Elevated plasma D-dimer levels in dermatomyositis patients with cutaneous manifestations.
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ABSTRACT:
SUBMITTER: Habe K
PROVIDER: S-EPMC6363793 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Dermatomyositis (DM) is a strikingly heterogenous disease characterized by a broad and ever-evolving spectrum of cutaneous manifestations that transcend the classic "hallmarks" defined by Peter and Bohan in 1975. Despite the increasing preponderance and ubiquity of autoantibody, radiologic, and electrophysiologic testing, the diagnosis of DM still hinges largely on prompt detection of cutaneous manifestations of this condition. While pathognomonic cutaneous features of DM are more readily recognizable, many patients present with subtle and/or atypical skin manifestations, and diagnosis of DM may require clinician identification of these cutaneous clues. In this review, we highlight several of the lesser-known skin manifestations of DM, specifically, panniculitis, diffuse subcutaneous edema, erythroderma, calcinosis, ulceration, flagellate erythema, Wong-type DM, gingival telangiectasias, and the ovoid palatal patch. We describe the clinical and histopathologic presentation of these cutaneous findings. While manifesting less frequently than the heliotrope rash, Gottron's papules, and Gottron's sign, these cutaneous clues are equally important for clinicians to recognize in order to facilitate timely diagnosis and early intervention.
| S-EPMC8033358 | biostudies-literature
Project description:BackgroundHemostatic alterations occur during the development of cancer. Plasma D-dimer is a hypercoagulability and fibrinolytic system marker that is increased in patients with various solid tumours. The aim of this study was to evaluate the hemostatic status of nasopharyngeal carcinoma (NPC) patients by assessing plasma D-dimer levels to investigate its value as a prognostic marker.MethodsWe retrospectively analysed 717 patients with nasopharyngeal carcinoma, and we applied Cox regression and log-rank tests to assess the association of D-dimer levels with disease-free survival (DFS), distant metastasis-free survival (DMFS), and overall survival (OS). D-dimer levels were measured using a quantitative D-dimer latex agglutination assay.ResultsUsing the 3rd quartile values (0.8 ?g/L) as the optimal cut-offs, we found that patients with high D-dimer levels have a shorter 3-year DFS, (79%, 95%CI (73.1-84.9)) vs. (69%, 95%CI (59.2-78.8)), DMFS (87%, 95%CI (83.1-90.9)) vs. (77%, 95%CI (69.2-84.8)), and overall survival (82%, 95%CI (76.1-87.9)) vs. (76%, 95%CI (66.2-85.8)). Multivariate analysis revealed that pre-treatment D-dimer levels and EBV DNA were significant independent factors for DFS, DMFS, and OS in NPC patients. Subgroup analyses indicated that the plasma D-dimer levels could effectively stratify patient prognosis for early cancer, advanced stage cancer, and patients with EBV DNA ?4000 copies/ml.ConclusionsHigh D-dimer levels were associated with poor disease-free survival, distant metastasis-free survival, overall survival, and increased risk of mortality in NPC patients. Prospective trials are required to assess the prognostic value of D-dimer levels.
| S-EPMC4242497 | biostudies-literature
Project description:PurposeWe aimed to explore the difference in coagulation function between healthy individuals and patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis and its relationship with disease severity.MethodsWe retrospectively compared coagulation function in 161 patients with first-attack anti-NMDAR encephalitis and 178 healthy individuals. The association between D-dimer levels and disease severity was analyzed using binary logistic regression. Receiver operating characteristic (ROC) curves were used to analyze the predictive value of D-dimer levels for the severity of anti-NMDAR encephalitis.ResultsCompared to control individuals, patients with anti-NMDAR encephalitis had higher D-dimer levels (median 0.14 vs. 0.05 mg/L, p < 0.001), blood white blood cell (WBC) count (median 8.54 vs. 5.95 × 109/L, p < 0.001), and neutrophil count (median 6.14 vs. 3.1 × 109/L, p < 0.001). D-dimers (median 0.22 vs. 0.10 mg/L, p < 0.001), blood WBC count (median 9.70 vs. 7.70 × 109/L, p < 0.001), neutrophil count (median 7.50 vs. 4.80 × 109/L, p < 0.001), and C-reactive protein (median 2.61 vs. 1.50 mg/l, p = 0.017) were higher; however, eosinophils (median 0.02 vs. 0.06 × 109/L, p < 0.001), and blood calcium (median 2.26 vs. 2.31 mmol/L, p = 0.003) were lower in patients with severe forms of anti-NMDAR encephalitis than in those with mild to moderate forms, and were associated with initial modified Rankin Scale scores. Multivariate analysis showed that D-dimer levels were significantly associated with severity [odds ratio =2.631, 95% confidence interval (CI) = 1.018-6.802, p = 0.046]. The ROC curve was used to analyze the predictive value of D-dimer levels for disease severity. The area under the curve was 0.716 (95% CI = 0.64-0.80, p < 0.001), and the best cut-off value was D-dimer = 0.147 mg/L (sensitivity 0.651; specificity, 0.705).ConclusionSerum D-dimer and neutrophil levels were independent predictors of disease severity in patients with first-attack anti-NMDAR encephalitis.
| S-EPMC9707621 | biostudies-literature
Project description:Background D-dimer has been shown as a valuable predictor for the prognosis of sepsis. But the prognostic association of an elevated D-dimer with adverse outcomes of all critical illnesses in pediatric intensive care unit (PICU) has received far less emphasis. Methods This was a single-center retrospective study, including 7,648 critical patients aged between 28 days and 18 years from the pediatric intensive care (PIC) database from 2010 to 2018. The primary outcome was the in-hospital mortality rate. Results Higher levels of D-dimer, INR, PT, APTT, and lower Fib were observed in the non-survivor group (all P < 0.001). D-dimer, INR, PT and APTT were independent risk factors for prognosis in critically ill children. There was the highest AUROC in D-dimer for predicting in-hospital mortality of critically ill patients compared with INR, PT, APTT, and Fib (D-dimer: 0.77 vs. INR: 0.73 vs. PT: 0.73 vs. APTT: 0.64 vs. Fib: 0.60). The cut-off value, sensitivity, and specificity of D-dimer were 1.53, 0.65, and 0.77, respectively. Subgroup analysis showed a stable evaluation effectiveness of D-dimer for predicting in-hospital mortality of critically ill patients in the age and gender groups. Conclusions We found poorer coagulation function in the non-survivors compared with the survivors. Among the coagulation indicators, D-dimer was most strongly associated with in-hospital mortality of unselected critically ill children.
| S-EPMC9537732 | biostudies-literature
Project description:INTRODUCTION:Progranulin (PGRN), a pleiotropic growth factor, has emerged as an immunoregulatory molecule. Because the roles of PGRN in dermatomyositis (DM) are still unknown, we investigated whether serum PGRN levels are associated with disease activity and prognosis in DM patients, particularly in those with DM complicated with interstitial lung disease (ILD). METHODS:The serum levels of PGRN were measured by enzyme-linked immunosorbent assay in patients with DM (n=57; acute/subacute interstitial pneumonia (A/SIP): n=17, chronic interstitial pneumonia (CIP): n=24, without ILD: n=16), polymyositis (PM, n=21; including 6 with ILD) and normal healthy controls (NHCs, n=60). We assessed the correlation between the serum PGRN levels and the activity indexes of ILD or prognosis in DM patients with ILD. RESULTS:Serum PGRN levels were significantly higher in DM patients than in PM patients (P=0.0025) and in NHCs (P<0.0001). In DM patients, the levels were significantly higher in patients with A/SIP than in those with CIP (P<0.0001) or without ILD (P=0.0003). The serum PGRN levels in DM patients with ILD significantly correlated with serum ferritin (rS=0.77, P<0.0001), lactate dehydrogenase (rS=0.54, P=0.0003) and C-reactive protein (rS=0.48, P=0.0015) levels. Moreover, in DM patients with ILD, the cumulative survival rate for 6 months was significantly lower in the group with serum PGRN levels?200 ng/ml (67%) than in the group with serum PGRN levels<200 ng/ml (100%) (P=0.0009). CONCLUSIONS:Serum PGRN is associated with disease activity and prognosis of DM with ILD. PGRN may play a role in the pathogenesis of DM and could be a useful biomarker.
| S-EPMC4354987 | biostudies-literature
Project description:Genome-wide association studies have recently identified 3p21.31, with lead variant pointing to the CXCR6 gene, as the strongest thus far reported susceptibility risk locus for severe manifestation of COVID-19. In order the determine its role, we measured plasma levels of Chemokine (C-X-C motif) ligand 16 (CXCL16) in the plasma of COVID-19 hospitalized patients. CXCL16 interacts with CXCR6 promoting chemotaxis or cell adhesion. The CXCR6/CXCL16 axis mediates homing of T cells to the lungs in disease and hyper-expression is associated with localised cellular injury. To characterize the CXCR6/CXCL16 axis in the pathogenesis of severe COVID-19, plasma concentrations of CXCL16 collected at baseline from 115 hospitalized COVID-19 patients participating in ODYSSEY COVID-19 clinical trial were assessed together with a set of controls. We report elevated levels of CXCL16 in a cohort of COVID-19 hospitalized patients. Specifically, we report significant elevation of CXCL16 plasma levels in association with severity of COVID-19 (as defined by WHO scale) (P-value < 0.02). Our current study is the largest thus far study reporting CXCL16 levels in COVID-19 hospitalized patients (with whole-genome sequencing data available). The results further support the significant role of the CXCR6/CXCL16 axis in the immunopathogenesis of severe COVID-19 and warrants further studies to understand which patients would benefit most from targeted treatments.
| S-EPMC8801318 | biostudies-literature
Project description:BackgroundNatriuretic peptides have been proposed as biomarkers of cardiovascular disease, especially heart failure. Brain natriuretic peptide (BNP) has also been shown to be upregulated at the transcriptional and translational levels by pro-inflammatory cytokines in cardiac myocytes. Although we often measure plasma BNP levels in cancer patients, it remains unknown whether cancer-related inflammation affects the plasma BNP levels. We investigated the relationship between the BNP and human cancers.MethodsWe retrospectively studied 2,923 patients in whom the plasma BNP levels and serum C-reactive protein (CRP) were measured and echocardiography was performed. Patients with clinically evident heart failure (NYHA II or higher), heart disease requiring medical treatment or surgery, renal dysfunction, and inflammatory disease were excluded. There were 234 patients in the final analysis. Blood sampling was performed before surgery and chemotherapy. In addition, we evaluated the relationship between the inflammation and plasma BNP levels in mouse models of colon cancer.ResultsOf the 234 patients, 80 were diagnosed with cancer. Both the plasma BNP and serum CRP levels were significantly higher in cancer patients than those without. There were no significant differences in the echocardiographic parameters. There was a significant positive correlation between the plasma BNP and serum CRP levels in cancer patients (r = 0.360, P<0.01) but not in those without. In cancer patients, only the CRP correlated with the BNP independent of the age, creatinine level, hypertension, and body mass index. In addition, in nude mice with subcutaneous colon cancer, the plasma BNP level was elevated compared with that in non-cancer mice, and there was a significant relationship between the plasma BNP and serum levels of the inflammatory markers.ConclusionsIn cancer patients, as well as colon cancer model mice, the plasma BNP levels were elevated, possibly due to cancer-related inflammation. The effect of cancer on the BNP levels should be considered when using BNP as an indicator of heart failure in cancer patients.
| S-EPMC5453551 | biostudies-literature
Project description:BackgroundThe pathogenesis of coronavirus disease 2019 (COVID-19) is still incompletely understood, but it seems to involve immune activation and immune dysregulation.ObjectiveWe examined the parameters of activation of different leukocyte subsets in COVID-19-infected patients in relation to disease severity.MethodsWe analyzed plasma levels of myeloperoxidase (a marker of neutrophil activation), soluble (s) CD25 (sCD25) and soluble T-cell immunoglobulin mucin domain-3 (sTIM-3) (markers of T-cell activation and exhaustion), and sCD14 and sCD163 (markers of monocyte/macrophage activation) in 39 COVID-19-infected patients at hospital admission and 2 additional times during the first 10 days in relation to their need for intensive care unit (ICU) treatment.ResultsOur major findings were as follows: (1) severe clinical outcome (ICU treatment) was associated with high plasma levels of sTIM-3 and myeloperoxidase, suggesting activated and potentially exhausted T cells and activated neutrophils, respectively; (2) in contrast, sCD14 and sCD163 showed no association with need for ICU treatment; and (3) levels of sCD25, sTIM-3, and myeloperoxidase were inversely correlated with degree of respiratory failure, as assessed by the ratio of Pao2 to fraction of inspired oxygen, and were positively correlated with the cardiac marker N-terminal pro-B-type natriuretic peptide.ConclusionOur findings suggest that neutrophil activation and, in particular, activated T cells may play an important role in the pathogenesis of COVID-19 infection, suggesting that T-cell-targeted treatment options and downregulation of neutrophil activation could be of importance in this disorder.
| S-EPMC7503135 | biostudies-literature
Project description:Interleukin (IL)-16, a polypeptide cytokine, plays a crucial role in the inflammatory process, acting as a chemoattractant for peripheral immune cells and has been linked to various inflammatory diseases. However, its role in patients with acute myocardial infarction (AMI) is unclear.We retrospectively analyzed serum levels of IL-16 in blood of patients with (STEMI, n?=?45) and without ST-segment elevation myocardial infarction (NSTEMI, n?=?42) compared with controls with excluded coronary artery disease (n?=?55). Furthermore, correlation analysis with inflammatory cells, C-reactive protein (CRP) levels, dendritic cell precursors (DCPs), and other clinical and biochemical markers was performed.Compared with controls, patients with STEMI and NSTEMI evidenced higher levels of IL-16 in pg/mL (STEMI: 759.38?±?471.54, NSTEMI: 677.77?±?438.8, control: 500.45?±?432.21; P?=?.002). IL-16 correlated with CRP (r?=?0.26, P?=?.001), leucocytes (r?=?0.38, P?<?.001), NT-proBNP (r?=?0.20, P?=?.02) and hsTnT (r?=?0.25, P?=?.004). Circulating myeloid DCPs, plasmacytoid DCPs, and total DCPs showed a significant inverse correlation to IL-16 levels (r?=?-0.21, P?=?.01; r?=?-0.23, P?=?.005; r?=?-0.26, P?=?.002, respectively).Interleukin-16 might play an important role in the inflammatory process of patients suffering from AMI and correlates with inflammatory cell activation and clinical and biochemical markers. The cytokine IL-16 might upregulate the proinflammatory response and recruitment of inflammatory cells into infarcted myocardium.
| S-EPMC5682786 | biostudies-literature
Project description:Emerging evidence suggests that two heparin-binding growth factor, midkine and pleiotrophin are implicated in the pathogenesis of autoimmune diseases including SLE. To investigate the plasma midkine and pleiotrophin levels in SLE patients, as well as their correlation with major clinical parameters and interleukin-17 (IL-17) level in SLE, 83 SLE patients and 123 controls including 20 rheumatoid arthritis (RA) patients, 21 Sjögren's syndrome (SS) patients and 82 healthy controls (HCs) were recruited. Plasma midkine, pleiotrophin and IL-17 levels were detected by ELISA. Midkine and pleiotrophin levels were significantly higher in SLE, RA and SS patients compared with HCs (all P < 0.05). There were significantly lower midkine and pleiotrophin levels in SLE compared to SS (P < 0.05 and P < 0.01, respectively). No significant differences in midkine and pleiotrophin levels were found between SLE and RA (P = 0.240 and P = 0.074, respectively). Both plasma midkine and pleiotrophin levels were associated with rash and anti-SSA in SLE. In addition, both midkine and pleiotrophin levels were positively associated with IL-17 level in SLE (both P < 0.001). Area under curve (AUC) of the receiver operating characteristic (ROC) curve for midkine and pleiotrophin were 0.606 (0.527-0.681) and 0.605 (0.526-0.680) respectively. In conclusion, elevated plasma midkine and pleiotrophin levels and their associations with rash, anti-SSA and IL-17 in SLE patients suggest their involvement in this disease.
| S-EPMC5522313 | biostudies-literature