of large artery atherosclerosis(LAA) cerebral infarction. MethodsBaseline data were collected from patients with first-ever acute cerebral infarction, serum Lp-PLA2 and MPO levels were measured. The etiology of cerebral infarction was classified according to the Chinese Ischemic Stroke Subtype Classification Standard. The risk factors associated with LAA cerebral infarction were identified by univariate and multivariate regression analysis. The diagnostic value of serum Lp-PLA2 and MPO for LAA cerebral infarction was assessed by the area under the receiver-operating characteristic (ROC) curve. ResultsOverall 368 patients were involved, 148 patients (40.22 %) were LAA. The serum La-PLA2 and MPO levels were higher in the LAA group than those in non-LAA group (23.06 ± 3.39 ng/mL versus 17.48 ± 3.26 ng/mL; 93.60 ± 9.58 ng/mL versus 75.98 ± 15.53 ng/mL; P < 0.001 for both). Multivariate analysis showed that elevated levels of serum Lp-PLA2 (OR 1.742, 95 %CI 1.499–2.025; P < 0.001) and MPO (OR 1.060, 95 % CI 1.026–1.096; P = 0.001) were the independent risk factors of LAA cerebral infarction. The area under curve of the serum Lp-PLA2 combined with MPO for the diagnosis of LAA cerebral infarction was 0.896 [0.866 ∼ 0.927] (P < 0.001). ConclusionSerum Lp-PLA2 combined with MPO could be valued as a predictor of acute cerebral infarction caused by large artery atherosclerosis.

Common mechanisms of placental dysfunction in preeclampsia, gestational diabetes, and COVID-19 in pregnant women

COVID-19 infection, preeclampsia and gestational diabetes mellitus in pregnancy cause similar changes in the placenta and influence development of the fetus between conception and birth in gestation. Proper uterine and placental vascularization is essential for normal fetal development. The transplacental exchange is regulated and maintained by the placental endothelium. During placental implantation, the trophoblast differentiates into two distinct layers, the inner cytotrophoblast and outer syncytiotrophoblast, which are key elements of the human placental barrier. Proinflammatory cytokines exacerbate ischemic events and create an upward spiral of an inflammatory reaction in the placenta. Placental pathology in gestational COVID-19 shows desquamation and damage of trophoblast and chronic histiocytic intervillositis. Similar lesions also occur in gestational diabetes mellitus and preeclampsia. The systemic inflammatory response of the mother, the increased inflammation in the placenta and cytokine production by placental trophoblasts should be monitored throughout pregnancy. Placental angiogenesis can be evaluated by serum vascular endothelial growth factor, Annexin A2, placental growth factor or sclerostin. Tissue damage can be assessed by measuring levels of serum lactate dehydrogenase and myeloperoxidase. Blood flow can be monitored with three-dimensional Doppler and pathological changes can be documented with paraffin-embedded tissue sections stained with hematoxylin and eosin, and electron microscope images as well as immunohistochemistry tests for vascular endothelial growth factor, placental growth factor, sclerostin and Annexin A2. The damage of maternal and fetal vascular perfusion (villitis and fibrin deposition) is a common mechanism of gestational diseases. The placenta lesions liberate anti-endothelial factors that lead to anti-angiogenic conditions and are the common mechanism of maternal placental vascular malperfusion in gestational diseases. Keywords: dysfunction, inflammation, pathology, placenta, pregnancy, vascularization

Long-term clinical outcomes of aspirin-exacerbated respiratory disease: Real-world data from an adult asthma cohort.

Aspirin-exacerbated respiratory disease (AERD) is a phenotype of severe asthma, but its disease course has not been well documented compared with that of aspirin-tolerant asthma (ATA). This study aimed to investigate the long-term clinical outcomes between AERD and ATA. AERD patients were identified by the diagnostic code and positive bronchoprovocation test in a real-world database. Longitudinal changes in lung function, blood eosinophil/neutrophil counts, and annual numbers of severe asthma exacerbations (AEx) were compared between the AERD and the ATA groups. Within a year after baseline, two or more severe AEx events indicated severe AERD, whereas less than two AEx events indicated nonsevere AERD. Among asthmatics, 353 had AERD in which 166 and 187 patients had severe and nonsevere AERD, respectively, and 717 had ATA. AERD patients had significantly lower FEV1%, higher blood neutrophil counts, and higher sputum eosinophils (%) (all p < .05) as well as higher levels of urinary LTE4 and serum periostin, and lower levels of serum myeloperoxidase and surfactant protein D (all p < .01) than those with ATA. In a 10-year follow-up, the severe AERD group maintained lower FEV1% with more severe AEs than the nonsevere AERD group. We demonstrated that AERD patients presented poorer long-term clinical outcomes than ATA patients in real-world data analyses.

Neutrophil extracellular trap burden correlates with the stenosis of coronary atherosclerosis.

Coronary atherosclerosis diseases (CADs) are associated with chronic inflammation. Neutrophil extracellular traps (NETs) are a type of novel proinflammatory cytokines whose levels are dramatically elevated in acute coronary syndrome. We conducted this study to further evaluate the association between circulating NET-associated markers and CAD in Chinese adults. A total of 174 patients with CAD and 55 healthy controls were screened using percutaneous coronary intervention or coronary computed tomography angiography. Blood lipid levels, blood glucose levels, and blood cell counts were determined using commercial kits. Serum levels of myeloperoxidase (MPO) and neutrophil elastase (NE) were measured using ELISA. Double-stranded DNA (dsDNA) in serum was quantified using the Quant-iT PicoGreen assay. We also compared the circulating NET levels with various parameters in the study subjects. The levels of serum NET markers, dsDNA, MPO, and NE, were significantly elevated in patients with CAD, particularly in the severe group, consistent with the increase in neutrophil counts. The levels of NET markers correlated with the risk factors of AS, increasing with the number of risk factors. NET markers were identified as independent risk factors for severe coronary stenosis and also as predictors of severe CAD. NETs may be related to AS and serve as indicators or predictors of stenosis in patients with severe CAD.

Relationship between disease severity and myeloperoxidase in chronic viral hepatitis: a prospective study.

Aim: To measure serum myeloperoxidase (MPO) levels and to evaluate the relationship between this parameter and histological findings in chronic hepatitis B and C patients. Materials & methods: Three groups were formed: chronic hepatitis B, chronic hepatitis C and a control group. Serum MPO levels were determined by ELISA. Results: MPO level was found to be higher in both patient groups compared with the control group (p<0.05). It was also higher in chronic hepatitis B and C patients with significant fibrosis compared with patients with mild fibrosis (p<0.05). Conclusion: Our results show that increased MPO level can be used as an important noninvasive marker in both the early detection of liver fibrosis and the prediction of significant fibrosis.