Inflammatory Profile In Patients Research Articles

A One-Month Advanced Glycation End Products-Restricted Diet Improves CML, RAGE, Metabolic and Inflammatory Profile in Patients with End-Stage Renal Disease Undergoing Haemodialysis.

Exogenous and endogenous advanced glycation end products (AGEs) contribute to the pathogenesis and progression of renal disease. This is a one-month controlled dietary counseling trial that restricts nutritional AGEs in patients with end-stage renal disease (ESRD) undergoing haemodialysis (n = 22 participants in the intervention and n = 20 participants in the control group). Haematological, biochemical markers, the soluble form of the receptor for AGEs (sRAGE), and carboxymethyl lysine (CML) were measured at baseline and at follow-up. Mononuclear cells were isolated and the protein expression of RAGE and the inflammatory marker COX-2 was measured using Western immunoblotting. The intervention group presented a lower increase in CML compared to the control group (12.39% median change in the intervention vs. 69.34% in the control group, p = 0.013), while RAGE (% mean change -56.54 in the intervention vs. 46.51 in the control group, p < 0.001) and COX-2 (% mean change -37.76 in the intervention vs. 0.27 in the control group, p < 0.001) were reduced compared to the control group. sRAGE was reduced in both groups. In addition, HbA1c (at two months), total cholesterol, and triglycerides were reduced in the intervention versus the control group. The adoption of healthy cooking methods deserves further research as a possible way of modulating inflammatory markers in patients with CKD.

Long-Term Impact of Nutritional Intervention with Increased Polyphenol Intake and Physical Activity Promotion on Oxidative and Inflammatory Profiles in Patients with Metabolic Syndrome.

Obesity and overweight pose significant risks to health, contributing to the prevalence of chronic conditions like type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVD). The current study aimed to assess the impact of a 6-year nutritional and lifestyle intervention on oxidative and inflammatory markers in individuals aged 55 to 75, specifically those at high risk of CVD. A study was carried out in a group of 80 participants with metabolic syndrome (MetS) residing in Mallorca, Spain, who underwent nutritional intervention based on a low-calorie Mediterranean diet (MedDiet) and promotion of physical activity. Before and after the intervention, several parameters including anthropometric data, haematological factors, blood pressure, and physical activity level were measured. Oxidative and inflammatory biomarkers in plasma were analysed. After the 6-year intervention, participants who managed to reduce their body mass index (BMI) had greater reductions in abdominal obesity, waist to heigh ratio (WHtR), diastolic blood pressure, and glucose levels, and increased high density protein cholesterol (HDL-c) compared to those who did not reduce BMI. This higher reduction in BMI was related to reduced energy intake and increased adherence to MedDiet, with greater polyphenol intake, and total physical activity (PA). Furthermore, improvements in oxidative stress and proinflammatory status were observed in participants who reduced their BMI. Significant reductions in the activity of the prooxidant enzyme, myeloperoxidase (MPO), levels of the lipid oxidation marker, malondialdehyde (MDA), and the proinflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1,) were found in those who reduced their BMI. In contrast, participants who did not improve their BMI exhibited higher levels of proinflammatory markers such as MCP-1 and tumour necrosis factor α (TNFα), as well as increased activity of the antioxidant enzyme catalase (CAT). Current findings suggest that an effective way to reduce BMI is a hypocaloric MedDiet combined with tailored physical activity to improve oxidative stress and proinflammatory status, and potentially reducing the risk of CVD.

Inflammasome activation in patients with Kaposi sarcoma herpesvirus–associated diseases

AbstractKaposi sarcoma herpesvirus (KSHV)–associated diseases include Kaposi sarcoma (KS), primary effusion lymphoma (PEL), KSHV-associated multicentric Castleman disease (MCD), and KS inflammatory cytokine syndrome (KICS). PEL, MCD, and KICS are associated with elevated circulating inflammatory cytokines. However, activation of the inflammasome, which generates interleukin-1β (IL-1β) and IL-18 via active caspase-1/4/5, has not been evaluated in patients with KSHV-associated diseases (KADs). Herein we report that patients with HIV and ≥1 KAD present with higher plasma levels of IL-18 and increased caspase-1/4/5 activity in circulating monocytes compared with HIV-negative healthy volunteers (HVs) or people with HIV (PWH) without KAD. Within KAD subtypes, KICS and MCD shared enhanced caspase-1/4/5 activity and IL-18 production compared with HVs and PWH, whereas patients with PEL showed remarkably high levels of inflammasome complex formation (known as apoptosis–associated speck-like protein containing a caspase recruitment domain). Moreover, caspase-1/4/5 activity and IL-18 plasma levels correlated with KSHV viral load, indicating KSHV-driven inflammasome activation in KAD. Accordingly, factors released by cells latently infected with KSHV triggered inflammasome activation and cytokine production in bystander monocytes in vitro. Finally, both supervised and unsupervised analyses with inflammasome measurements and other inflammatory biomarkers demonstrate a unique inflammatory profile in patients with PEL, MCD, and KICS as compared with KS. Our data indicate that detrimental inflammation in patients with KAD is at least partially driven by KSHV-induced inflammasome activation in monocytes, thus offering novel approaches to diagnose and treat these complex disorders. These trials were registered at www.ClinicalTrials.gov as #NCT01419561, NCT00092222, NCT00006518, and NCT02147405.

#2866 The CompAct-HD trial reports a persistent inflammatory profile in patients undergoing haemodialysis, acutely exacerbated with each treatment

Abstract Background and Aims Inflammation induced by haemodialysis (HD) treatment has been recognised for several decades. Despite significant advances in technology, there is evidence that incompatibility between the dialyser, a foreign surface, and the patients’ blood, results in activation of the immune system. With each session, blood-membrane interaction leads to a repetitive activation of the innate complement system and a subsequent inflammatory response. It is now widely acknowledged that the consequences of long-term inflammation include fibrosis and accelerated cardiovascular disease, a common cause of mortality in patients with renal failure. The aim of the CompAct-HD trial is to characterize complement activation and biomarker response to blood-membrane-circuit interaction during HD. Method For a single session, six timed intradialytic blood samples were collected from HD patients during standard treatment with ultrapure water and high flux “biocompatible” membranes. Complement activity potential was determined from timepoint 1 and inflammatory biomarkers from timepoints 2 to 6. Single time point samples were also collected from 7 healthy donors. Highly multiplexed assays enabled to determine 30 biomarkers of inflammation, including cytokines, chemokines, growth factors and complement proteins, from a single blood sample. Data analysis was performed using Microsoft® Excel Version 16.80 and GraphPad Prism 10.1.0. Results 354 patients were recruited from 8 dialysis units across Greater Manchester, UK. An interim analysis was performed on 150 HD patients receiving standard care as well as 7 healthy donors. Dialysis appears to generate an acute inflammatory response, that is, within 15 minutes of commencing treatment which does not appear to resolve by the end of the session. This heightened inflammatory state was observed in HD patients in comparison to healthy donors (Fig. 1) with most pronounced changes seen in cytokines IL-1β, IL-10, IL-12p40 and TNF-α during dialysis. Established markers such as IL-6 also showed a 6-fold increase at the 75th percentile. Similarly, an exaggerated intradialytic response was observed in complement proteins, including the terminal complement complex (TCC) C5b-9 and anaphylatoxin C5a with spikes of up to 7-fold and 10-fold respectively (Fig. 2). A session of HD was shown to cause a relative increase in complement proteins and inflammatory biomarkers. The magnitude of response seen in patients was variable (Fig. 3) with the greatest rise seen in the top quartile (above the Q3 boundary). Conclusion Our findings evidence a sharp inflammatory response to modern day HD treatment across a large cohort of dialysis patients. When compared to healthy donors, we observed heightened levels of inflammation in dialysis patients that is further exacerbated with each treatment session. This study shows that HD has a significant role to play in the chronic inflammatory state of patients with end stage renal failure. Furthermore, here we describe potential targets, in both cytokine and complement proteins, which could be the key to downregulation of inflammation. Using targeted therapeutics, we have an opportunity to deliver a more biocompatible treatment, improving patient outcomes.

Thyroid Hormonal, Lipidic and Inflammatory Profiles in Patients with Hepatic Encephalopathy

Thyroid Hormonal, Lipidic and Inflammatory Profiles in Patients with Hepatic Encephalopathy

LOW HIGH-DENSITY LIPOPROTEIN LEVEL PROMOTES INFLAMMATORY RESPONSE IN LONG COVID PATIENTS UNDERGOING HEMODIALYSIS ONE YEAR AFTER INFECTION

Objective: Long COVID, a syndrome characterized by persistent symptoms post-acute SARS-CoV-2 infection, poses unique challenges for patients undergoing hemodialysis (HD). Low levels of high-density lipoprotein (HDL) (&lt;1.2 mmol/L) have been implicated in heightened COVID-19 risk and associated cardiovascular complications in this patient population. This study aimed to explore the potential association between low HDL and inflammatory responses in long COVID among HD patients. Design and method: A total of 80 hemodialysis (HD) patients, aged 55 (44-62.5) years, with a dialysis vintage of 45 (21-78.6) months and a history of COVID-19, were enrolled in this cross-sectional cohort study. Among them, 45 (56.2%) were diagnosed with long COVID, while 35 (43.8%) had fully recovered. Lipid profiles and inflammatory markers, such as serum interleukin (IL)-6, IL-17, and C-reactive protein (CRP), were assessed one year post-infection. The cytokines were measured using ELISA. Data were presented as median and interquartile interval [Me (Q25-Q75)] and compared using the Mann-Whitney test. Results: Patients experiencing long COVID exhibited significantly lower HDL levels compared to fully recovered individuals: 1.19 (1.06-1.76) vs 1.66 (1.32-1.92) mmol/L (p = 0.02). Among those with low HDL levels (&lt;1.2 mmol/L), elevated concentrations of CRP, IL-6, and IL-17 were evident in comparison to patients with HDL concentrations exceeding 1.2 mmol/L (Fig. 1). Subsequent subgroup analysis revealed a more pronounced inflammatory profile in patients concurrently experiencing long COVID and exhibiting low HDL levels (Fig. 2). Conclusions: Our findings indicate that low HDL levels may enhance the inflammatory response in patients with long COVID undergoing HD one year post-infection, potentially promoting cardiovascular complications. Future research should focus on elucidating the pathways underlying this association and exploring novel strategies to mitigate inflammation and improve outcomes in long COVID among HD patients.

Inflammatory markers changes following acceptance-based behavioral psychotherapy in generalized anxiety disorder patients: Evidence from a randomized controlled trial

IntroductionGeneralized anxiety disorder (GAD) has been associated with elevated levels of C-reactive protein (CRP) and proinflammatory cytokines. Despite robust evidence as an effective treatment for GAD, research on the effects of cognitive-behavioral therapies (CBT) in the inflammatory profile of patients with clinical anxiety has presented mixed results. ObjectiveThe present study aimed to investigate the effect of an acceptance-based behavior therapy (ABBT) on inflammatory biomarkers and their association with anxiety levels in GAD patients in comparison to supportive therapy as an active control. MethodsPeripheral inflammatory biomarkers (CRP, IL-1β, IL-4, IL-6, IL-10, TNF-α) were measured in 77 GAD patients who participated in a 14-week 10-session randomized clinical trial of group ABBT (experimental, n = 37) or supportive group therapy (ST: active control group, n = 40). ResultsThe concentrations of IL-1β decreased in the control group and the concentrations of IL-6 increased in the experimental group from baseline to post-treatment, whereas no difference was identified in IL-4, IL-10, TNF, or CRP. Although anxiety and depression levels decreased in both treatment conditions, no correlation with inflammation markers was found for most clinical and biological variables. A negative correlation between changes in IL-6 and IL-10 and anxiety symptom score changes was identified. ConclusionsThe present study results found that a short trial of acceptance-based behavior therapy did not change the proinflammatory profile which may be associated with GAD. Additional research is needed to evaluate the influence of other inflammation-related variables, longer periods of follow-up as well as the effect of supportive therapy on peripheral inflammatory biomarkers in GAD patients.

Inflammatory profile in patients with rheumatoid arthritis and sarcopenia.

Sarcopenia is characterized by the loss of muscle mass and strength associated with aging; however, individuals with chronic diseases are at risk at the early stages. In rheumatoid arthritis (RA), sustained chronic inflammation influences muscle deterioration. It may expedite the development of sarcopenia, which has been linked to physical disability, cardiovascular events, disease activity of RA, and premature death. We aimed to compare the inflammatory profiles of patients with RA with and without sarcopenia. This cross-sectional study involved 165 women with RA. Sarcopenia was diagnosed according to criteria established by the European Working Group on Sarcopenia in Older People. To assess the inflammatory profile, concentrations of cytokines such as EGF, IL-17, IL-1α, IL-1β, IL-6, TNFα, TNFβ, and creatine kinase (CK) were measured. The prevalence of sarcopenia was 15.8% (95% CI: 8.9-18.2). The median age of patients with sarcopenia was 59.5years (49.8-65.3), compared to 50years (43-59years) p = 0.001. The disease duration was also longer in patients with sarcopenia, 21years (15-30), compared to those without sarcopenia, 13years (7.3-20) p = 0.001. The inflammatory profile differed between patients with and without sarcopenia, revealing that the cytokines IL-1α, IL-6, and TNFβ concentrations were significantly higher (p < 0.05) in patients with sarcopenia, adjusted for BMI, age, and disease duration. Patients with RA and sarcopenia were older and exhibited longer disease duration and higher levels of inflammatory cytokines compared to those without sarcopenia. These findings suggest potential implications for clinical outcomes. Key Points • The prevalence of sarcopenia in women with rheumatoid arthritis was 15.8% (95% CI, 8.9-18.2). • Levels of IL-1α, IL-6, and TNFβ cytokines were significantly higher in women with rheumatoid arthritis and sarcopenia compared with those without sarcopenia, adjusted for BMI, age, and disease duration.

Vitamin D and tear fluid cytokines in predicting outcomes in viral conjunctivitis - A new outlook.

To determine the association between systemic vitamin D (VD) and immunoglobulin E (IgE) levels with severity and ocular surface inflammatory profile in patients with epidemic keratoconjunctivitis (EKC). 210 eyes of 105 patients who were clinically diagnosed with EKC were included in the study. The levels of serum VD and serum IgE were measured. Schirmer's strip-based tear fluid (TF) was used to determine levels of IL-1β, IL-6, IL-10, IL-17A, TNFα, MMP9, sICAM1, and VEGF-A in a subset of patients. Levels of VD were significantly ( P < 0.05) lower and levels of IgE were significantly higher in patients with severe forms of conjunctivitis compared to those with nonsevere forms. Majority of the patients with severe forms of the disease exhibited VD deficiency and/or abnormally high IgE. A negative correlation (r = -0.682; P < 0.0001) was observed between VD and IgE levels. TF levels of IL-1β, IL-6, TNFα, and sICAM1 were significantly higher in eyes with severe forms of conjunctivitis compared to those with nonsevere forms and controls. These factors showed a positive correlation ( P < 0.05) with IgE levels and a negative correlation ( P < 0.05) with VD levels. Patients with severe forms of EKC exhibited VD deficiency and higher levels of IgE. Increased TF inflammatory factors demonstrated a disease causal relationship with VD and IgE. Hence, restoring the altered levels of VD and IgE to normal range would be pivotal in the prevention and management of severe conjunctivitis.

Inflammatory profiles in women with eating disorder: Linking inflammatory biomarkers to clinical phenotypes

IntroductionEating disorders (ED) represent a group of very complex and serious diagnoses characterized by emotional dysregulation and impulsivity. New approaches are necessary to achieve effective diagnosis and treatments. Shifting biomarker research away from the constraints of diagnostic categories may effectively contribute to a dimensional differentiation across disorders according to neurobiology (e.g., inflammatory biomarkers). Thus, the aim of our study was to identify inflammatory profiles in patients with ED. MethodsA sample of 100 women with an ED (23.4 ± 8.55 years) and 59 healthy controls (HC) (20.22 ± 4.18 years) was used. K-means cluster analysis was followed to identify inflammatory clusters considering seven blood biomarkers (iNOS, TNFα, COX2, p38, ERK, TBARS and PPARγ). Moreover, a wide assessment of clinical features was conducted. ResultsTwo distinct clusters were identified. Cluster 1 patients were characterized by higher inflammatory levels of TNF-α, COX2, p38, and ERK, and had more restrictive anorexia diagnosis than cluster 2. Cluster 2 participants showed higher inflammatory levels of iNOS and were older than cluster 1 and controls and had lower BMI than HC. In addition, they had higher levels of bulimic symptoms than those from the cluster 1 and HC, and higher impulsivity than HC. All ED patients (regardless of cluster) showed higher ED symptoms and more trauma than HC. ConclusionsOur study revealed that inflammatory dysfunction may be linked with clinical endophenotypes in ED, one more restrictive (cluster 1) with an inflammation/oxidative endophenotype more cytokine and MAPK/ERK mediated, and the other more impulsive, with more bulimic symptoms (cluster 2) with NO free radical high output source iNOS. Trauma seems to be a vulnerability factor for both endophenotypes.

LOW HIGH-DENSITY LIPOPROTEIN LEVEL ASSOCIATED WITH ENHANCED INFLAMMATORY RESPONSE AND ONE-YEAR PERSISTENCE OF LONG COVID IN PATIENTS UNDERGOING HEMODIALYSIS: A CROSS-SECTIONAL COHORT STUDY

Background: Long-term consequences of COVID-19, known as long COVID, present distinctive hurdles for patients receiving hemodialysis treatment. Reduced levels of high-density lipoprotein (HDL) (&lt; 1.22 mmol/L) have previously been demonstrated to be associated with heightened susceptibility to COVID-19 and immediate COVID-19-related adverse outcomes in this patient population. However, the potential association between HDL levels and the persistence of long COVID has not been examined within the hemodialysis cohort. The present study aimed to explore the relationship between HDL levels and inflammatory responses one year after COVID-19 among patients undergoing hemodialysis. Methods: A total of 80 patients treated with hemodialysis, aged 55 (44-62.5) years, with a dialysis vintage of 45 (21-78.6) months and a history of COVID-19, were enrolled in this cross-sectional cohort study. Among them, 45 (56.2%) were diagnosed with long COVID, while 35 (43.8%) had fully recovered. Lipid profiles and inflammatory markers, such as serum C-reactive protein, and interleukins -6 and -17, were assessed one year post-infection. Results: Patients experiencing long COVID exhibited significantly lower HDL levels compared to fully recovered individuals: 1.19 (1.06-1.76) vs 1.66 (1.32-1.92) mmol/L (p &lt; 0.0001). The HDL cut-off point of less than 1.22 mmol/L demonstrated a sensitivity of 84.9% and specificity of 95.3% to predict one-year long COVID persistence in our cohort. Among the patients with HDL levels &lt; 1.22 mmol/L, elevated concentrations of C-reactive protein (р = 0.003), interleukin-6 (p = 0.005), and interleukin-17 (p &lt; 0.0001) were evident compared to those with HDL concentrations exceeding 1.22 mmol/L. Subsequent subgroup analysis revealed a more pronounced inflammatory profile in patients concurrently experiencing long COVID and exhibiting low HDL levels. Conclusion: The obtained results suggest that a low level of HDL (&lt; 1.22 mmol/L) may exacerbate the inflammatory response in patients undergoing hemodialysis, potentially contributing to the persistence of long COVID even a year after infection. Future research is necessary to elucidate the pathogenetic mechanisms of this relationship and explore potential strategies to improve patient outcomes.

Inflammatory profile of patients with different weight diagnoses and similar periodontal condition: A systematic review.

This study aimed to systematically review the literature regarding the inflammatory profiles, measured by cytokines and chemokines, of individuals with different diagnoses of weight, but with the similar periodontal condition. Searches were performed in five databases (Scopus, EMBASE, PubMed, Web of Science, and Cochrane-Central). Studies that compared the inflammatory profile of normal-weight individuals to those with obesity and evaluated the same cytokine, collection method, and periodontal diagnosis (periodontal health, gingivitis, or periodontitis) were included. Cross-sectional studies underwent evaluation by independent researchers using the Joanna Briggs Institute Critical Appraisal Checklist. The GRADE (Grades of Recommendation, Assessment, Development and Evaluation) system assessed evidence certainty. Twelve studies were included. The diagnosis of obesity was done on the basis of body mass index, waist circumference, and waist-hip ratio. Pro-inflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor-α [TNF]-α, IL-1β, IL-31, and IL-34) were analyzed in serum, saliva, gingival crevicular fluid (GCF), and plasma. Periodontal diagnoses varied across studies. TNF-α expression was significantly higher in individuals with obesity and periodontal health or periodontitis. Serum IL-1β levels showed mixed results, but salivary IL-1β levels were elevated in obese individuals. IL-6 levels were higher in obese individuals, regardless of periodontal status. IL-34 and IL-10 showed no significant differences across groups. Monocyte chemoattractant protein-4 (MCP-4) levels were higher in obese individuals with periodontitis or periodontal health. IL-31 and IL-34 in GCF showed no significant differences between obese and nonobese individuals, without periodontitis. Heterogeneous results were noted for IL-6, IL-1β, IL-31, IL-34, TNF-α, and MCP-4, hindering conclusions on weight's impact on inflammatory profiles in periodontal patients.

Uremic toxins and inflammatory profile of patients with chronic kidney disease: A cross-sectional study involving non-dialysis, hemodialysis and peritoneal dialysis

Uremic toxins and inflammatory profile of patients with chronic kidney disease: A cross-sectional study involving non-dialysis, hemodialysis and peritoneal dialysis

The Effects of a Cardiac Rehabilitation Program on Endothelial Progenitor Cells and Inflammatory Profile in Patients with Chronic Heart Failure of Different Severity.

Endothelial dysfunction and inflammation are common pathophysiological characteristics of chronic heart failure (CHF). Endothelial progenitor cells (EPCs) are recognized as useful markers of vascular damage and endothelial repair. The aim of this study was to investigate the effects of a cardiac rehabilitation program on EPCs and inflammatory profile in CHF patients of different severity. Forty-four patients with stable CHF underwent a 36-session cardiac rehabilitation program. They were separated into two different subgroups each time, according to the median peak VO2, predicted peak VO2, VE/VCO2 slope, and ejection fraction. EPCs, C-reactive protein (CRP), interleukin 6 (IL-6), interleukin 10 (IL-10), and vascular endothelial growth factor (VEGF) were measured. Flow cytometry was used for the quantification of EPCs. Mobilization of EPCs increased and the inflammatory profile improved within each severity group (p < 0.05) after the cardiac rehabilitation program, but there were no statistically significant differences between groups (p > 0.05). A 36-session cardiac rehabilitation program has similar beneficial effects on the mobilization of EPCs and on the inflammatory profile in patients with CHF of different severity.

Not just snot: Local inflammatory profiles in patients with aspirin-exacerbated respiratory disease differ from patients with aspirin-tolerant chronic rhinosinusitis.

IL-5, CCL2, and CXCL8 in sinus mucous are higher in patients with AERD relative to aspirin-tolerant patients with CRS These mediators are pleiotropic, leading to widescale inflammatory processes contributing to AERD AERD is not only a T2 disease but heterogeneous: this may explain the refractory nature of AERD.

#3195 PATIENTS ON HD WITH CENTRAL CATHETERS LOCKED WITH TAUROLIDINE HAVE A SIMILAR INFLAMMATORY PROFILE TO SUBJECTS WITH NATIVE ARTERIOVENOUS FISTULA

Abstract Background and Aims Inflammation is a near-universal condition in haemodialysis (HD) patients, which contributes to increased complications, morbidity and mortality. The inflammatory profile is enhanced in subjects who need a central venous catheter (CVC) as vascular access in comparison with patients with native arteriovenous fistula (AVF), the optimal vascular access for HD. The aim of the present study was to analyse the inflammatory profile of HD patients according to their vascular access (CVC vs AVF), and to evaluate whether Taurolidine-citrate-heparin lock solution (TCH; taurolidine 1.35%, citrate 4% and heparin 500 IU) is able to modulate the inflammatory state of patients with CVC towards an inflammatory profile similar to that observed in subjects with AVF. Method A total of 109 patients with AVF or tunneled CVC under regular haemodialysis for more than 6 months were screened. Exclusion criteria included intercurrent infections in the previous 3 months, active inflammatory or immunologic diseases, and treatment with antibiotics or drugs affecting the immune system. Finally, 85 patients were included in the study and classified according to the vascular access: 25 patients with AVF and 60 with CVC. Subsequently, two subgroups were formed from the group of patients with tunneled CVC according to a heparin-containing catheter lock solution with (CVC-TCH) and without taurolidine-citrate (CVC-Hep). Subsequently, high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) concentrations in serum and messenger ribonucleic acid (mRNA) gene expression levels of IL-6 and TNF-alpha in peripheral blood mononuclear cells (PBMC) were measured at inclusion and after three months follow-up. Results Altogether eighty-five subjects (42 males and 43 females; mean age 61 ± 9 yrs; 39% diabetics) were initially included in the study. In 25 subjects the vascular access was AVF, while the rest used tunneled CVC; of these 31 used standard CVC-Hep and 29 used CVC-TCH. Five patients dropped out the study and thus 80 patients completed the 3-month follow-up and were finally evaluated. At inclusion, patients with CVC had significantly higher serum and expression levels of inflammatory parameters compared to subjects with AVF. After 3 months, there were no significant changes in inflammatory markers in subjects with AVF compared to baseline, whereas in subjects with CVC-Hep a significant increase in serum and gene expression of IL-6 could be observed. On the contrary, subjects with CVC-TCH experienced a decrease of all parameters compared to baseline, of which differences in serum IL-6 and gene expression levels of IL-6 and TNF-alpha were significant. After 3 months of follow-up there was no significant difference in any inflammatory parameter when comparing patients with CVD-TCH with those with AVF (Table). Conclusion In patients under HD with cuffed tunneled CVC, the use of TCH lock solution after each HD session is associated with a significant improvement in the inflammatory serum and gene expression state. Thus, the inflammatory profile of patients with CVC using TCH does not differ from that of patients with native AVF after at least three months of CVC-TCH use.

THU-348 - Distinct changes in the inflammatory profile of patients with EASL-CLIF- versus APASL-acute-on-chronic liver failure

THU-348 - Distinct changes in the inflammatory profile of patients with EASL-CLIF- versus APASL-acute-on-chronic liver failure

P071 Exercise as an anti-inflammatory treatment in axial spondyloarthritis (axSpA): a proof-of-concept study

Abstract Background/Aims Axial spondyloarthritis (axSpA) is an inflammatory arthritis affecting 0.5-1.0% of people in the UK. The inflammatory profile with axSpA causes pain and loss of mobility but can also contribute to other manifestations such as cardiovascular disease (CVD). Current management of axSpA relies on biologic medication; however, they are expensive, and effectiveness is influenced by disease duration, baseline inflammation and age. Monocytes, a type of white blood cell, express the cell surface markers CD14 ++CD16- (classical), CD14 ++CD16 + (intermediate), and CD14+CD16 ++ (non-classical). CD16+ monocytes are pro-inflammatory and are elevated in populations with CVD. Importantly, regular exercise reduces the relative proportion of CD16+ cells in other populations, but this is unknown in axSpA. Therefore, the present randomised control trial investigated whether exercise reduced the relative percentage of CD16+ monocytes in response to 12-weeks of home-based walking. Subjective measures of disease activity, physical function, spinal pain, and work productivity are included to supplement the findings. Methods 20 participants (10 control, 10 exercise; 8 vs 7 presented here due to ongoing data collection) were recruited, provided written informed consent, and completed baseline assessments before being assigned into a control or exercise group. The control group carried on as normal. The exercise group completed 5 x 30-minute bouts of ‘somewhat hard’ walking per week which was confirmed via heart rate monitoring and a rating of perceived exertion scale. At baseline (week 0) and follow-up (week 12), participants completed questionnaires to assess BASDAI, BASFI, ASAS-HI, WPAI, and spinal pain. Blood samples were also collected for the analysis of monocyte subsets. Data were analysed using a two-way mixed analysis of variance (ANOVA) with time as the within factor. Statistical significance was accepted as P &amp;lt; 0.05. However, description of trends is used throughout due to this being preliminary data with a small sample size. Results Group-by-time interactions revealed a significant reduction in the proportion of non-classical monocytes in the exercise group and an increase in the control group (P &amp;lt; 0.001). This coincided with a significant interaction for the proportion of less inflammatory classical monocytes, with an increase in the exercise group and decrease in the control group (P &amp;lt; 0.001). Overall, the exercise group also responded more favourably for BASDAI (P = 0.026) and spinal pain (P = 0.088) than the control group. Conclusion Preliminary findings suggest regular walking reduces pro-inflammatory immune cell populations in axSpA which coincides with favourable BASDAI and spinal pain responses compared to a control group. This highlights the importance of regular exercise to improve underlying inflammatory profiles in patients with axSpA. Disclosure M. Roberts: None. M. Hamrouni: None. V. Linsley: None. A. Moorthy: Consultancies; A.M has received speaker fees from Lilly, Novartis, Galapagos and UCB. Grants/research support; A.M has received funding from the National Axial Spondyloarthritis Society for this work. N. Bishop: Grants/research support; N.B has received funding from the National Axial Spondyloarthritis Society for this work.

Spotlight on the September 27 Issue

![Graphic][1]</img>#### Notable in Neurology This Week This issue features an article that investigates the association of self-reflection with cognition and brain health in cognitively unimpaired older adults; another analyzes the preferences and user experiences of wearable devices in epilepsy. A featured Research Article examines the comparative risk of opioid overdose with concomitant use of prescription opioids and skeletal muscle relaxants. ### Association of Thrombin Generation With Leukocyte Inflammatory Profile in Patients With Acute Ischemic Stroke This study investigates the association between thrombin generation and leukocyte gene expression in patients with acute ischemic stroke. … [1]: /embed/inline-graphic-1.gif

Nutritional Status, Body Composition, and Inflammation Profile in Older Patients with Advanced Chronic Kidney Disease Stage 4-5: A Case-Control Study.

Nutritional status is a predictor of adverse outcomes and mortality in patients with advanced chronic kidney disease (ACKD). This study aimed to explore and evaluate risk factors related to nutritional status, body composition, and inflammatory profile in patients with ACKD compared with age- and sex-matched controls in a Mediterranean cohort of the Spanish population. Out of 200 volunteers recruited, 150 participants (64%) were included, and a case-control study was conducted on 75 ACKD patients (stages 4–5), matched individually with controls at a ratio of 1:1 for both age and sex. At enrolment, demographic, clinical, anthropometric, and laboratory parameters were measured. Bioimpedance analysis (BIA) was used to assess both body composition and hydration status. ACKD patients had lower body cell mass (BCM%), muscle mass (MM%) phase angle (PA), s-albumin, and higher C-reactive protein (s-CRP) than controls (at least, p < 0.05). PA correlated positively with BCM% (cases: r = 0.84; controls: r = 0.53, p < 0.001), MM% (cases: r = 0.65; controls: r = 0.31, p < 0.001), and inversely with s-CRP (cases: r = −0.30, p < 0.001; controls: r = −0.31, p = 0.40). By univariate and multivariate conditional regression analysis, total body water (OR: 1.186), extracellular mass (OR: 1.346), s-CRP (OR: 2.050), MM% (OR: 0.847), PA (OR: 0.058), and s-albumin (OR: 0.475) were significantly associated among cases to controls. Nutritional parameters and BIA-derived measures appear as prognostic entities in patients with stage 4–5 ACKD compared to matched controls in this Mediterranean cohort.