C-reactive Protein Concentrations In Patients Research Articles

Systemic low-grade C-reactive protein is associated with proximal symptom spread in carpal tunnel syndrome.

Neuropathic pain is a highly prevalent condition associated with persistent disability. Some patients with neuropathic pain experience symptom spread outside neuroanatomical boundaries; these patients report more severe sensory symptoms and greater disability. However, the mechanisms behind such symptom spread are not fully understood. We used pre-surgical carpal tunnel syndrome (CTS) as a human model system of neuropathic pain to identify differences in the concentration of serologic inflammatory mediators between patients with CTS with territorial symptoms and those with proximal symptom spread to either the elbow or shoulder/neck. We performed a post-hoc analysis, comparing levels of serologic inflammatory mediators in a discovery cohort among 3 symptoms spread profiles (n = 55; n = 25 no spread, n = 21 spread to elbow, n = 9 spread to shoulder/neck). We then de-novo analysed the significantly dysregulated mediators in an independent validation cohort (n = 72; n = 34 no spread, n = 16 spread to elbow, n = 22 spread to shoulder/neck). The discovery cohort revealed higher serum concentrations of C-reactive protein (CRP) and interleukin-6 in patients with any symptom spread proximal to the wrist; interferon-γ was higher in patients with symptom spread to the elbow compared with those without proximal spread. The validation study replicated the association of higher CRP concentrations in patients with proximal spread to the elbow (no spread: median [interquartile range] 2.5 [5.4]; spread to elbow 6.2 [4.6]; spread to shoulder/neck 2.6 [3.7], P = 0.006). No other markers replicated in the validation cohort. Our findings suggest that proximal symptom spread in the context of neuropathic symptoms is associated with low-grade inflammation.

Identification of kynurenine and quinolinic acid as promising serum biomarkers for drug-induced interstitial lung diseases

BackgroundDrug-induced interstitial lung disease (DILD) is a lung injury caused by various types of drugs and is a serious problem in both clinical practice and drug development. Clinical management of the condition would be improved if there were DILD-specific biomarkers available; this study aimed to meet that need.MethodsBiomarker candidates were identified by non-targeted metabolomics focusing on hydrophilic molecules, and further validated by targeted approaches using the serum of acute DILD patients, DILD recovery patients, DILD-tolerant patients, patients with other related lung diseases, and healthy controls.ResultsSerum levels of kynurenine and quinolinic acid (and kynurenine/tryptophan ratio) were elevated significantly and specifically in acute DILD patients. The diagnostic potentials of these biomarkers were superior to those of conventional lung injury biomarkers, Krebs von den Lungen-6 and surfactant protein-D, in discriminating between acute DILD patients and patients with other lung diseases, including idiopathic interstitial pneumonia and lung diseases associated with connective tissue diseases. In addition to identifying and evaluating the biomarkers, our data showed that kynurenine/tryptophan ratios (an indicator of kynurenine pathway activation) were positively correlated with serum C-reactive protein concentrations in patients with DILD, suggesting the potential association between the generation of these biomarkers and inflammation. Our in vitro experiments demonstrated that macrophage differentiation and inflammatory stimulations typified by interferon gamma could activate the kynurenine pathway, resulting in enhanced kynurenine levels in the extracellular space in macrophage-like cell lines or lung endothelial cells. Extracellular quinolinic acid levels were elevated only in macrophage-like cells but not endothelial cells owing to the lower expression levels of metabolic enzymes converting kynurenine to quinolinic acid. These findings provide clues about the molecular mechanisms behind their specific elevation in the serum of acute DILD patients.ConclusionsThe serum concentrations of kynurenine and quinolinic acid as well as kynurenine/tryptophan ratios are promising and specific biomarkers for detecting and monitoring DILD and its recovery, which could facilitate accurate decisions for appropriate clinical management of patients with DILD.

Characteristics of persistent arthritis with refractory Kawasaki disease: a single-center retrospective study

Arthritis is one complication of Kawasaki disease (KD); however, the clinical features of arthritis in KD have not been well clarified. We retrospectively investigated the characteristics of persistent arthritis beyond the subacute phase of KD. In this cohort, 49 of 243 patients (20%) developed arthritis, with 33 patients (14%) experiencing persistent arthritis. Among these 33 patients, 31 (94%) had complete KD. Thirty (91%) were resistant to first intravenous immunoglobulin, and 15 (45%) required additional infliximab. Five patients (15%) developed coronary artery lesions, and 24 (73%) had oligoarthritis, mainly in large lower-extremity joints. Twenty-four patients (73%) complained of arthralgia. At arthritis onset, 16 patients (48%) presented with fever, including recurrent fever in 10 patients. Serum C-reactive protein concentration in patients with active arthritis significantly increased compared with after acute KD treatment (2.4 vs. 0.7 mg/dL, p < 0.001). Serum matrix metalloproteinase-3, a biomarker of arthritis, was significantly higher in patients with active arthritis than in remission (93.7 vs. 20.3 ng/mL, p < 0.001). Thirty (91%) and 14 (42%) patients, respectively, were treated with non-steroidal anti-inflammatory drugs and prednisolone, and they completely recovered. To summarize, persistent arthritis is a common complication in refractory KD, and adequate diagnosis and treatment are necessary.

Clinical Validation of a Capillary Blood Home-Based Self-Sampling Technique for Monitoring of Infliximab, Vedolizumab, and C-Reactive Protein Concentrations in Patients With Inflammatory Bowel Disease.

Therapeutic drug monitoring provides important guidance for treatment of patients with inflammatory bowel disease (IBD) and could help to early identify treatment failure. This study aimed to validate a finger prick-based capillary blood sampling technique to measure biological trough levels and C-reactive protein (CRP) and evaluate patient performance and -support. In this prospective cohort study, patients with IBD receiving infliximab (IFX) or vedolizumab (VEDO) therapy performed finger prick-based capillary blood sampling at home. Additionally, blood was collected through routinely performed in-hospital venepuncture prior to biological infusion. IFX, VEDO, and CRP concentrations were measured by enzyme-linked immunosorbent assay. The concordance between methods was statistically evaluated and a survey was conducted to assess practicality and patient support. In total, 81 patients (46 IFX, 35 VEDO) were enrolled. Mean differences between both methods were 0.42 (95% confidence interval, -1.74 to 2.58) μg/mL for IFX and 0.72 (95% confidence interval, -5.50 to 6.94) μg/mL for VEDO. Passing-Bablok regressions demonstrated no evidence for systematic or proportional biases. Venous and capillary IFX (ρ = 0.96, P < .001) and VEDO (ρ = 0.97, P < .001) levels strongly correlated and showed high intermethod agreement (Cohen's kappa: IFX = 0.82; VEDO = 0.94). Similarly, venous and capillary CRP levels were strongly correlated (ρ = 0.99, P < .001). Most patients (>95%) were able to successfully perform the self-sampling at home without prior instructions. This study clinically validated a finger prick-based capillary blood self-sampling technique allowing concomitant home monitoring of biological levels and CRP for patients with IBD, who reported substantial support, tolerability, and practicality.

Concentrations of selected acute phase proteins in patients with chronic venous insufficiency treated with Sulodexide. Part 1.

Chronic venous insufficiency (CVI) is a widespread and serious social problem. The pathogenesis of the disease is multifactorial and one of the important factors in its development is inflammation. Assessment of the concentration of selected acute phase proteins: C-reactive protein (CRP) and α1 antitrypsin (AAT) in the blood serum of patients with CVI before and after treatment with Sulodexide. The study was carried out in 88 people, including 39 clinically healthy subjects as the reference group and 49 patients with CVI at various stages of the disease. The concentrations of CRP and AAT were determined. The concentration of CRP in patients before the use of Sulodexide, compared to the results in the reference group, was statistically significantly higher. The concentration decreased significantly after the applied treatment. AAT concentration was significantly (p < 0.05) higher in the group of patients compared to the reference group. After treatment with Sulodexide, AAT concentration decreased in all study groups, which was statistically significant compared to the reference group. Elevated levels of acute phase proteins: CRP and AAT in patients indicate the participation of the inflammatory component in the pathogenesis of CVI. Monitoring levels of acute phase protein, especially AAT, may be useful in tracking the course of the disease, the body's response to treatment, and in making prognosis. Sulodexide, which acts mainly as an anticoagulant and profibrinolytic, also has an anti-inflammatory effect, which may contribute to the inhibition of the development of subsequent stages of CVI.

Increased C-reactive protein concentrations in patients admitted to the emergency department with troponin level elevations decreases the probability of myocardial ischemia

Abstract Funding Acknowledgements Type of funding sources: None. Background Patients frequently present to the emergency department (ED) with chest pain, dyspnea, or other symptoms with elevated troponin level. This finding prompts a provisional diagnosis of myocardial ischemia and raises the need to exclude this possibility. However, elevated blood troponin may be the result of a systemic inflammatory or infectious state merely representing cardiac injury and not myocardial ischemia. Purpose We hypothesized that the ratio of CRP/troponin could reflect the extent of the systemic inflammatory state that induces an attendant cardiac injury, which if sufficiently high could exclude myocardial ischemia. Methods Study population included 10774 patients admitted to the ED during the years 2016-2019 with cTn level higher &amp;gt; 14 ng/liter. CRP level was measured in all patients and CRP/troponin ratio was assessed against discharge diagnosis of myocardial ischemia, in order to evaluate its ability to exclude ischemic etiology of symptoms. The incidence of myocardial ischemia among study patients decreased with increasing CRP/troponin value. Results The prevalence of myocardial ischemia was 760/2694 patients (28.2%), 415/2694 (15.4%), 294/2695 (10.9%) and 130/2694 (4.8%) with 1st-4th CRP/troponin quartile, respectively (p &amp;lt; 0.0001). Logistic regression has shown that the probability of myocardial ischemia decreased by 53%, 68%, and 87% in the second to fourth CRP/troponin quartile compared with the first quartile, respectively (p &amp;lt; 0.0001). Conclusion The present study has shown that increased CRP level seems to modulate the specificity of simultaneous troponin as a marker of ischemia. As CRP level increases, so increases the likelihood that concomitant elevated troponin is due to myocardial injury and not due to myocardial ischemia. The clinical implication is that in the presence of a high CRP/troponin ratio, admission to the cardiology department and coronary investigation are unnecessary, whereas appropriate investigation of the actual medical problem is warranted.

The relation between healthy lifestyle changes and decrease in systemic inflammation in patients with stable cardiovascular disease

Background and aimsPharmacological lowering of inflammation has proven effective in reducing recurrent cardiovascular event rates. Aim of the current study is to evaluate lifestyle changes (smoking cessation, weight loss, physical activity level increase, alcohol moderation, and a summary lifestyle improvement score) in relation to change in plasma C-reactive protein (CRP) concentration in patients with established cardiovascular disease. MethodsIn total, 1794 patients from the UCC-SMART cohort with stable cardiovascular disease and CRP levels ≤10 mg/L, who returned for a follow-up study visit after median 9.9 years (IQR 5.4–10.8), were included. The relation between changes in smoking status, weight, physical activity, alcohol consumption, a summary lifestyle improvement score and change in plasma CRP concentration was evaluated with linear regression analyses. ResultsSmoking cessation was related to a 0.40 mg/L decline in CRP concentration (β-coefficient −0.40; 95%CI -0.73,-0.07). Weight loss (per 1SD = 6.4 kg) and increase in physical activity (per 1 SD = 48 MET hours per week) were related to a decrease in CRP concentration (β-coefficients −0.25; 95%CI -0.33,-0.16 and −0.09; 95%CI -0.17,-0.01 per SD). Change in alcohol consumption was not related to CRP difference. Every point higher in the summary lifestyle improvement score was related to a decrease in CRP concentration of 0.17 mg/L (β-coefficient −0.17; 95%CI -0.26,-0.07). ConclusionsSmoking cessation, increase in physical activity, and weight loss are related to a decrease in CRP concentration in patients with stable cardiovascular disease. Patients with the highest summary lifestyle improvement score have the most decrease in CRP concentration. These results may indicate that healthy lifestyle changes contribute to lowering systemic inflammation, potentially leading to a lower cardiovascular risk in patients with established cardiovascular disease.

Serum fetuin-A, tumor necrosis factor alpha and C-reactive protein concentrations in patients with hereditary angioedema with C1-inhibitor deficiency

Background and aimsHereditary angioedema with C1-inhibitor deficiency (C1-INH-HAE) is characterized by localized, non-pitting, and transient swelling of submucosal or subcutaneous region. Human fetuin-A is a multifunctional glycoprotein that belongs to the proteinase inhibitor cystatin superfamily and has structural similarities to the high molecular weight kininogen. Fetuin-A is also known a negative acute phase reactant with anti-inflammatory characteristics. In this study we aimed to determine serum fetuin-A, C-reactive protein (CRP) and tumor necrosis factor alpha (TNFα) concentrations in patients with C1-INH-HAE during symptom-free period and during attacks and compare them to those of healthy controls. Further we analyzed possible relationship among these parameters as well as D-dimer levels which was known as marker of HAE attacks.Patients and methodsSerum samples of 25 C1-INH-HAE patients (8 men, 17 women, age: 33.1 ± 6.9 years, mean ± SD) were compared to 25 healthy controls (15 men, 10 women, age: 32.5 ± 7.8 years). Serum fetuin-A and TNFα concentrations were determined by ELISA, CRP and D-dimer by turbidimetry.ResultsCompared to healthy controls patients with C1-INH-HAE in the symptom-free period had significantly decreased serum fetuin-A 258 μg/ml (224–285) vs. 293 μg/ml (263–329), (median (25–75% percentiles, p = 0.035) and TNFα 2.53 ng/ml (1.70–2.83) vs. 3.47 ng/ml (2.92–4.18, p = 0.0008) concentrations. During HAE attacks fetuin-A levels increased from 258 (224–285) μg/ml to 287 (261–317) μg/ml (p = 0.021). TNFα and CRP levels did not change significantly. We found no significant correlation among fetuin-A CRP, TNFα and D-dimer levels in any of these three groups.ConclusionsPatients with C1-INH-HAE have decreased serum fetuin-A concentrations during the symptom-free period. Given the anti-inflammatory properties of fetuin-A, the increase of its levels may contribute to the counter-regulation of edema formation during C1-INH-HAE attacks.

High-sensitivity C-Reactive Protein concentration in Patients with Acute Coronary Syndrome of Central India

High-sensitivity C-Reactive Protein concentration in Patients with Acute Coronary Syndrome of Central India

Meta-analysis of serum C-reactive protein and cartilage oligomeric matrix protein levels as biomarkers for clinical knee osteoarthritis

BackgroundThe roles of C-reactive protein (CRP) and cartilage oligomeric matrix protein (COMP) in knee osteoarthritis (KOA) remain controversial, thus the present study is aimed to explore the relationships between CRP, COMP, and the incidence/progression of KOA.MethodsA systematic search was conducted on PubMed and Embase until September, 2016 for all the relevant studies. The pooled mean difference (MD) with its 95% confidence interval (95% CI) based on fixed effects model or random effects model was calculated to assess the potential role of CRP and COMP in the incidence or progression of KOA. Heterogeneity was evaluated by Cochran’s Q and I2 tests. When P < 0.05 or I2 > 50%, a random effects model was chosen, otherwise, a fixed effects model was used. Moreover, the role of CRP in different degrees of pain was also analyzed. Sensitivity analysis was performed to evaluate the strength of the meta-analysis.ResultsFourteen studies were enrolled in the meta-analysis. No difference was found between baseline CRP and CRP levels in the last follow-up period of KOA (MD = − 0.09, 95% CI: -0.30, 0.13). Pooled data showed higher CRP concentration in patients with incident KOA when compared with controls (MD = 0.33, 95% CI: 0.04, 0.63). Moreover, higher serum COMP levels were found in patients with incident KOA (MD = 1.69, 95% CI: 0.61, 2.76) Additionally, significant higher CRP concentration was observed in KOA patients with highest degree of pain (MD = 1.60, 95% CI: 0.52, 2.67).ConclusionCRP and COMP serum levels were both associated with the incidence of KOA. Patients with a higher CRP and COMP concentration might have an increased probability of developing KOA. However, higher CRP serum levels was not related with KOA progression. Furthermore, KOA patients with more pain had higher CRP concentrations.

C-reactive protein concentrations across the mood spectrum in bipolar disorder: a systematic review and meta-analysis

Inflammatory processes and neural-immune interactions have been implicated in the pathogenesis of psychiatric conditions, but studies in bipolar disorder are inconclusive so far. We aimed to investigate whether peripheral concentrations of C-reactive protein (CRP), an acute-phase response protein of inflammatory activity, are increased in bipolar disorder across the mood spectrum. In this systematic review and meta-analysis, we searched MEDLINE, the Cochrane Library, Scopus, and Web of Knowledge from database inception to Aug 14, 2016, for studies that measured serum and plasma CRP concentrations in adult patients with bipolar disorder (as defined by DSM-IV-TR) and healthy controls. We extracted data from published reports. We did three between-group meta-analyses comparing CRP concentrations in patients in mania, depression, or euthymia, with those in healthy controls (cross-sectional studies), and two within-group meta-analyses comparing changes in CRP concentrations before and after treatment of an index manic or depressive episode (longitudinal studies). We used Hedges' adjusted g to calculate effect sizes and pooled results using random-effect models. We also did meta-regression analyses by mood state to investigate possible moderators of CRP concentrations. We identified 27 studies representing 2161 patients with bipolar disorder and 81 932 healthy controls. Compared with healthy individuals, CRP concentrations were moderately increased in people with bipolar disorder during depression (g 0·67, 95% CI 0·23 to 1·11; p=0·003) and euthymia (0·65, 0·40 to 0·90; p<0·0001) and more substantially increased during mania (0·87, 0·58 to 1·15; p<0·0001). The extent of the increases in CRP concentrations in mania and depression was not related to symptom severity (p=0·256 for mania and p=0·626 for depression). CRP concentrations were moderately decreased after resolution of an index manic episode (-0·36, -0·66 to -0·05; p=0·022) and slightly decreased after resolution of an index depressive episode (-0·18, -0·30 to -0·07; p=0·002). CRP concentrations are increased in bipolar disorder regardless of mood state, but are higher during mania than in depression and euthymia, suggesting an increased inflammatory burden in mania. None.

Serum levels of magnesium and their relationship with CRP in patients with OSA.

Low levels of magnesium (Mg) are associated with chronic inflammatory stress. Some animal studies have reported that a moderate deficiency of Mg, similar to that which occurs in humans, may increase inflammatory or oxidative stress stimulated by other factors, such as disrupted sleep or sleep deficiency. This cross-sectional study evaluated the relationship between serum levels of Mg and the inflammatory response in patients with a new diagnosis of obstructive sleep apnea (OSA). This clinical, retrospective study registered 68 patients with newly diagnosed mild to severe OSA and 30 without OSA. The Apnea-Hypopnea Index (AHI), oxygen desaturation index (ODI), time until blood hemoglobin oxygen saturation <90% (SpO2 <90%), and mean blood hemoglobin SpO2 were measured. Serum levels of Mg, plasma C-reactive protein (CRP), and total sleep time (TST) by polysomnography were also measured. Mg levels were lower in patients with OSA than those in controls matched for age, sex, and body mass index (BMI). Patients with OSA had substantially higher plasma CRP concentrations than controls. A negative correlation was observed between the AHI and ODI and Mg levels. Significant differences in Mg and CRP levels were observed between patients with AHI scores of 5-15 and scores ≥30 based on OSA severity but independent of BMI. Furthermore, the AHI, ODI, TST <90%, and mean SpO2 significantly correlated with CRP. A significant negative correlation was observed between Mg and CRP levels (p<0.0001). Our results show that Mg levels changed depending on the presence and severity of OSA. Low levels were associated with a higher CRP concentration in patients with OSA.

Serum C-reactive protein distribution in minimally invasive total knee arthroplasty do not differ with distribution in conventional total knee arthroplasty.

Minimally invasive total knee arthroplasty (MITKA) has been developed to reduce surgical trauma and facilitate rehabilitation after arthroplasty. A plausible hypothesis is that this reduced trauma results in lower concentrations of circulating inflammatory biomarkers, such as C-reactive protein (CRP). In this study, we compared CRP concentrations in patients undergoing MITKA to those undergoing conventional TKA (CTKA). Eight hundred and seven patients undergoing MITKA were prospectively recruited. CRP was measured before operation and on days 2, 4, 21, and 42 after operation. Two hundred and forty-seven patients who had CTKA were collected retrospectively, with the same inclusion and exclusion criteria as those who had MITKA. We found in both groups, that CRP values rose abruptly after operation, with peak values reached on day 2 or 4. Values then declined so that by days 21 and 42 they were only modestly above baseline values. Throughout the entire study period, mean CRP in MITKA patients did not differ significantly from those in CTKA patients. However, a significantly higher proportion of CTKA patients than of MITKA patients had peak CRP values at day 4 rather than at day 2 (76.8% vs 42.5%), a difference that was more pronounced in women. Also, by day 42, CRP values were still above baseline in 18.5% of MITKA patients and 28.8% of CTKA patients without known complications. In conclusion, CRP distribution pattern was similar in patients who received MITKA or CTKA,. CRP values remained slightly elevated in both MITKA and CTKA patients for as long 42 days after operation. These findings suggest that MITKA is no less traumatic than CTKA, as determined by CRP values, and the patterns of postoperative CRP may be useful in the management of TKA patients.

Prognostic evaluation of preoperative serum C-reactive protein concentration in patients with epithelial ovarian cancer.

The aim of the present study was to evaluate correlations between preoperative C-reactive protein (CRP) serum concentration and the clinical-pathological parameters of epithelial ovarian cancer (EOC), as well as cancer antigen 125 (CA125) concentration, in patients with EOC. The preoperative serum CRP concentrations of 107 patients with EOC were compared with values of 44 control patients and defined as positive if values were >8 mg/l. Correlations between CRP expression and serum CA125 concentrations, International Federation of Gynecologists and Obstetricians (FIGO) staging, lymph node metastasis, ascites and size of postoperative residual lesions were evaluated for the EOC cases. A total of 69% (74/107) of the EOC cases were CRP-positive, with a mean serum CRP concentration of 14.32 mg/l (versus 2.18 mg/l in the control patients) (P<0.001). A rank correlation analysis showed a positive correlation between serum CRP and CA125 concentrations (P<0.001). The five-year survival rate of the CRP-positive patients with EOC was significant lower than that of the patients that were CRP-negative (33.3 vs. 75.8%, P<0.001). Non-parametric and multivariate analyses showed significant correlations between CRP concentrations and FIGO staging (P=0.001), lymph node metastasis (P=0.001) and ascites (P=0.033). In contrast to previous reports, the mean CRP serum concentration of the CRP-positive patients with EOC also correlated significantly with the CA125 values, and the increases in the CRP serum concentration in the Chinese patients were lower than those described for Caucasian EOC cases. In conclusion, the CRP serum concentration may be a useful clinical marker, solely or in combination with CA125, in patients with EOC.

Does increased peripheral C-reactive protein predate the occurrence of a short cervical length?

Objective: Shortened cervical length is an important predictor of preterm birth, though the etiology of cervical length variation has not been fully elucidated. Our objective was to evaluate the potential association between peripheral C-reactive protein (CRP), a first trimester peripheral marker of inflammation, and second trimester decreased cervical length.Methods: Cases and controls were defined by second trimester cervical length >/<25 mm. CRP concentrations were measured in archived first trimester screen serum via commercial assay. The association between CRP and cervical length was evaluated via Wilcoxon’s rank test. Both logistic and linear regressions were performed.Results: A total of 49 cases were matched to 98 controls. No statistically significant difference in first trimester CRP was demonstrated between cases and controls overall. Among subjects with decreased cervical lengths, however, there was a significant linear association between the degree of shortening and first trimester CRP concentrations (p = 0.022).Conclusion: First trimester CRP was not associated with decreased second trimester cervical length overall. However, the degree of shortening correlated with increased first trimester CRP concentrations in patients with a short cervix. This suggests that systemic inflammation in early pregnancy may underlie variation in second trimester cervical lengths among higher risk individuals.

Estimation of intercommunications between insulin resistance, endothelial dysfunction, dyslipidemia, plasma adiponectin and C-reactive protein concentrations in patients with type 2 the diabetes mellitus

Under a supervision there were 80 patients with type 2 diabetes mellitus (DM) in age from 41 to 74. It is set that for patients with newly diagnosed type 2 DM in combination with obesity there are hyperglycemia, hyperinsulinemia and insulin resistance (IR). Maximal hyperinsulinemia is marked at disease duration up to 5 years. At duration of disease the insulin secretion goes down from 6 to 10 years, and IR increases. For patients with newly diagnosed type 2 DM the atherogenic type IIb dyslipidemia was marked. Hypoadiponectinemia assists to IR development, forming the atherogenic lipid profile and endothelial dysfunction, bulge of intima-media complex. Between IR and endothelial dysfunction from data of correlation analysis there is high positive connection that increases with the increase of DM duration for women. By principal reasons of endothelial dysfunction the type 2 DM patients during the moment of diagnosis have a chronic hyperglycemia, IR, dyslipidemia, hypoadiponectiemia, vascular inflammation.

Association between C-reactive Protein Concentration and Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-analysis

This meta-analysis was conducted to summarize the association between the serum concentration of C-reactive protein (CRP) and chronic obstructive pulmonary disease (COPD). MEDLINE(®), Cochrane Central Register of Controlled Trials, and EMBASE databases were searched for relevant studies. Data were extracted; pooled weighted mean differences (WMDs) and 95% confidence intervals (CIs) were calculated. Twenty studies were selected for final inclusion in this analysis. Patients with COPD had higher serum CRP concentrations than healthy controls (WMD 4.72 mg/l, 95% CI 2.98, 6.47). In addition, patients with severe COPD had higher serum CRP concentrations than those with moderate COPD (WMD 1.26 mg/l, 95% CI 0.78, 1.73). There was no significant difference in serum CRP concentration between patients with mild and moderate COPD (WMD 0.67 mg/l, 95% CI -0.08, 1.42). This meta-analysis suggested that patients with stable COPD had higher serum CRP concentrations than healthy controls. CRP might be an indicator of disease severity in patients with COPD, thus highlighting the importance of measuring serum CRP concentrations in patients with stable COPD.

C-Reactive Protein and the Framingham Coronary Risk Score in Patients Newly Diagnosed With Intermittent Claudication

To investigate the relationship between serum C-reactive protein (CRP) levels and the calculated 10-year Framingham risk score (FRS) in patients newly diagnosed with intermittent claudication. Serum CRP levels were measured in 90 patients newly diagnosed with intermittent claudication over a 12-month period. In all, 76 patients (53 males [70%], mean age 63.3 ± 9.3) were included in the analysis. Log-transformed CRP levels significantly correlated with total FRS (r = .34, P = .002). Participants were divided into 4 groups according to log-CRP levels. Analysis of variance showed a statistically significant difference between the 4 groups in terms of mean FRS, P = .003. Post hoc comparisons indicated that group 1 was significantly different from group 4, P = .002. Analysis of covariance showed a significant difference between the 4 groups of log-CRP levels in terms of mean FRS, P = .008. There is an increased 10-year risk of coronary heart disease associated with increased plasma concentration of CRP in patients newly diagnosed with intermittent claudication.

C‐reactive protein and seizures in focal epilepsy: A video‐electroencephalographic study

C-reactive protein (CRP) has been studied extensively in many noninflammatory neurologic conditions, but there has been little study of CRP in the context of seizures or epilepsy. The purpose of this study was to examine CRP concentrations in patients with refractory focal epilepsy who were undergoing video-electroencephalography (EEG) monitoring compared with healthy controls, and CRP change during 24 h after a seizure. CRP levels were measured in serum at the onset of video-EEG recording (CRP-0h) and at 3, 6, 12, and 24 h after index seizure (the first verified localized-onset seizure) in 31 patients during inpatient video-EEG monitoring by using high sensitivity measurement of CRP concentration. The patients were categorized into two groups: temporal lobe epilepsy (TLE; n = 15) and extratemporal lobe epilepsy (XLE; n = 16). Eighty healthy volunteers served as controls. CRP-0h concentration was significantly higher in patients with refractory focal epilepsy than in controls (3.5 vs. 0.7 mg/ml, p < 0.001). All five patients with elevated CRP-0h (>mean + 2 standard deviations in controls) had TLE (vs. none in XLE; p = 0.018). Index seizure type was associated with CRP increase from baseline to maximum level after index seizure (p = 0.005). The most important predictor of increase in CRP level was secondarily generalized tonic-clonic seizure (SGTCS; p = 0.030). The higher baseline levels in patients with epilepsy compared with healthy controls demonstrates that CRP concentrations are also affected in refractory epilepsy. Our data suggest that SGTCS stimulates CRP production. These results emphasize the association between inflammation and refractory epilepsy.

Value of C-Reactive Protein in Predicting Left Ventricular Remodelling in Patients with a First ST-Segment Elevation Myocardial Infarction

Objective. To assess the value of C-reactive protein (CRP) in predicting postinfarct left ventricular remodelling (LVR). Methods. We measured in-hospital plasma CRP concentrations in patients with a first ST-segment elevation myocardial infarction (STEMI). Results. LVR was present at 6 months in 27.8% of 198 patients. CRP concentration rose during the first 24 h, mainly in LVR group. The prevalence of LVR was higher in patients from the highest quartile of CRP concentrations at 24 h as compared to those from any other quartile (odds ratio (OR) 3.48, 95% confidence interval (95% CI) 1.76–6.88). Multivariate analysis identified CRP concentration at 24 h (OR for a 10 mg/L increase 1.29, 95% CI 1.04–1.60), B-type natriuretic peptide at discharge (OR for a 100 pg/mL increase 1.21, 95% CI 1.05–1.39), body mass index (OR for a 1 kg/m2 increase 1.10, 95% CI 1.01–1.21), and left ventricular end-diastolic volume (OR for a 1 mL increase 0.98, 95% CI 0.96-0.99) as independent predictors of LVR. The ROC analysis revealed a limited discriminative value of CRP (area under the curve 0.61; 95% CI 0.54–0.68) in terms of LVR prediction. Conclusions. Measurement of CRP concentration at 24 h after admission possesses a significant but modest value in predicting LVR after a first STEMI.