Biomarker Of Disease Activity Research Articles

Chronic Inflammatory Demyelinating Polyneuropathy and Evaluation of the Visual Evoked Potentials: A Review of the Literature.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a rare autoimmune disorder characterised by the progressive demyelination of peripheral nerves, resulting in motor and sensory deficits. While much research has focused on clinical and electrophysiological aspects of CIDP, there is an emerging interest in exploring its impact on the visual system through visual evoked potentials (VEPs). This comprehensive review synthesises existing literature on VEP findings in CIDP patients, shedding light on their potential diagnostic and prognostic value. The review thoroughly examines studies spanning the last two decades, exploring VEP abnormalities in CIDP patients. Notably, VEP studies have consistently revealed prolonged latencies and reduced amplitudes in CIDP patients compared to healthy controls. These alterations in VEP parameters suggest that the demyelinating process extends beyond the peripheral nervous system to affect the central nervous system, particularly the optic nerve and its connections. The correlation between VEP abnormalities and clinical manifestations of CIDP, such as visual impairment and sensory deficits, underscores the clinical relevance of VEP assessment in CIDP management. Furthermore, this review addresses the potential utility of VEPs in aiding CIDP diagnosis and monitoring disease progression. VEP abnormalities may serve as valuable biomarkers for disease activity, helping clinicians make timely therapeutic decisions. Moreover, this review discusses the limitations and challenges associated with VEP assessment in CIDP, including variability in recording techniques and the need for standardised protocols. In conclusion, this review highlights the evolving role of VEPs as a non-invasive tool in CIDP evaluation. The consistent VEP abnormalities observed in CIDP patients suggest the involvement of the central nervous system in this demyelinating disorder. As our understanding of CIDP and its pathophysiology continues to evolve, further research in this area may lead to improved diagnostic accuracy and monitoring strategies, ultimately enhancing the clinical management of CIDP patients.

The emerging role of Growth Differentiation Factor 15 as a potential disease biomarker in juvenile dermatomyositis.

We aimed to investigate the potential of Growth Differentiation Factor 15 (GDF-15) as a novel biomarker for disease activity in Juvenile Dermatomyositis (JDM). We recruited children with juvenile myositis including juvenile dermatomyositis (n = 77), polymyositis (n = 6), and healthy controls (n = 22). GDF-15 levels in plasma were measured using ELISA. Statistical analyses were performed using non-parametric tests. Levels of GDF-15 were significantly elevated in JDM compared with healthy controls (p< 0.001). GDF-15 levels exhibited strong positive correlations with disease activity scores, including the Disease Activity Score (DAS) total score, DAS skin score, DAS muscle score, and Childhood Myositis Assessment Scale (CMAS). Additionally, GDF-15 levels could differentiate between active disease and remission based on the Physician Global Assessment of muscle score. Positive correlations were observed between levels of GDF-15 and creatine kinase, neopterin, and nailfold end row loops, indicating the potential involvement of GDF-15 in muscle damage, immune activation, and vascular pathology. ROC curve analysis showed GDF-15 to be more effective in assessing disease activity in JDM than creatine kinase (AUC 0.77, p= 0.001 and AUC 0.6369, p= 0.0738, respectively). GDF-15 may serve as a valuable biomarker for assessing disease activity in JDM. It exhibits better sensitivity and specificity than creatine kinase, and the levels correlate with various disease activity scores and functional measures. GDF-15 may provide valuable information for treatment decision-making and monitoring disease progression in JDM.

ANCA-Associated Vasculitis: Practical Issues in Management.

ANCA associated vasculitides are multi-system autoimmune diseases which are increasing in prevalence. In this review we will discuss the clinical manifestations and review the management options. We highlight the various trials of induction and maintenance therapy and discuss the areas of unmet need. These include understanding which patients are at highest risk of relapse, clinical adaptation of improved biomarkers of disease activity and tools to discuss long term prognosis.

Tape strips detect molecular alterations and cutaneous biomarkers in skin of patients with hidradenitis suppurativa

Hidradenitis suppurativa (HS) has a high unmet need for better treatments. Biopsies are considered the gold standard for studying molecular alterations in skin. A reproducible, minimally invasive approach is needed for longitudinal monitoring in trials and in pediatric populations. To determine whether skin tape strips can detect molecular alterations in HS and identify biomarkers of disease activity. We performed RNA sequencing on tape strips collected from lesional and healthy-appearing (nonlesional) HS skin (n=22) and healthy controls (n=21). We correlated the expression of skin biomarkers between tape strips and a previously published gene-signature of HS biopsies. Tape strips detected upregulation of known HS biomarkers (eg, Interleukin[IL]-17A) in nonlesional and/or lesional skin and also identified novel clinically actionable targets, including OX40 and JAK3. The expression of Th17 and tumor necrosis factor-α pathways were highly correlated between tape strips and biopsies. HS clinical severity was significantly associated with expression of biomarkers (eg tumor necrosis factor-α , IL-17A/F, OX40, JAK1-3, IL-4R) in HS lesional and/or nonlesional skin. Sample size. Tape stripping is limited in depth. This study validates tape strips as a minimally-invasive approach to identify cutaneous biomarkers in HS. This provides a novel avenue for monitoring treatment efficacy and a potential step toward individualized therapy in HS.

Serum Neurofilament Light Chain as a Biomarker for Disease Activity in Relapsing Remitting Multiple Sclerosis Patients

Serum Neurofilament Light Chain as a Biomarker for Disease Activity in Relapsing Remitting Multiple Sclerosis Patients

Cerebrospinal Fluid Neurofilament Light Chain as a Biomarkers of Disease Activity and Disability in NMOSD

Cerebrospinal Fluid Neurofilament Light Chain as a Biomarkers of Disease Activity and Disability in NMOSD

Serum profiling identifies CCL8, CXCL13, and IL-1RA as markers of active disease in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a clinically heterogeneous disease that presents a challenge for clinicians. To identify potential biomarkers for diagnosis and disease activity in SLE, we investigated a selected yet broad panel of cytokines and autoantibodies in patients with SLE, healthy controls (HC), and patients with other autoimmune diseases (AIDs). Serum samples from 422 SLE patients, 546 HC, and 1223 other AIDs were analysed within the frame of the European PRECISESADS project (NTC02890121). Cytokine levels were determined using Luminex panels, and autoantibodies using different immunoassays. Of the 83 cytokines analysed, 29 differed significantly between patients with SLE and HC. Specifically, CCL8, CXCL13, and IL-1RA levels were elevated in patients with active, but not inactive, SLE versus HC, as well as in patients with SLE versus other AIDs. The levels of these cytokines also correlated with SLE Disease Activity Index 2000 (SLEDAI-2K) scores, among five other cytokines. Overall, the occurrence of autoantibodies was similar across SLEDAI-2K organ domains, and the correlations between autoantibodies and activity in different organ domains were weak. Our findings suggest that, upon validation, CCL8, CXCL13, and IL-1RA could serve as promising serum biomarkers of activity in SLE.

Circulating tumor DNA for monitoring classic Hodgkin lymphoma patients: Correlation with FDG-PET/CT.

The value of circulating tumor DNA (ctDNA) as a biomarker of disease activity in classic Hodgkin lymphoma (cHL) patients has not yet been well established. By profiling primary tumors and ctDNA, we identified common variants between primary tumors and longitudinal plasma samples in most of the cases, confirming high spatial and temporal heterogeneity. Although ctDNA analyses mirrored HRS cell genetics overall, the prevalence of variants shows that none of them can be used as a single biomarker. Conversely, the estimation of hGE/mL, based on measures of total ctDNA, reflects disease activity and is almost perfectly correlated with standard parameters such as PET/CT that are associated with refractoriness.

Assessing vitamin D as a biomarker in inflammatory bowel disease.

A reliable serum biomarker for inflammatory bowel disease (IBD) activity is needed. Vitamin D is involved in inflammation and has been demonstrated to be low in IBD patients with active disease. It is routinely measured in IBD patients. Therefore, vitamin D may have a role as a serum biomarker in IBD. This study aims to investigate whether serum vitamin D may be useful as a biomarker in IBD in a real-world IBD population. Patients were identified by review of fecal calprotectin (FCP) results, and those who had a clinical review, vitamin D test, and FCP performed within 3 months were included. Clinical scores were calculated from chart review. Nonparametric tests were used to investigate vitamin D and FCP levels, serum biomarkers, and clinical scores. Of 616 patients identified, 325 episodes of matched vitamin D level and biomarker data were obtained. A statistically significant correlation was found between vitamin D levels and FCP levels for all patients (r = -0.19 [s -0.29 to -0.080], P < 0.001]. This remained true when patients were divided into IBD subsets. Low vitamin D was associated with partial Mayo scores and C-reactive protein (CRP) to albumin ratio in ulcerative colitis, and CRP and CRP/albumin ratio in Crohn's disease. Vitamin D level is negatively correlated with FCP and it may be considered as an adjunct biomarker at this stage. A prospective study would be beneficial to investigate further correlations between vitamin D and existing biomarkers of inflammation in IBD.

Metabolomics of Cerebrospinal Fluid Amino and Fatty Acids in Early Stages of Multiple Sclerosis.

Multiple sclerosis (MS) is a demyelinating and neurodegenerative autoimmune disease of the central nervous system (CNS) damaging myelin and axons. Diagnosis is based on the combination of clinical findings, magnetic resonance imaging (MRI) and analysis of cerebrospinal fluid (CSF). Metabolomics is a systematic study that allows us to track amounts of different metabolites in a chosen medium. The aim of this study was to establish metabolomic differences between the cerebrospinal fluid of patients in the early stages of multiple sclerosis and healthy controls, which could potentially serve as markers for predicting disease activity. We collected CSF from 40 patients after the first attack of clinical symptoms who fulfilled revised McDonald criteria of MS, and the CSF of 33 controls. Analyses of CSF samples were performed by using the high-performance liquid chromatography system coupled with a mass spectrometer with a high-resolution detector. Significant changes in concentrations of arginine, histidine, spermidine, glutamate, choline, tyrosine, serine, oleic acid, stearic acid and linoleic acid were observed. More prominently, Expanded Disability Status Scale values significantly correlated with lower concentrations of histidine. We conclude that these metabolites could potentially play a role as a biomarker of disease activity and predict presumable inflammatory changes.

IMMU-48. SOLUBLE CIRCULATING IMMUNE CHECKPOINT MOLECULES IN MALIGNANT BRAIN TUMORS

Abstract Immune checkpoint therapy has been shown to be effective in several types of cancer, and tumor-directed immune activation is also a promising strategy in glioblastoma (GBM) patients. Our goal was to discover alterations in the circulating immunome of GBM patients and other cerebral tumor entities to identify soluble immune biomarkers and novel therapeutic targets. We analyzed 30 markers in plasma of 208 patients and healthy donors, using bead-based multiplex assays and flow cytometry. In a smaller cohort we further applied a high-sensitivity discovery biomarker platform with 368 markers. We included patients with 1) primary GBM (n=68), 2) recurrent GBM (n=25), 3) cerebral metastases (NSCLC, n=61; breast cancer, n=19), 4) meningioma (n=15) as well as 5) healthy donors (HD, n=20). We detected a distinct immune signature in the peripheral blood of patients with GBM, which was defined by an increased prevalence of soluble immune checkpoint markers (sCD27, sPD-L2, sGal-9), whereas soluble chemokines (CX3CL, CXCL12) were underrepresented. This signature was similar in primary and recurrent GBM, but differed markedly from other cerebral tumor entities as well as from HD. Primary GBM, but not their recurrent counterparts, additionally exhibited increased levels of neurotrophic factors (BDNF, b-NGF) and signs of immune activation with significantly increased levels of IL-18. The biomarker discovery platform further identified 76 proteins that were specifically regulated in GBM compared to HD, offering the potential to serve as biomarkers for disease activity. GBM patients with higher levels of BDNF displayed a significantly shorter survival than patients with lower levels (9.33 vs. 21.90 months; p=0.0001). Likewise patients with high concentrations of VEGF survived significantly shorter than those with low concentrations (12.97 vs. 21.90 months, p=0,0166). Taken together, we were able to delineate a specific immune profile of soluble markers in GBM patients compared to other cerebral tumor entities and to healthy individuals.

CNSC-22. CANCER NEUROSCIENCE IN THE OR: ELECTROPHYSIOLOGIC INSIGHTS AT THE TIME OF BRAIN TUMOR RESECTION

Abstract Pioneering works by Venkatesh and Venkataramani demonstrated that formation of functional neural-glial synapses fosters development and growth of glial neoplasms. Resultant peritumoral neural hyperexcitability associates with tumor progression, though limited in vivo human data have been evaluated to date. We sought to enrich our understanding of these mechanisms by obtaining thin film intraoperative micro-electrocorticography (µECoG) recordings from patients undergoing primary brain tumor resection. METHODS: Intraoperative µECoG data for 8 patients with low- (LGG) and high-grade glioma (HGG, WHO grades 3 and 4) of various tumor histology were included. Analyses excluded any operative behavioral or cognitive tasks and evaluated data prior to stimulation for language or motor mapping. Following low pass (&amp;lt; 200 Hz) and notch filtering at 60, 120, and 180 Hz for ambient electrical noise, bandpower was calculated using multitaper spectral analysis for low frequency (LF, &amp;lt; 1 Hz), delta (1-4 Hz), beta (12-30 Hz), gamma (30-80 Hz), and high gamma (80-200 Hz) bands. RESULTS: Compared to isocitrate dehydrogenase (IDH) wild-type tumors, those with IDH-mutation (n = 3; two WHO grade 3, one grade 4) demonstrated the highest proportion of power within the LF band (92.2% vs 71.4%) with relatively lower proportional beta (3.6% vs 18.3%) and gamma (2.2% vs 8.7%) bandpower. The same pattern was seen in HGG (n = 5) vs LGG (n = 3) tumors with higher LF (84.5% vs 70.3%) and lower beta (10.3% vs 16.8%) and gamma (3.5% vs 10.8%) bandpower, perhaps driven by three HGGs with IDH mutation. Absolute bandpower was highest at all bands in a patient with left frontal glioblastoma. CONCLUSIONS: Interesting patterns are emerging that corroborate differential high and low frequency neural activity among patients with primary brain tumors. Disparities in LF and beta/gamma bands may represent therapeutic targets or a non-invasive biomarker of disease activity but require further, ongoing data collection and analyses.

FAR in systemic lupus erythematosus: a potential biomarker of disease activity and lupus nephritis.

The fibrinogen-to-albumin ratio (FAR), a novel inflammatory marker, has been studied in various diseases. However, the significance of FAR in systemic lupus erythematosus (SLE) has not been fully elucidated. This study was to investigate the connection between FAR and SLE. A retrospective analysis of 154 SLE patients and 77 healthy individuals was performed. The clinical and laboratory data were reviewed. Receiver operating characteristic (ROC) curves were conducted for FAR at baseline to predict disease activity and lupus nephritis (LN) in SLE patients. Pearson correlation was also applied. FAR in the SLE group was found to be significantly higher than that of the healthy control group (83.71mg/g vs. 53.14mg/g, P < 0.001). It was also significantly higher in patients with LN than that in patients without (107.64mg/g vs. 67.75mg/g, P < 0.001). The ROC curve for predicting LN showed that the area under the curve (AUC) of FAR (0.859, 95% CI 0.803-0.914) was the largest when compared to albumin (0.852, 95% CI 0.789-0.916) or fibrinogen (0.736, 95% CI 0.659-0.814) alone. In addition, FAR was a good predictor of severe disease activity in SLE (AUC = 0.721, 95% CI 0.612-0.830) and LN patients (AUC = 0.789, 95% CI 0.680-0.898). Pearson correlation analysis indicated that FAR demonstrated a strong correlation with SLE disease activity index 2000 (r = 0.4288, P < 0.001). FAR was significantly increased in SLE patients. It is a possible biomarker for disease activity and renal involvement in SLE.

Laboratory biomarkers for multiple sclerosis and their role in clinical practice

Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) most commonly diagnosed in young adults. In recent decades, new treatments have emerged that have radically changed the prognosis and quality of life of these patients. However, this has also raised new challenges in predicting the course and activity of the disease before the development of new neurological deficits that aggravate the disability and in prescribing the most appropriate disease-modifying therapy for the individual patient in a timely manner. One of the possible solutions that could help answer these questions is the use of laboratory biomarkers in MS. In addition to the oligoclonal bands (OGB) and the immunoglobulin G index, which are already well known and clinically useful laboratory tests, other biomarkers have been discovered that can assess the inflammatory and neurodegenerative processes occurring in the CNS. Kappa free light chains and K-index have been identified as new potential diagnostic biomarkers for MS, with similar sensitivity and specificity to OGB. Some biomarkers have also shown the ability to differentiate a clinically isolated syndrome from MS and to identify the clinical course of MS. The concentration of chitinase-3-like protein in the cerebrospinal fluid is currently the only biomarker that can help distinguish MS from a clinically isolated syndrome. Levels of glial fibrillary acidic protein in cerebrospinal fluid and blood serum can help distinguish primary progressive MS from the relapsing-remitting course of this disease. Serum neurofilament light chain levels are considered the most useful biomarker for monitoring disease activity and treatment efficiency. This article discusses the most promising biomarkers for MS diagnosis, disease activity, and treatment response.

Phase 1/2 Study of Pacritinib in Combination with Azacitidine in Chronic Myelomonocytic Leukemia

Introduction and preclinical rationale Treatment options for chronic myelomonocytic leukemia (CMML) are limited. Hypomethylating agents (HMAs) are the only approved therapies but are associated with unsatisfactory response rates and do not impact disease evolution (Merlevede Nat Comm 2016). JAK inhibition can reduce GM-CSF signaling, which contributes to CMML pathobiology; ruxolitinib has been clinically evaluated in CMML demonstrating promising, but insufficient clinical activity. Pacritinib is a JAK inhibitor that has a unique profile which suggests it may be uniquely well suited for the treatment of CMML, including targeting of CSF1R and IRAK1, both of which are upregulated in CMML and related diseases (Obba Autophagy 2015, Rhyasen Cancer Cell 2013). Additionally, pacritinib was recently shown to be a potent inhibitor of ACVR1 (Oh AJH 2023), potentially allowing for increased iron availability and improvement in anemia. Pacritinib has been evaluated preclinically in CMML primary samples and mouse models where it demonstrated significant, albeit heterogenous activity (Yoshimi Blood 2017). To enhance the activity of pacritinib in CMML, it was also evaluated in combination with azacitidine in GM-CSF hypersensitive cell lines and primary CMML cells where profound synergy was noted (Ma ASH 2015). Based on encouraging preclinical data, we hypothesize that the combination of pacritinib with azacitidine will be an effective treatment strategy in CMML patients. Methods In this phase 1/2 trial, we will evaluate the safety and efficacy of pacritinib and azacitidine in newly diagnosed or previously treated CMML. Patients must be JAK inhibitor and HMA naïve (≤1 cycle of HMA allowed). Phase 1 will follow a ‘3+3‘ dose de-escalation design and will enroll 6-12 patients. The primary objective of this phase is to determine the recommended phase 2 dose (RP2D) of pacritinib in combination with a fixed dose of azacitidine. Pacritinib will be administered at 200mg twice daily (with a lower dose of 100mg twice daily being explored in the case of dose limiting toxicity) in combination with azacitidine 75mg/m 2 for 7 days. Phase 2 will utilize a Simon's two stage design to assess the preliminary efficacy of pacritinib in combination with azacitidine at the RP2D. In the first stage, after treating 6 patients at the RP2D, there will be an interim response assessment as part of the phase 2 portion. If at least 4 among these 6 patients show a response, the trial will proceed to a second stage and enroll an additional 12 patients. Patients will be treated for 6 cycles of 28 days each with an interim bone marrow biopsy after cycle 3. The primary endpoint of the phase 1 portion is the recommended RP2D through the assessment of dose limiting toxicities and of the phase 2 portion is the overall response rate (ORR) by the end of cycle 6 as defined by a clinical benefit or greater by myelodysplastic syndrome/myeloproliferative neoplasm International Working Group response criteria (Savona 2015). Secondary endpoints include duration of response, disease free survival, overall survival, changes in MPN-SAF total symptom scores, palpable splenomegaly, and adverse events. Several correlative studies are planned as part of this clinical trial. Modulation of biomarkers of disease activity with treatment including GM-CSF dependent STAT5 phosphorylation, MAPK, and PI3K signaling will be analyzed. We will also evaluate changes in mutational and cytogenetic burden with treatment as well as at baseline to identify predictive biomarkers of response.

Proteomics reveal biomarkers for diagnosis, disease activity and long-term disability outcomes in multiple sclerosis

Sensitive and reliable protein biomarkers are needed to predict disease trajectory and personalize treatment strategies for multiple sclerosis (MS). Here, we use the highly sensitive proximity-extension assay combined with next-generation sequencing (Olink Explore) to quantify 1463 proteins in cerebrospinal fluid (CSF) and plasma from 143 people with early-stage MS and 43 healthy controls. With longitudinally followed discovery and replication cohorts, we identify CSF proteins that consistently predicted both short- and long-term disease progression. Lower levels of neurofilament light chain (NfL) in CSF is superior in predicting the absence of disease activity two years after sampling (replication AUC = 0.77) compared to all other tested proteins. Importantly, we also identify a combination of 11 CSF proteins (CXCL13, LTA, FCN2, ICAM3, LY9, SLAMF7, TYMP, CHI3L1, FYB1, TNFRSF1B and NfL) that predict the severity of disability worsening according to the normalized age-related MS severity score (replication AUC = 0.90). The identification of these proteins may help elucidate pathogenetic processes and might aid decisions on treatment strategies for persons with MS.

COX5A as a potential biomarker for disease activity and organ damage in lupus.

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease with limited therapeutic targets or clinical outcome predictors. This study aimed to gain more insights into the underlying immunological pathways and prognostic biomarkers of SLE. Integrated analyses of RNA-seq data from 64 SLE and 62 healthy controls, examining 27 immune cell types to explore the key pathways and driver genes in SLE pathogenesis. Single-cell RNA sequencing data from the skin and kidney were used to determine the association of COX5A expression with organ damage. The associations of COX5A with SLE phenotypes were further evaluated in two independent cohorts, and receiver operating characteristic (ROC) curves were constructed to assess the value of COX5A as a biomarker for disease activity and organ damage in SLE. We found that oxidative phosphorylation (OXPHOS) is the most significantly altered metabolic pathway in SLE, especially in effector T cells. Notably, we identified an OXPHOS-related enzyme, COX5A, whose expression was significantly higher in effector T cells than in naïve T cells and showed associations with disease activity, organ damage, and steroid treatment of SLE. Furthermore, ROC curves showed that COX5A is a robust biomarker for disease activity, kidney involvement, and new-onset skin lesions, with the area under the curve (AUC) values of 0.880, 0.801, and 0.805, respectively. Our results identified the OXPHOS signature as a prominent feature in SLE T cells, and COX5A as a potential candidate biomarker for disease activity and organ damage in SLE.

Proximity extension assay-based discovery of biomarkers for disease activity in chronic inflammatory demyelinating polyneuropathy

BackgroundObjective disease activity biomarkers are lacking in chronic inflammatory demyelinating polyneuropathy (CIDP), impacting treatment decisions in clinical care and outcomes in clinical trials. Using a proximity extension assay, we aimed...

Whole-joint histogram analysis of different models of diffusion weighted imaging in evaluating disease activity of axial spondyloarthritis.

To assess whole-joint histogram analysis of mono-exponential and bi-exponential diffusion weighted and diffusion kurtosis imaging in evaluating disease activity of axial spondyloarthritis (axSpA). A total of 82 patients with axSpA who underwent both DKI and multi b diffusion weighted imaging of the sacroiliac joints were divided into active and inactive disease groups based on clinical activity indices. Another 17 patients with nonspecific low back pain were included as a control group. The SPARCC scoring system was used to assess the level of sacroiliac joint bone marrow edema. Histogram parameters of apparent diffusion coefficient (ADC), true diffusion coefficient (D), perfusion fraction (f), pseudodiffusion coefficient (D*), mean kurtosis (MK), and mean diffusivity (MD) were calculated. Regions of interest were placed covering the entire sacroiliac joint. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic performance of imaging parameters in distinguishing different groups. Regression analysis was applied to determine the correlation between imaging parameters and clinical activity indices. All of the histogram parameters distinguished the active from inactive groups with a low area under the curve (AUC) (max AUCs≤0.71), while the SPARCC score failed to differentiate the two groups (p = 0.08). MD, MK, D, D*, and ADC showed good performance in differentiating active and inactive from control groups (max AUC = 0. 81 ~ 0.98). f50 differentiated the active from control groups with an AUC of 0.72, significantly lower than the maximum AUC for MD, MK, D, ADC, and SPARCC score (all p < 0.05). The max AUC of MD in differentiating inactive from control groups was significantly higher than that of D* and the SPARCC score. MD, D, D*, f, and ADC were positively correlated with BASDAI, while MK was negatively correlated with BASDAI. Only MD was positively correlated with hsCRP. Whole-joint histogram analysis of mono-exponential, bi-exponential diffusion weighted, and diffusion kurtosis imaging showed good diagnostic performance in differentiating active and inactive axSpA from patients with non-specific back pain. All the imaging parameters were correlated with BASDAI except for SPARCC score. Only DKI-derived MD was correlated with an increase in hsCRP, suggesting its potential use as an imaging biomarker for disease activity in axSpA. 1. No significant difference was found between the three models of diffusion weighted imaging in evaluating disease activity of axial spondyloarthritis.2. Only DKI-derived MD was correlated with an increase in hsCRP, suggesting its potential use as an imaging biomarker for disease activity in axSpA.

The role of plateletcrit in Takayasu arteritis: A potential biomarker for disease activity and 6-month treatment response.

To determine the role of plateletcrit as a potential biomarker for disease activity and treatment response in Takayasu arteritis (TAK). Totally, 215 newly diagnosed TAK patients were consecutively enrolled. Demographic data, clinical manifestations, laboratory and imaging examinations, and treatment strategy were recorded at baseline and at each visit during the 6-month treatment period. Normal plateletcrit (0.1%-0.4%) and hyper-plateletcrit (>0.4%) observed at baseline were used as group criteria. At baseline, the overall plateletcrit was 0.32 (0.24-0.38)%, with a normal and high level observed in 172 (80.00%) and 43 (20.00%) patients, respectively. Baseline plateletcrit was significantly higher in patients with active disease and associated with inflammatory biomarkers, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and interleukin (IL)-6 (all p < .01). At 6 months, complete remission was achieved in 171 (79.53%) patients, and a significant decrease in plateletcrit was observed in these cases (p < .01). Patients with a normal baseline plateletcrit were more likely to achieve complete remission compared to those with a high baseline plateletcrit (HR = 4.65, 95% CI: 2.38-19.08, p < .01). In addition, ESR (p = .01) and IL-6 (p = .02) levels were still higher in patients with a high baseline plateletcrit at 6 months. Progression of vascular lesions was indicated in 18 (8.37%) patients at 6 months, and these patients also had significantly higher baseline plateletcrit (p = .03). Plateletcrit levels were positively related to disease activity and inflammatory index in TAK. Importantly, patients with high baseline plateletcrit levels may show a worse treatment response at 6 months.