Higher Plasma C-reactive Protein Levels Research Articles

GUİLLAİN-BARRÉ SENDROMUNDA AĞIR ÖZÜRLÜLÜĞÜN ERKEN BELİRTEÇLERİ

Objective
 Guillain-Barré syndrome (GBS) is an autoimmune
 neurological disorder with non-negligible morbidity
 and mortality. This study aimed to evaluate different
 patient characteristics and laboratory findings as early
 predictors of severe disability in GBS patients.
 Material and Method
 We retrospectively reviewed the medical records of
 121 patients diagnosed with GBS between January
 1, 2018, and December 31, 2021. Data regarding
 demographic characteristics, presenting complaints,
 co-morbidities, previous infection history, neurological
 examination findings, GBS Disability Scores (GDS)
 on the 1st day and by the end of the first month,
 laboratory parameters of serological and cerebrospinal
 fluid (CSF) examination, electromyoneurography
 results, GBS subtypes, treatments, treatment-related
 complications, and prognoses were recorded.
 Results
 The median age of the 121 patients was 58 (20–87)
 years (n = 73 males, 60%). The average GDS was
 3 on admission and 2 at the end of the first month.
 The serum C-reactive protein (CRP) and CSF protein
 levels were raised, while vitamin D levels were
 reduced. Advanced age, cranial nerve involvement,
 history of infection, admission to the intensive care
 unit (ICU), need for mechanical ventilation (MV),
 presence of complications, high plasma CRP levels,
 neutrophil-lymphocyte ratio (NLR), and plateletlymphocyte
 ratio (PLO) were significantly associated
 with severe disability in GBS patients at day 1 and at
 the end of the first month.
 Conclusion
 We identified multiple characteristics that can predict
 severe disability in GBS patients.

Psychosocial and behavioral factors affecting inflammation among pregnant African American women

African American women are reported to have greater inflammation compared with women from other racial groups. Higher inflammation during pregnancy has been associated with increased risk of adverse perinatal outcomes. We hypothesized that maternal inflammation is related to depressive symptoms and social and behavioral risk factors among pregnant African American women. Pregnant African American women (n ​= ​187) were recruited at prenatal clinics in the Midwest. Women completed questionnaires and had blood drawn at a prenatal visit. Plasma levels of cytokines (interferon gamma [IFN]-γ, interleukin [IL]-6, IL-8, IL-10, tumor necrosis factor [TNF]-α) and C-reactive protein (CRP) were measured by multiplex assays. Women had a mean age of 26.58±5.42 years and a mean gestational age at data collection of 16.35±5.95 weeks. Twenty-six percent of women had Center for Epidemiological Studies-Depression (CES-D) scores ≥23 (scores that have been correlated with clinical diagnosis of depression), 15.5% smoked cigarettes, 16.6% used marijuana, and 5.3% reported experiencing intimate partner violence (IPV). Higher CES-D scores were correlated with higher plasma CRP levels (r ​= ​0.16, p ​= ​0.046). Women who reported any experiences of IPV during pregnancy had higher levels of IL-8 (p ​= ​0.018) and lower levels of IFN-γ (p ​= ​0.012) compared with women who did not report IPV. Cigarette smoking during pregnancy was associated with lower levels of the anti-inflammatory cytokine IL-10 (p ​= ​0.003). These findings suggest that depressive symptoms, IPV, and cigarette smoking during pregnancy relate to select inflammatory markers in pregnant African American women. The relationships of inflammation with these factors should be further investigated to better understand the mechanisms which influence maternal and fetal health outcomes.

Cortical inflammation and brain signs of high-risk atherosclerosis in a non-human primate model.

Atherosclerosis is a chronic systemic inflammatory disease, inducing cardiovascular and cerebrovascular acute events. A role of neuroinflammation is suspected, but not yet investigated in the gyrencephalic brain and the related activity at blood−brain interfaces is unknown. A non-human primate model of advanced atherosclerosis was first established using longitudinal blood samples, multimodal imaging and gene analysis in aged animals. Non-human primate carotid lesions were compared with human carotid endarterectomy samples. During the whole-body imaging session, imaging of neuroinflammation and choroid plexus function was performed. Advanced plaques were present in multiple sites, premature deaths occurred and downstream lesions (myocardial fibrosis, lacunar stroke) were present in this model. Vascular lesions were similar to in humans: high plaque activity on PET and MRI imaging and systemic inflammation (high plasma C-reactive protein levels: 42 ± 14 µg/ml). We also found the same gene association (metabolic, inflammatory and anti-inflammatory markers) as in patients with similar histological features. Metabolic imaging localized abnormal brain glucose metabolism in the frontal cortex. It corresponded to cortical neuro-inflammation (PET imaging) that correlated with C-reactive protein level. Multimodal imaging also revealed pronounced choroid plexus function impairment in aging atherosclerotic non-human primates. In conclusion, multimodal whole-body inflammation exploration at the vascular level and blood−brain interfaces identified high-risk aging atherosclerosis. These results open the way for systemic and central inflammation targeting in atherosclerosis in the new era of immunotherapy.

Association between visceral/subcutaneous adipose tissue ratio and plasma inflammatory markers and score for cardiovascular risk prediction in a Brazilian cohort: Pró-Saúde Study.

Visceral adipose tissue (VAT) is associated with various metabolic disorders, and adipokines, secreted by adipose tissue, are involved in their pathogenesis. This study investigated associations between VAT/subcutaneous adipose tissue (SAT) ratio, inflammatory markers, and cardiovascular (CV) risk-score in adults. Plasma levels of adipokines, plasma lipid profile, blood pressure, and body composition (using dual-emission x-ray absorptiometry) were determined. CV risk-score based on the American College of Cardiology and the American Heart Association (ACC/AHA) score was calculated in a sample of 309 Brazilian civil servants aged <60 years. Participants' VAT/SAT ratio were categorized into quartiles. Among males, plasma leptin (2.8 ng/mL) and C reactive protein (CRP) (0.2 mg/dL) (P<0.05) levels were higher at P75 and P50 than P5, and the highest calculated CV risk-score was observed at P75 (7.1%). Among females, higher plasma adiponectin levels were observed at P25 (54.3 ng/mL) compared with P75 (36 ng/mL) (P<0.05). Higher plasma CRP levels were observed at P75 (0.4 mg/dL) compared with P5 (0.1 mg/dL) (P<0.05). Higher CV risk-score was observed at P75 (2.0%) compared with P5 (0.7%). In both sexes, VAT and VAT/SAT ratio were directly associated with plasma leptin, CRP, and CV risk-score, and inversely associated with adiponectin; SAT was directly associated with plasma leptin and CRP (P<0.01); interleukin (IL)-10 and CRP were directly associated with adiponectin and leptin, respectively (P<0.05). Among men only, IL-10 (inversely) and CRP (directly) were associated with CV risk-score (P=0.02). Our results strengthened the relevance of the VAT/SAT ratio in cardiovascular risk.

Investigation of the curative effects of palm vitamin E tocotrienols on autoimmune arthritis disease in vivo

The tocotrienol-rich fraction (TRF) from palm oil contains vitamin E, which possesses potent antioxidant and anti-inflammatory activities. Rheumatoid arthritis (RA) is a chronic joint inflammatory disease characterised by severe joint pain, cartilage destruction, and bone erosion owing to the effects of various pro-inflammatory mediators and cytokines. Here, we investigated the therapeutic effects of TRF in a rat model of collagen-induced arthritis (CIA). Arthritis was induced by a single intradermal injection of collagen type II in Dark Agouti (DA) rats. Rats were then treated with or without TRF by oral gavage from day 28 after the first collagen injection. Arthritic rats supplemented with TRF showed decreased articular index scores, ankle circumferences, paw volumes, and radiographic scores when compared with untreated rats. The untreated arthritic rats showed higher plasma C-reactive protein levels (p < 0.05) and production of pro-inflammatory cytokines than arthritic rats fed TRF. Moreover, there was a marked reduction in the severity of histopathological changes observed in arthritic rats treated with TRF compared with that in untreated arthritic rats. Overall, the results show that TRF had beneficial effects in this rat model of RA.

Pentraxin levels in non-eosinophilic versus eosinophilic asthma.

Innate immunity has been thought to be involved in asthma pathogenesis. Pentraxins, acting as soluble pattern recognition molecules, play an important role in humoral innate immunity. Asthma is a heterogeneous inflammatory disease of airways and can be classified as eosinophilic or non-eosinophilic asthma. To investigate whether pentraxin levels differ in subjects with eosinophilic versus non-eosinophilic asthma. Furthermore, to access the predictive performance of pentraxin levels for discriminating asthma inflammatory phenotypes. A total of 80 asthmatic patients and 24 healthy control subjects underwent sputum induction at study inclusion. Differential leucocyte counts were performed on selected sputum. Plasma C-reactive protein (CRP), serum amyloid P (SAP), pentraxin 3 (PTX3), and sputum SAP, PTX3, IL-8 levels were determined by enzyme-linked immunosorbent assay. Subjects with non-eosinophilic asthma had significantly increased pentraxin levels compared with those with eosinophilic asthma and healthy controls, with median (interquartile range) plasma CRP levels of 0.86 (0.28-2.07), 0.26 (0.14-0.85), and 0.15 (0.09-0.45)mg/L (P<.001), respectively, plasma SAP levels of 33.69 (19.79-58.39), 19.76 (16.11-30.58), and 20.06 (15.68-31.11)mg/L (P=.003), respectively, and sputum PTX3 levels of 4.9 (1.35-18.72), 0.87 (0.30-2.07), and 1.08 (0.31-4.32)ng/mL (P<.001), respectively. Conversely, sputum SAP concentrations of eosinophilic asthmatics (median, 21.49ng/mL; IQR, 6.86-38.79ng/mL) were significantly higher than those of non-eosinophilic patients (median, 8.15ng/mL; IQR, 2.82-18.01ng/mL) and healthy controls (median, 8.79ng/mL; IQR, 2.00-16.18ng/mL). Asthma patients with high plasma CRP (P=.004), SAP (P=.005) and sputum PTX3 levels (P<0.001) also had significantly lower sputum eosinophil percentages. Sputum PTX3 levels had the best power (11.18-fold, P<.001) to predict non-eosinophilic airway inflammation in asthma patients. Pentraxin levels differed significantly between patients with non-eosinophilic asthma and those with eosinophilic asthma. Furthermore, elevated pentraxin expressions may predict non-eosinophilic airway inflammation in asthmatic patients.

The Additive Impact of Periodic Limb Movements during Sleep on Inflammation in Patients with Obstructive Sleep Apnea

Both periodic limb movements during sleep (PLMS) and obstructive sleep apnea (OSA) are major causes of sleep disorders and have been associated with systemic inflammation and cardiovascular events. However, it is uncertain whether in combination they promote a higher inflammatory response and greater risk of cardiovascular events than each condition alone. To investigate whether the presence of PLMS is associated with increased inflammation in patients suspected of having OSA. In 342 patients who underwent polysomnography to diagnose OSA, plasma C-reactive protein (CRP) and fibrinogen levels were measured. OSA was found in 254 patients, with 46 also having PLMS. Among the 88 patients who did not have OSA, 8 had PLMS. Plasma CRP and fibrinogen levels in the group with both PLMS and OSA were higher than in patients with neither OSA nor PLMS and in patients with OSA only (CRP: 0.20 ± 0.48 vs. 0.09 ± 0.15 vs. 0.13 ± 0.18 mg/dl, P = 0.03; fibrinogen: 298.2 ± 76.1 vs. 269.0 ± 57.1 vs. 270.0 ± 52.6 mg/dl, P < 0.01). Multivariate analysis showed that the presence of PLMS was associated with higher plasma CRP levels (β = 0.1401, P < 0.01) and fibrinogen levels (β = 0.1359, P = 0.01) independently from other clinical variables such as body mass index and the severity of OSA. PLMS were positively associated with plasma CRP and fibrinogen levels in patients suspected of having OSA. Because plasma levels of these proteins have been established as predictive factors of future cardiovascular events, the presence of PLMS may be a useful clinical sign to identify patients with OSA at high risk of cardiovascular events.

Anemia is Associated with Bone Mineral Density in Chronic Obstructive Pulmonary Disease

Objective: Patients with chronic obstructive pulmonary disease (COPD) often suffer from systemic co-morbidities, including anemia. However, anemia is related to multiple outcomes in COPD and in other chronic diseases, but it's impact is underestimated in COPD. The objective of the present study was to relate anemia in patients with COPD with disease-related outcomes, systemic inflammation and COPD related co-morbidities. Methods: Data of 321 patients with COPD admitted for pulmonary rehabilitation were analysed. Besides general characteristics, lung function, body composition, arterial gases and plasma haemoglobin concentration, disease-related outcomes (health-related quality of life by St. George's Respiratory Questionnaire, 6-minute walking distance, mMRC dyspnea scale, and BODE index), systemic inflammation (C-reactive protein (CRP)) and self-reported and objectified co-morbidities (low muscle mass, osteoporosis, renal failure, risk for undernutrition) were taken into account. Results: First, 20% of the patients were anemic, and 8% was polycythemic. Polycythemic patients had a lower proportion of men and a lower proportion of low muscle mass compared to the other groups. Anemic patients had higher plasma CRP levels and lower total body bone mineral density compared to the other groups. There was no difference in disease-related outcomes or other co-morbidities in the patients with and without anemia. Even after adjustment for confounders, anemia was an independent determinant for higher CRP levels and lower bone mineral density. Conclusion: Anemia is frequently present in patients with COPD and there is evidence that it is associated with lower whole body bone mineral density.

Genetic contribution to C-reactive protein levels in severe obesity

Obese individuals are characterized by a chronic, low-grade inflammatory state. Increased levels of C-reactive protein (CRP), a marker of inflammation, have been observed in subjects with the metabolic syndrome. We have previously reported that genes encoding proteins involved in the anti-inflammatory and immune response are differentially expressed in visceral adipose tissue of obese men with or without the metabolic syndrome. Among these genes, the interferon-gamma-inducible protein 30 (IFI30), CD163 molecule (CD163), chemokine (C-X-C motif) ligand 9 (CXCL9) and thymic stromal lymphopoietin (TSLP), were selected for further genetic analyses. The aim of the study was to verify whether IFI30, CD163, CXCL9 and TSLP gene polymorphisms contribute to explain the inter-individual variability of the inflammatory profile of obesity assessed by plasma high-sensitivity CRP concentrations. A total of 1185 severely obese individuals were genotyped for single nucleotide polymorphisms (SNPs) covering most of the sequence-derived genetic variability at the IFI30, CD163, CXCL9 and TSLP gene loci (total of 27 SNPs). Following measurement of plasma CRP levels, subjects were divided into two groups, low vs. high using the median value of plasma CRP levels (8.31mg/L) as a cutoff point. Genotype frequencies were compared between groups. Associations between genotypes and plasma CRP levels (continuous variable) were also tested after adjustments for age, sex, smoking and BMI. The rs11554159 and rs7125 IFI30 SNPs showed a significant difference in genotype frequencies (p<0.05) between subgroups of low vs. high plasma CRP levels (wild type homozygotes: rs11554159=47% vs. 55%, rs7125=31% vs. 24%, for low vs. high CRP groups, respectively). The association between rs11554159 and CRP levels as a continuous variable remained significant (p=0.004). Both carriers of the GA and AA genotypes demonstrated, on average, a 13% lower CRP levels in comparison with GG homozygotes. No association was observed between SNPs in the CD163, CXCL9 and TSLP genes and CRP levels. The IFI30 rs11554159 polymorphism could partially explain the inter-individual variability observed in the inflammatory profile associated with obesity.

Genetically Elevated C-Reactive Protein and Ischemic Vascular Disease

Conclusion: Polymorphisms of the C-reactive protein (CRP) gene are associated with increases in CRP levels but are not in themselves associated with an increased risk of ischemic vascular disease. Summary: It is well known that elevated plasma levels of CRP are associated with an increased risk of ischemic cerebrovascular and ischemic cardiac disease. What is unknown is whether CRP levels themselves contribute to causation of ischemic cerebrovascular or cardiac disease, or are merely markers of the existence of ischemic cerebrovascular or cardiovascular disease. The CRP gene has genetic variations that increase levels of CRP to different degrees and therefore can theoretically be used to assess the consequences of lifelong high CRP levels independent of additional risk factors. The authors of this study sought to determine whether genetically elevated CRP levels caused an increased risk of ischemic heart disease and ischemic cerebrovascular disease. The study included 10,276 people from a general population cohort. Ischemic heart disease developed in 1786, and ischemic cerebrovascular disease developed in 741. In an additional cohort of 31,992 persons from the general population, 2521 had ischemic heart disease and 1483 had ischemic cerebrovascular disease. The authors also studied an additional 2238 patients with ischemic heart disease and 4474 control participants along with 612 patients with ischemic cerebrovascular disease and an additional 1224 control participants. High-sensitivity CRP was measured, followed with genotyping of four CRP polymorphisms and two apolipoprotein E polymorphisms. In persons with CRP levels >3 mg/L, compared with those with CRP levels <1 mg/L, ischemic heart disease was increased by a factor of 1.6 and ischemic cerebrovascular disease was increased by a factor of 1.3. The four CRP polymorphisms resulted in an increase in CRP levels of up to 64%. Theoretically, this would predict an increased risk of 32% for ischemic heart disease and 25% for ischemic cerebrovascular disease. However, no genotype combination was associated with an increased risk of either ischemic cerebrovascular or ischemic cardiac disease. Apolipoprotein E genotypes were associated with an increased risk of ischemic heart disease and elevated cholesterol levels. Comment: Drugs are being developed to specifically target lowering CRP levels (Curr Atheroscler Rep 2006;8:421-8). The ultimate goal would be to lower CRP levels and, if CRP is associated with causing atherosclerosis, ultimately prevent the development of vascular disease. This study suggests that such a strategy is likely to be “barking up the wrong tree.” Although epidemiologic studies have observed an increased risk of ischemic vascular disease associated with higher plasma CRP levels, the current data indicate that increased CRP levels are perhaps more a marker for atherosclerosis than a cause of atherosclerosis. Please see also the abstract for a related article (N Engl J Med 2008;359:2195-207).

The association of endothelial nitric oxide synthase G894T polymorphism with C-reactive protein level and metabolic syndrome in a Chinese study group

Some studies have reported a possible relationship between endothelial nitric oxide synthase (eNOS) and metabolic syndrome (MS), which is associated with an increased risk for cardiovascular disease. A recent meta-analysis study found the eNOS G894T polymorphism to be associated with ischemic heart disease. Here, we examine the association of eNOS G894T polymorphism with MS in a Chinese population (n = 397). The eNOS T+ (TT and GT) genotypes (56.92% vs 38.86%; odds ratio, 2.08; 95% confidence interval, 1.21-3.56; P = .007) and T allele (33.08% vs 23.34%; odds ratio, 1.62; 95% confidence interval, 1.08-2.44; P = .019) were significantly more frequent in subjects who had MS. Furthermore, subjects with eNOS T+ genotypes had significantly higher plasma C-reactive protein levels as compared with GG subjects ( P = .004). This study shows that, in a Chinese population, eNOS G894T polymorphism is associated with an elevated C-reactive protein level and MS.

Contribution of the Lean Body Mass to Insulin Resistance in Postmenopausal Women With Visceral Obesity: A Monet Study

Some insulin-resistant obese postmenopausal (PM) women are characterized by an android body fat distribution type and higher levels of lean body mass (LBM) compared to insulin-sensitive obese PM women. This study investigates the independent contribution of LBM to the detrimental effect of visceral fat (VF) levels on the metabolic profile. One hundred and three PM women (age: 58.0+/-4.9 years) were studied and categorized in four groups on the basis of their VF (higher vs. lower) and lean BMI (LBMI=LBM (kg)/height (m2); higher vs. lower). Measures included: fasting lipids, glucose homeostasis (by euglycemic/hyperinsulinemic clamp technique and 2-h oral glucose tolerance test (OGTT)), C-reactive protein (CRP) levels, fat distribution (by computed tomography (CT) scan), and body composition (by dual-energy X-ray absorptiometry). Women in the higher VF/higher LBMI group had lower glucose disposal and higher plasma insulin levels compared to the other groups. They also had higher plasma CRP levels than the women in the lower VF/lower LBMI group. VF was independently associated with insulin levels, measures of glucose disposal, and CRP levels (P<0.05). LBMI was also independently associated with insulin levels, glucose disposal, and CRP levels (P<0.05). Finally, significant interactions were observed between LBMI and VF levels for insulin levels during the OGTT and measures of glucose disposal (P<0.05). In conclusion, VF and LBMI are both independently associated with alterations in glucose homeostasis and CRP levels. The contribution of VF to insulin resistance seems to be exacerbated by increased LBM in PM women.

The TNF-α G-308A polymorphism is associated with C-reactive protein levels: The HERITAGE Family Study

Objective Pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), stimulate the release of C-reactive protein (CRP). We investigated the association between the TNF-α G-308A polymorphism and plasma CRP levels. Methods Subjects were 456 White (225 men, 231 women) and 232 Black (83 men, 149 women) healthy adults who underwent a 20-week standardized exercise program in the HERITAGE Family Study. The TNF-α gene promoter polymorphism was determined using PCR amplification followed by NcoI digestion. Plasma CRP was measured using a high-sensitivity assay. Results Genotype frequencies were in Hardy–Weinberg equilibrium. After adjustment for age, smoking, alcohol consumption, maximal oxygen uptake and, in women, hormone use, the AA homozygotes for the G-308A polymorphism had higher baseline CRP levels than other genotypes in White and Black men ( P < 0.001 and P = 0.044, respectively) and in Black women ( P = 0.032). Body mass index partly explained these associations in Blacks. The exercise program results provided further evidence for an association with the polymorphism. Among those with high CRP at baseline (≥ 3.0 mg/L), regular exercise decreased CRP less in AA homozygotes than in other genotypes ( P = 0.043). Conclusion The AA genotype of the TNF-α G-308A polymorphism is associated with higher plasma CRP levels and less favorable CRP response to regular exercise.

Defining the Proinflammatory Phenotype Using High Sensitive C-Reactive Protein Levels as the Biomarker

Inflammation is pivotal in atherosclerosis. The prototypic marker of inflammation is C-reactive protein (CRP). Numerous studies have confirmed that high CRP levels in normal volunteers predict cardiovascular events. The objective of this study was to define proximal and associated abnormalities of the proinflammatory phenotype using CRP levels as the biomarker. Two groups of normal, healthy subjects, selected by stringent criteria from an initial cohort of 252, were studied over the period of 12 months. Group 1 included subjects with consistently low CRP (<0.004 microM or <0.5 mg/liter; low CRP group; n = 15). Group 2 included subjects with consistently high CRP (>2.0 or >0.016 microM to <10 mg/liter or <0.085 microM; high CRP group; n = 13). Fasting blood (50 ml) was obtained, and the following parameters were assayed: high sensitivity CRP, fibrinogen, lipid profile, insulin, whole blood cytokines after stimulation with lipopolysaccharide (LPS; 100 ng/ml for 24 h), soluble cell adhesion molecules, plasminogen activator inhibitor-1, CD40, CD40 ligand, leptin, adiponectin, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-3 (MMP-3), and MMP-9. Genomic DNA was obtained from peripheral blood leukocytes, and the TNF-alpha -308 genotype was determined. The median CRP levels were 0.0018 microM (0.21 mg/liter) and 0.031 microM (3.7 mg/liter) for the low and high groups, respectively. High CRP subjects were older and had significantly higher body mass indexes, triglycerides, insulin, homeostasis model assessment, and leptin levels compared with low CRP subjects. The markers of inflammation, plasminogen activator inhibitor-1, MMP-9, fibrinogen, and vascular cell adhesion molecule-1 levels were significantly higher in the high compared with the low CRP group. LPS-stimulated levels of whole blood IL-1beta, IL-6, and TNF were significantly higher, and IL-4 levels were significantly lower in the high CRP group. After age- and body mass index-adjusted analysis of covariance, only plasma MMP-9 levels and LPS-stimulated whole blood IL-1beta and TNF levels were significantly higher in the high CRP group. The frequency of the rare A allele at TNF-alpha -308 was equivalent in high and low CRP groups. A phenotype characterized by increased plasma inflammatory mediators as well as increased LPS-stimulated whole blood TNF-alpha and IL-1beta levels is associated with high plasma CRP levels. This systemic inflammatory phenotype may contribute to vascular inflammation or may reflect inflammation in vessels or at other sites.

Serologic markers of persistent chlamydia pneumonia infection and long-term prognosis after successful coronary stenting

Background Previous studies have shown an incremental role of inflammation in late prognosis following coronary stenting (CS). In particular, high preprocedural levels of plasma C-reactive protein (CRP) have been related to increased hazard of late ischemic complications. Persistent Chlamydia pneumoniae (Cp) infection, detected by positive IgA anti-Cp titers, may be associated with this inflammatory process and portend a high risk of late adverse prognosis after CS. Methods A total of 483 consecutive patients with either stable or unstable coronary syndromes were followed-up for 1 year after successful CS. The composite of cardiac death, myocardial infarction, rehospitalization for rest-unstable angina, and exertional angina, whichever occurred first, was the clinical end point. Additionally, the rate of in-stent restenosis and progression of coronary artery disease during this period were evaluated. Anti-Cp titers and plasma CRP levels were measured before the procedure. Results Positive immunoglobulin A (IgA), but not positive immunoglobulin G (IgG), titers were significantly associated with high plasma CRP levels in patients with unstable coronary syndromes ( P = .005), but not in those with stable angina ( P = .7). Moreover, positive IgA titers were significantly related to increased risk of both the composite clinical end point ( P = .04) and progression of coronary artery disease ( P < .001) in patients with unstable coronary syndromes but not in those with stable angina. Neither positive IgA nor positive IgG titers were associated with the rate of in-stent restenosis. Conclusions Persistent Cp infection may drive an inflammatory response in the coronary vasculature and portends an adverse late outcome after CS in patients with unstable coronary syndromes.

C-reactive protein predicts the deterioration of glycemia in chinese subjects with impaired glucose tolerance.

Recent studies have shown that C-reactive protein (CRP) predicts future risk of diabetes in healthy Caucasians. We determined whether plasma CRP level was elevated in Chinese subjects with impaired glucose tolerance (IGT) and whether CRP level could be used to predict progression to type 2 diabetes or reversion to normal glucose tolerance (NGT) in these high-risk individuals. A total of 228 subjects with IGT at baseline from the Hong Kong Cardiovascular Risk Factors Prevalence Study underwent repeat oral glucose tolerance testing after 2 years. Plasma high-sensitivity CRP was measured from their stored baseline samples and from 228 subjects with NGT matched for age and BMI by an immunoturbidimetric assay. Subjects with IGT at baseline had higher plasma CRP levels than subjects with NGT: 1.18 mg/l (0.52-2.52) vs. 0.87 mg/l (0.37-1.84), median (interquartile range), P = 0.01. At 2 years, 117 subjects with IGT reverted to NGT, 84 remained in IGT, and 21 progressed to diabetes. Individuals who progressed to diabetes had the highest plasma CRP levels at baseline (P < 0.0001). Those with baseline CRP levels in the third and top quartile had a relative risk of remaining in IGT or progressing to diabetes of 2.87 (95% CI 1.06-7.82) and 2.76 (1.06-7.31), respectively, after adjusting for anthropometric measure and lifestyle factors. CRP independently predicts the risk of remaining in IGT or progressing to diabetes in Chinese subjects with IGT. CRP might provide an adjunctive measure for identifying subjects with the highest risk of progression to diabetes who would derive the greatest benefits from preventive interventions.

Plasma C-reactive protein concentrations in relation to 5-year body weight change among children: the Taipei Children Heart Study.

C-reactive protein (CRP), a nonspecific inflammatory marker, may be associated with the development of cardiovascular disease (CVD) among adults. The purpose of this study is to evaluate the relation between plasma CRP levels and 5-y body weight and body mass index (BMI) change among school children in Taiwan. In 1995, we conducted an epidemiological survey to evaluate the anthropometric characteristics and CVD risk factors among 1500, aged 12-15 y, school children in Taipei. We measured plasma high sensitivity CRP levels using nephelometric method. In 2000, we followed these children to evaluate their changes in body height, weight and BMI during 5 y. In general, boys were taller, heavier and had higher BMI than girls at the baseline (1995) and at the 5-y follow-up (2000). Baseline plasma CRP levels were positively correlated with body weight and BMI in both 1995 and 2000. However, plasma CRP levels were negatively correlated with 5-y BMI change in both genders. We further divided the children into three subgroups based on their baseline CRP levels (nondetected, 0.188-1.00 and >1.0 mg/dl). Children in the higher plasma CRP levels (>1.0 mg/dl) were heavier and had higher BMI (both in 1995 and 2000) than those children with nondetected CRP levels. However, children with higher CRP subgroup had a lower 5-y increasing of BMI and there was even a decrease of BMI levels among the higher CRP girls. From this prospective study, we found that baseline plasma CRP levels were positively correlated with the baseline and the 5-y follow-up body weight and BMI in both genders. However, plasma CRP levels may not be a good predictor of 5-y body weight and BMI changes among children in Taiwan.

Effect of Plasma C-Reactive Protein Levels in Modulating the Risk of Coronary Heart Disease AssociatedWith Small, Dense, Low-Density Lipoproteins in Men(The Quebec Cardiovascular Study)

This purpose of this study was to investigate how plasma C-reactive protein (CRP), a nonspecific acute-phase reactant, modulates the risk of coronary heart disease (CHD) associated with the small, dense, low-density lipoprotein (LDL) phenotype. LDL particle size and plasma CRP were measured in the Quebec Cardiovascular Study cohort of 2,025 men free of CHD at baseline, among whom 103 had a first CHD event during a 5-year follow-up period. Plasma CRP levels were measured using the Behring Latex-Enhanced (highly sensitive) CRP assay. LDL particle size phenotype was characterized using 2% to 16% polyacrylamide gradient gel electrophoresis. There were weak but significant associations between plasma CRP levels and features of LDL size, such as the proportion of LDL with a diameter <255 Å (r = 0.09, p <0.001) and LDL peak particle size (r = −0.09, p <0.001). Variations in plasma CRP levels modulated the risk of CHD associated with small LDL peak particle size (relative risk 4.3 vs 2.5 in men with high vs low plasma CRP levels, respectively) and with an elevated proportion of LDL <255 Å (relative risk 6.6 vs 3.0). Thus, increased plasma CRP levels further elevate the risk of CHD associated with having small, dense LDL particles.

C-reactive protein and rapidly progressive coronary artery disease--is there any relation?

High plasma C-reactive protein (CRP) levels have been associated with an unfavorable outcome in patients with coronary artery disease (CAD), and a direct participation of CRP in the atherosclerotic process has been postulated. The aim of this study was to evaluate the possible relationship of high plasma CRP levels with the rapid progression of coronary atherosclerosis (RPCAD). In all, 194 patients who were readmitted and underwent repeat coronary angiography because of recurrence of symptoms following successful percutaneous coronary intervention were studied. Median angiographic follow-up time was 6 months. Rapid progression CAD was defined as the presence of a new lesion, > 25% in luminal diameter stenosis, in a previously nondiseased vessel, or deterioration of a known, nontreated lesion by at least 25%. By multivariate analysis, patients with high plasma CRP levels upon first admission were at higher risk of RPCAD. In particular, odds ration (OR) = 1.8; 95% confidence interval (CI) = 1.3-3.6; p value = 0.02 in patients with CRP = 0.5-2 mg/dl versus patients with CRP < 0.5 mg/dl, and OR = 7.1; 95% CI = 3.8-9.5; p value < 0.001 in patients with CRP > 2 mg/dl versus patients with CRP < 0.5 mg/dl. Increased plasma CRP levels could possibly identify patients at high risk for the development of RPCAD.

IGF-I, IGF-I-binding proteins and GH-binding protein in malnourished elderly patients with inflammation receiving refeeding therapy.

To investigate the mechanisms determining the success or failure of refeeding therapy in malnourished elderly patients with inflammation by studying changes in plasma IGF-I, GH-binding protein (GHBP) and IGF-binding protein (IGFBP) levels and IGFBP-3 proteolysis. We studied 15 severely malnourished hospitalized elderly patients. Weight, food intake, plasma albumin, transthyretin, C-reactive protein (CRP), orosomucoid, interleukin-6 (IL-6), IGF-I, intact and proteolytically degraded IGFBP-3 and GHBP levels were determined on admission and during refeeding therapy designed to increase food intake to 40 kcal/kg body weight per day (15% protein). Plasma IGF-I, IGFBP-3 and GHBP levels were significantly low for age on admission in all malnourished elderly patients. They increased in nine patients as nutritional status improved (albuminemia >30 g/l; transthyretinemia >200 mg/l or weight gain >5% of initial body weight) and levels of inflammation markers decreased (group 1). In contrast, plasma IGF-I, IGFBP-3 and GHBP levels remained low in six patients in whom nutritional status failed to improve and levels of inflammation markers increased (group 2). IGF-I showed greater variations than IGFBP-3 or GHBP with respect to nutritional status. High plasma CRP and IL-6 levels were associated with high levels of IGFBP-3 proteolysis. Efficient refeeding therapy was associated with a significant increase in IGF-I plasma levels. In patients with severe and persistent inflammation, high levels of proteolysis of IGFBP-3 may have contributed to the low plasma IGF-I levels, persistence of hypercatabolism and lack of improvement in nutritional status.