Degree Of Inflammation In Patients Research Articles

Association between morphological manifestations of inflammatory bowel disease and biochemical markers of inflammation

Aim. To determine morphological and morphometric changes in the structure of the mucous membrane of the large intestine and their relationship with the content of short-chain volatile fatty acids and fecal calprotectin in patients with inflammatory bowel disease. Materials and methods. We examined 68 patients with inflammatory bowel disease, including 30 women and 38 men aged 20–66 years, 55 patients were with ulcerative colitis and 13 patients – with Crohn’s disease. Histological examination focused on changes in the mucous membrane of the large intestine. Determination of short-chain volatile fatty acids in feces was performed using gas chromatography. Calprotectin content was measured in fecal samples by enzyme-linked immunosorbent assay. Results. Significant correlations were found between epithelial disruption and changes in crypt architecture, infiltration density, and histological activity. The higher degree of inflammation in patients with severe course was combined with a lower level of tissue nonspecific protection, which was detected by the number of goblet cells, eosinophilic and neutrophilic leukocytes. There was a decrease in the fecal concentration of butyric acid in patients with nonspecific ulcerative colitis and Crohn’s disease compared with controls, but a more significant decrease was observed in patients with severe nonspecific ulcerative colitis. The data have confirmed the association between inflammatory bowel disease and the content of short-chain volatile fatty acids, fecal calprotectin in coprofiltrate, which was evidenced by the presence of correlations between low content of short-chain volatile fatty acids and eosinophilic infiltration (r = -0.412; fecal calprotectin levels and disease severity (r = 0.589; P = 0.001), atrophy (r = 0.458; Р < 0.05), infiltration density (r = 0.434; Р < 0.05). Conclusions. All patients with inflammatory bowel disease are characterized by a specific histological picture, which reflected the different degrees of inflammation. Morphometric parameters more accurately show significant atrophic changes in the mucous membrane of the large intestine. The data have confirmed the association between inflammatory bowel disease and the content of short-chain volatile fatty acids and calprotectin in coprofiltrate.

Inflammation and hemodialysis adequacy: are C-reactive protein levels influenced by the dose of dialysis?

IntroductionChronic inflammation and the underlying cardiovascular comorbidity are still current problems in chronic hemodialysis patients. There are few studies comparing the "dialysis dose" with the degree of inflammation in the patient. Our main objective was to determine whether there is a relationship between serum C-reactive protein (CRP) levels and the “dialysis dose” (Kt / V) using ionic dialysance. MethodsMulticenter cross-sectional study. 536 prevalent chronic hemodialysis patients were included. CRP levels, neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) were collected. Kt was obtained by ionic dialysance and urea distribution volume was calculated from the Watsonˈs formula. The sample was divided into two groups, taking the median CRP as the cut-off point. Dialysis adequacy obtained in each group was compared. Finally, a logistic regression model was carried out to determine the variables with the greatest influence. ResultsMedian CRP was 4.10 mg/L (q25-q75: 1.67-10) and mean Kt/V was 1.48 ± 0.308. Kt/V was lower in the patients included in the high inflammation group (p = 0.01). In the multivariate logistic regression, the "high" levels of CRP were directly correlated with the Log INL (p < 0.001) and inversely proportional with serum albumin values (p = 0.014), Kt/V (p = 0.037) and serum iron (p < 0.001). ConclusionThe poorer adequacy in terms of dialysis doses, lower Kt / V values, may contribute to a higher degree of inflammation in chronic hemodialysis patients

Neutrophil-to-Lymphocyte Ratio (NLR) as An Inflammation Degree Marker in Tongue Cancer Patient

Tongue cancer is one of the most common malignancies of all oral malignancies. Cancer staging is induced by a systemic inflammatory response with one of the markers, one of them is neutrophil-lymphocyte ratio (NLR). This study aims to provide an overview of the NLR as a marker of the degree of inflammation in patients with tongue cancer. This systematic literature review was conducted online from January 2021 to March 2021 against articles reporting RNL as a marker of inflammatory action in patients with tongue cancer. The search for articles referred to Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) and conducted through PubMed, PMC, ScienceDirect, and EBSCOhost with the publication year 2015-2020. Selected articles met the criteria according to the PICO framework (Population, Intervention, Comparison, Outcome). Article screening is done by reading the title and abstract, checking for duplication, and reading the entire text. Sixteen in 841 research articles with observational study design were identified, the NLR cut-off value ranges from 2.04-2.95. Nine in ten research articles suggested a relationship between the NLR value and several clinicopathological characteristics of the patient. Twelve articles mentioned that there was the association of RNL with patient overall survival (OS), disease-free survival (DFS), and disease-specific survival (DSS). The NLR value can be an indicator of the degree of inflammation in patients with tongue cancer as assessed from the parameters of the clinicopathological assessment and can be a predictive factor for patient's prognosis or survival status.

Association of Serum Neuron-Specific Enolase and C-Reactive Protein With Disease Location and Endoscopic Inflammation Degree in Patients With Crohn's Disease.

Objective: The objective of this study was to explore the association between serum markers neuron-specific enolase (NSE) and C-reactive protein (CRP) with intestinal lesion location and degree of inflammation in patients with Crohn's disease (CD).Design: The levels of serum NSE, CRP, and fecal calprotectin (FC) in patients with CD were analyzed retrospectively. The severity of inflammatory lesions in the intestinal wall was accessed using the Simple Endoscopic Score for Crohn's disease (SES-CD).Results: The levels of NSE in patients with CD were higher than those of healthy individuals (14.87 vs. 12.68 ng/ml, P < 0.001). The levels of CRP in patients with CD were higher than those of healthy individuals (12.30 vs. 3.40 mg/l, P < 0.001). The FC levels in patients with CD were higher than those of patients with non-inflammatory bowel disease (1,143.90 vs. 114.21 μg/g, P < 0.05). The levels of NSE in CD with ileal lesions and simultaneous ileal and colon lesions were significantly higher than those in patients with CD with colonic lesions. However, the CRP was higher in patients with colonic lesions than those with ileal lesions. The levels of NSE in patients with severe inflammation were higher than those in patients with moderate inflammation (15.95 vs. 13.89 ng/ml, P < 0.05). Similarly, the NSE levels in patients with CD with severe inflammation were higher than those in patients with CD with mild inflammation (15.95 vs. 13.53 ng/mL, P < 0.05). The levels of CRP in severe inflammation were higher than those in moderate inflammation (29.80 vs. 19.60 mg/l, P < 0.05). In addition, the CRP levels in severe inflammation were higher than those in mild inflammation (29.80 vs. 5.86 mg/l, P < 0.05). ROC curve analysis showed that when NSE was combined with CRP for distinguishing between patients with CD and those without CD, sensitivity increased to 80.41%, specificity increased to 74.66%, and a highest AUC was equal to 0.843.Conclusion: Our study shows that serum NSE and CRP can be used to assess the severity of CD as well as the location of intestinal involvement. Therefore, NSE and CRP could be used as the non-invasive tests in detecting the location and severity of disease in patients with CD in daily routine practice.

Inflamación y adecuación de la hemodiálisis: ¿están los niveles de proteína C reactiva influidos por la dosis de diálisis recibida?

IntroductionChronic inflammation and the underlying cardiovascular comorbidity are still current problems in chronic hemodialysis patients. There are few studies comparing the “dialysis dose” (Kt/V) with the degree of inflammation in the patient. Our main objective was to determine whether there is a relationship between serum C-reactive protein (CRP) levels and the Kt/V using ionic dialysance. MethodsMulticenter cross-sectional study. A total of 536 prevalent chronic hemodialysis patients were included. CRP levels, neutrophil-lymphocyte ratio and platelet-lymphocyte ratio were collected. Kt was obtained by ionic dialysance and urea distribution volume was calculated from the Watson's formula. The sample was divided into 2 groups, taking the median CRP as the cut-off point. Dialysis adequacy obtained in each group was compared. Finally, a logistic regression model was carried out to determine the variables with the greatest influence. ResultsMedian CRP was 4.10mg/L (q25-q75: 1.67-10) and mean Kt/V was 1.48±0.308. Kt/V was lower in the patients included in the high inflammation group (P=.01). In the multivariate logistic regression, the “high” levels of CRP were directly correlated with the Log neutrophil-lymphocyte ratio (P<.001) and inversely proportional with serum albumin values (P=.014), Kt/V (P=.037) and serum iron (P<.001). ConclusionThe poorer adequacy in terms of dialysis doses (lower Kt/V values) may contribute to a higher degree of inflammation in chronic hemodialysis patients.

MO762RELATIONSHIP BETWEEN INFLAMMATION AND PERIPHERAL ARTERIAL DISEASE MEASURED BY ANKLE-BRACHIAL INDEX IN CHRONIC HEMODIALYSIS PATIENTS

Abstract Background and Aims Peripheral arterial disease (PAD) is very common in patients with chronic kidney disease. There are predisposing factors such as high blood pressure, diabetes mellitus, and dyslipidemia that are highly prevalent in this population. The ankle-brachial index (ABI) is a widely validated diagnostic method for the diagnosis of PAD. A value below 0.9 is suggestive of this pathology. On the other hand, inflammation is a phenomenon that favors development of atherosclerosis and therefore could be another predisposing factor for PAD. There are emerging markers of inflammation such as the neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and systemic immune-inflammation index (SII) that have an excellent correlation with classic markers such as C-reactive protein (CRP). The objective of our study was to determine whether there is a relationship between ABI values and the degree of inflammation in patients. Method A retrospective observational cross-sectional study was conducted in our prevalent hemodialysis population between April-May 2019. ABI was measured through the Microlife WatchBP Office ABI™ device. The sample was divided into two groups using 0.9 as a cut-off point: group 1 (ABI &amp;lt;0.9) and group 2 (ABI&amp;gt; 0.9). Inflammatory ratios (NLR, PLR and SII) and other parameters of bone kidney disease such as serum calcium, bicarbonate, phosphorus, parathyroid hormone (PTH), magnesium and vitamin D were determined. Results 100 patients with chronic kidney disease on chronic hemodialysis belonging to our Avericum Negrin center were analyzed. 42% (N = 42) of the sample were women and 42% (N = 42) were diabetic. The etiology of kidney disease was: 12% (N = 12) renal nephroangiosclerosis, 35% (N = 35) diabetic nephropathy, 14% (N = 14) chronic glomerulonephritis, 8% (N = 8) polycystic kidney disease, 17% (N = 17) unknow and 14% (N = 14) others. 19% (N = 19) had a central venous catheter as vascular access. The mean values of inflammatory and renal bone disease parameters are described in Table 1. The values of PLR and SII index were significantly higher in patients with ABI &amp;lt;0.9. (Figures 1 and 2). Conclusion Patients with peripheral arterial disease (ABI &amp;lt;0.9) had higher PLR and SII values

Cullin3 aggravates the inflammatory response of periodontal ligament stem cells via regulation of SHH signaling and Nrf2

ABSTRACT It is found that the activation of Sonic Hedgehog (SHH) signaling pathway is related to the degree of inflammation in patients suffering from periodontitis. Cullin3 (CUL3), an important ubiquitin ligase, can control SHH signaling. In this study, we were dedicated to clarify the roles of SHH and CUL3 in P. gingivalis-LPS (Pg-LPS)-treated periodontal ligament stem cells (PDLSCs). In this study, cell viability was detected using cell counting kit-8 (CCK-8). The inflammatory cytokines of PDLSCs were estimated by enzyme-linked immunosorbent assay (ELISA). With the application of western blots, the protein levels of SHH, Gli1 and NF-E2-related factor 2 (Nrf2) were determined. Alkaline phosphatase staining and Alizarin red staining were performed to evaluate the differentiation and mineralization capabilities of PDLSCs. The apoptotic cells were screened using TUNEL staining. The results showed that Pg-LPS inhibited cell viability and triggered inflammation of PDLSCs. Overexpression of CUL3 weakened the differentiation and mineralization capabilities of PDLSCs. Moreover, CUL3 overexpression aggravated inflammation and cell apoptosis induced by Pg-LPS. It is worth noting that although the protein levels of SHH, Gli1 and Nrf2 were elevated in PDLSCs treated with Pg-LPS, overexpression of CUL3 decreased the expressions of Gli1 and Nrf2. Overall, SHH/Gli1 and Nrf2 were involved in the inflammation and cell apoptosis of PDLSCs, which was dominated by CUL3.

Identification of differentially expressed genes in ulcerative colitis and verification in a colitis mouse model by bioinformatics analyses.

BACKGROUNDUlcerative colitis (UC) is an inflammatory bowel disease that is difficult to diagnose and treat. To date, the degree of inflammation in patients with UC has mainly been determined by measuring the levels of nonspecific indicators, such as C-reactive protein and the erythrocyte sedimentation rate, but these indicators have an unsatisfactory specificity. In this study, we performed bioinformatics analysis using data from the National Center for Biotechnology Information-Gene Expression Omnibus (NCBI-GEO) databases and verified the selected core genes in a mouse model of dextran sulfate sodium (DSS)-induced colitis.AIMTo identify UC-related differentially expressed genes (DEGs) using a bioinformatics analysis and verify them in vivo and to identify novel biomarkers and the underlying mechanisms of UC.METHODSTwo microarray datasets from the NCBI-GEO database were used, and DEGs between patients with UC and healthy controls were analyzed using GEO2R and Venn diagrams. We annotated these genes based on their functions and signaling pathways, and then protein-protein interactions (PPIs) were identified using the Search Tool for the Retrieval of Interacting Genes. The data were further analyzed with Cytoscape software and the Molecular Complex Detection (MCODE) app. The core genes were selected and a Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was performed. Finally, colitis model mice were established by administering DSS, and the top three core genes were verified in colitis mice using real-time polymerase chain reaction (PCR).RESULTSOne hundred and seventy-seven DEGs, 118 upregulated and 59 downregulated, were initially identified from the GEO2R analysis and predominantly participated in inflammation-related pathways. Seven clusters with close interactions in UC formed: Seventeen core genes were upregulated [C-X-C motif chemokine ligand 13 (CXCL13), C-X-C motif chemokine receptor 2 (CXCR2), CXCL9, CXCL5, C-C motif chemokine ligand 18, interleukin 1 beta, matrix metallopeptidase 9, CXCL3, formyl peptide receptor 1, complement component 3, CXCL8, CXCL1, CXCL10, CXCL2, CXCL6, CXCL11 and hydroxycarboxylic acid receptor 3] and one was downregulated [neuropeptide Y receptor Y1 (NYP1R)] in the top cluster according to the PPI and MCODE analyses. These genes were substantially enriched in the cytokine-cytokine receptor interaction and chemokine signaling pathways. The top three core genes (CXCL13, NYP1R, and CXCR2) were selected and verified in a mouse model of colitis using real-time PCR Increased expression was observed compared with the control mice, but only CXCR2 expression was significantly different.CONCLUSIONCore DEGs identified in UC are related to inflammation and immunity inflammation, indicating that these reactions are core features of the pathogenesis of UC. CXCR2 may reflect the degree of inflammation in patients with UC.

The Influence of Propolis Compress on Phelebitis Score Reduction in Hospitalized Patients

Phlebitis is complications of intravenous therapy. Warm compress can reduce degree of inflammation in patients with phlebitis. While propolis compress generally used to reduce the degree of dermatitis. This study aims to examine the effect of propolis compress to the score reduction of phlebitis. The study used Quasy-experimental. The independent variabel is propolis compress and dependent variable is phlebitis scores. The sample of the study are 10 respondents with phlebitis taken by Non-Randomized Sampling technique. The results showed average scores of phlebitis before treatment are an early sign of phlebitis, early stage, and moderate phlebitis stage with their respective percentage (30%). Furthemore, it’s found 60% with score 0 or no phlebitis after the propolis compress treatment. Based on the test of Paired T-Test, there’s different score between before and after propolis compress treatment that’s marked by p-value (0,000) < α = 0,05 Furthermore, the test result of Independent T-Test showed the p-value (0,000) < α = 0,01. In conclusion, There’s the effect of giving propolis compress to reduce the score of phlebitis. It’s hoped to Paramedic’s, especially nurses to perform alternative measures in handling the problem of nosocomial infections.

Magnetic resonance enterography, colonoscopy, and fecal calprotectin correlate in colonic Crohn\u2019s disease

BackgroundFecal calprotectin (FCP), magnetic resonance enterography (MRE), and colonoscopy are complementary biometric tests that are used to assess patients with Crohn’s Disease (CD). While prior studies have evaluated the association between combinations of these tests, no study has established a correlation between all three: FCP, MRE, and colonoscopy. We prospectively investigated if there is correlation between these three tests, which may result in improved clinical outcomes that can then be used to streamline patient monitoring and treatment modification.MethodsOne hundred fifty-six patients with colonic CD were prospectively examined between March 2017 and December 2018. FCP levels, MRE, and colonoscopy were assessed in parallel on all 156 patients. Clinical CD activity was measured with the Crohn’s Disease Activity Index (CDAI). CD activity with FCP was measured with a quantitative immunoassay. CD activity on MRE was measured with the Magnetic Resonance Index of Activity (MaRIA). CD activity on colonoscopy was measured with the Crohn’s Disease Endoscopic Index of Severity (CDEIS).ResultsOne hundred twelve patients (72%) had active disease (Crohn’s Disease Activity Index > 150) and 44 patients (28%) were in clinical remission disease (Crohn’s Disease Activity Index < 150). FCP levels, MaRIA, and CDEIS are highly correlated with positive and significant Pearson and Spearman coefficients, respectively (P < 0.0001), in univariate analyses. Regression analysis (multivariate analyses) demonstrates significant, positive correlation between FCP and MaRIA (r = 1.07, P < 0.0001) and between FCP and CDEIS (r = 0.71, P = 0.03), and between.MaRIA and CDEIS (r = 0.63, P = 0.01).ConclusionsFCP levels significantly correlate with the degree of active inflammation in patients with colonic Crohn’s Disease. Improved clinical results may be achieved by using a biometric strategy that incorporates FCP, colonoscopy, and MRE together. This strategy may in-turn be used in the future to streamline monitoring disease activity and adjustment of therapy to improve long term patient outcomes.

Curative effect of teprenone capsule combined with quadruple therapy in the treatment of chronic atrophic gastritis

Objective To analyze the curative effect of teprenone capsule combined with quadruple therapy in the treatment of chronic atrophic gastritis. Methods From June 2013 to June 2017, one hundred and fifty patients with chronic atrophic gastritis admitted to the First Hospital of Ninghai County were retrospectively selected.According to different treatment schemes, they were divided into control group and observation group, with 75 patients in each group.The control group was treated with routine quadruple therapy, and the observation group was treated with teprenone capsule combined with quadruple therapy.The effective rate of the two groups was compared. Results The total effective rate of the observation group was 97.33%, which was higher than 85.33% of the control group, the difference between the two groups was statistically significant(χ2=3.197, P<0.05). After treatment, the levels of interleukin-8 and tumor necrosis factor-alpha in the observation group were (7.04±1.03)ng/L, (41.02±1.72)ng/L, respectively, which in the control group were (10.81±1.63)ng/L, (57.35±2.95)ng/L, respectively, the differences between the two groups were statistically significant (t=6.028, 7.281, all P<0.05). The gastric mucosa score and the gastrin concentration in the observation group were (1.13±0.32)points, (8.97±2.33)pmol/L, respectively, which in the control group were (1.82±0.61)points, (5.36±1.52)pmol/L, respectively, the differences between the two groups were statistically significant(t=5.661, 6.024, all P<0.05). Conclusion Teprenone capsule combined with quadruple therapy can improve the clinical efficacy and reduce the degree of inflammation in patients with chronic atrophic gastritis, which is worthy of clinical application. Key words: Gastritis, atrophic; Teprenone; Rabeprazole; Tinidazole; Claricid; Colloidal bismuth pectin; Interleukin-8; Tumor necrosis factor-alpha

Histological assessment of the liver explant in transplanted hepatitis C virus patients achieving sustained virological response with direct-acting antiviral agents.

The use of direct-acting anti-viral agents (DAAs) has resulted in extremely high sustained virological response (SVR) rates in patients being treated while on liver transplantation (LT) waiting lists. The aim of this study was to evaluate the histological findings of hepatitis C virus (HCV) patients who achieved SVR after receiving DAA treatment [SVR(+)] prior to LT, and compare them with HCV patients who had not achieved SVR [SVR(-)]. Fifty-eight adult HCV patients who underwent LT at our institution from 2014 to 2016 were included in the study. Two pathologists, blinded to SVR status, simultaneously evaluated the histological sections. Assessment included the Histology Activity Index (HAI/modified Knodell score), fibrosis stage (Ishak score), and Laennec cirrhosis stage. The study group comprised 25 SVR(+) patients (56% male; mean age, 63.8 years), and the control group comprised 33 SVR(-) patients (69% male; mean age, 61.7 years). There was no significant difference in HAI between the groups (P = 0.414). Patients who achieved SVR also did not show less portal inflammation (P = 0.787), interface hepatitis (P = 0.999), confluent necrosis (P = 0.627) or spotty necrosis (P = 0.093) than the control group. There was a trend towards a higher degree of inflammation in patients who achieved SVR in <24 weeks (P = 0.07). The degree of focal lytic necrosis/apoptosis and portal inflammation was more prominent in SVR(+) patients with shorter SVR-LT intervals. Our study is the first to report persistent inflammation in HCV patients who received DAAs prior to LT. This supports the notion that inflammation is immunologically driven and that inflammation persists despite the absence of virus.

Oxidative stress as a potential biomarker for determining disease activity in patients with Rheumatoid Arthritis

Rheumatoid arthritis is an inflammatory, autoimmune disease where oxidative stress has been proposed to contribute to the joint tissue damage. To establish whether measurement of the redox status in blood mirrors the oxidant status at sites of inflammation in patients with rheumatoid arthritis, we concomitantly examined their oxidant status by spectrophotometry and/or flow cytometry. The basal levels of total reactive oxygen species (ROS), superoxide and hydroxyl radicals were significantly raised in neutrophils sourced from peripheral blood and synovial infiltrate, as also showed a strong positive correlation; however, there was no major increase in the reactive nitrogen species RNS generated in monocytes from both sources. Furthermore, raised levels of superoxide in neutrophils of synovial infiltrate showed a positive correlation with NADPH oxidase activity in synovial fluid. Additionally, as ROS generated in both peripheral blood and synovial infiltrate correlated positively with both DAS 28 and CRP/anti-CCP levels, its measurement can serve as an indirect measure of the degree of inflammation in patients with RA.

Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis

The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.

No apparent association between periocular and ocular microcolonization and the degree of inflammation in patients with atopic keratoconjunctivitis.

The cause of the chronic inflammation in atopic keratoconjunctivitis (AKC), the ocular manifestation of atopic eczema/dermatitis syndrome, is largely unknown. To investigate the possibility that microorganisms may be important in the inflammatory activity in AKC. Fifteen patients with AKC participated in the study. The presence of aerobic bacteria and fungi was related to the severity of clinical signs, the numbers of inflammatory cells in tears and conjunctival biopsies, and the concentration of various cytokines in tears. In addition, serological evidence for IgE sensitization to Staphylococcus aureus B antigen and Malassezia sympodialis antigen was investigated. Twelve healthy subjects were included for control purposes. The patients exhibited moderate clinical signs of AKC. No relation was found between the severity of AKC and the presence of microorganisms, despite the fact that S. aureus was frequently isolated. AKC patients showed significantly higher levels of IFN-gamma, TNF-alpha (tumour necrosis factor-alpha), IL-2, IL-4, IL-5 and IL-10 than controls. An association was found between conjunctival signs and the levels of all cytokines except IL-5. We found no evidence to suggest that periocular and ocular microcolonization are related to inflammatory parameters in AKC. However, confirmation of the present results in a longitudinal study with repeated clinical examinations and samplings in the same individual is required before the contribution of S. aureus to on-going inflammation in AKC can be dismissed.

M.550 Acute alterations of homocysteine plasma levels in relation to the degree of inflammation in patients with an acute coronary syndrome

M.550 Acute alterations of homocysteine plasma levels in relation to the degree of inflammation in patients with an acute coronary syndrome

M.550 Acute alterations of homocysteine plasma levels in relation to the degree of inflammation in patients with an acute coronary syndrome

M.550 Acute alterations of homocysteine plasma levels in relation to the degree of inflammation in patients with an acute coronary syndrome