Showing papers on "C-reactive protein published in 1998"
TL;DR: Evidence of inflammation after MI is associated with increased risk of recurrent coronary events, and therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent.
Abstract: Background —We studied whether inflammation after myocardial infarction (MI) is a risk factor for recurrent coronary events and whether randomized treatment with pravastatin reduces that risk. Methods and Results —A nested case-control design was used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood samples from 391 participants in the Cholesterol and Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal coronary event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (control subjects). Overall, CRP and SAA were higher among cases than control subjects (for CRP P =0.05; for SAA P =0.006) such that those with levels in the highest quintile had a relative risk (RR) of recurrent events 75% higher than those with levels in the lowest quintile (for CRP RR=1.77, P =0.02; for SAA RR=1.74, P =0.02). The study group with the highest risk was that with consistent evidence of inflammation (elevation of both CRP and SAA) who were randomly assigned to placebo (RR=2.81, P =0.007); this risk estimate was greater than the product of the individual risks associated with inflammation or placebo assignment alone. In stratified analyses, the association between inflammation and risk was significant among those randomized to placebo (RR=2.11, P =0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P =0.5). Conclusions —Evidence of inflammation after MI is associated with increased risk of recurrent coronary events. Therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent.
1,450 citations
TL;DR: It is indicated that among apparently healthy men, baseline levels of CRP predict future risk of developing symptomatic PAD and thus provide further support for the hypothesis that chronic inflammation is important in the pathogenesis of atherothrombosis.
Abstract: Background—Among apparently healthy men, elevated levels of C-reactive protein (CRP), a marker for systemic inflammation, predict risk of myocardial infarction and thromboembolic stroke. Whether increased levels of CRP are also associated with the development of symptomatic peripheral arterial disease (PAD) is unknown. Methods and Results—Using a prospective, nested, case-control design, we measured baseline levels of CRP in 144 apparently healthy men participating in the Physicians’ Health Study who subsequently developed symptomatic PAD (intermittent claudication or need for revascularization) and in an equal number of control subjects matched on the basis of age and smoking habit who remained free of vascular disease during a follow-up period of 60 months. Median CRP levels at baseline were significantly higher among those who subsequently developed PAD (1.34 versus 0.99 mg/L; P=.04). Furthermore, the risks of developing PAD increased significantly with each increasing quartile of baseline CRP concentr...
983 citations
TL;DR: Enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial, and improves disease severity and clinical outcome despite unchanged pancreatic injury on CT scan.
Abstract: Background—In patients with major trauma and burns, total enteral nutrition (TEN) significantly decreases the acute phase response and incidence of septic complications when compared with total parenteral nutrition (TPN).Poor outcome in acute pancreatitis is associated with a high incidence of systemic inflammatory response syndrome (SIRS) and sepsis. Aims—To determine whether TEN can attenuate the acute phase response and improve clinical disease severity in patients with acute pancreatitis. Methods—Glasgow score, Apache II, computed tomography (CT) scan score, C reactive protein (CRP), serum IgM antiendotoxin antibodies (EndoCAb), and total antioxidant capacity (TAC) were determined on admission in 34 patients with acute pancreatitis. Patients were stratified according to disease severity and randomised to receive either TPN or TEN for seven days and then re-evaluated. Results—SIRS, sepsis, organ failure, and ITU stay, were globally improved in the enterally fed patients. The acute phase response and disease severity scores were significantly improved following enteral nutrition (CRP: 156 (117‐222) to 84 (50‐ 141), p<0.005; APACHE II scores 8 (6‐10) to 6 (4‐8), p<0.0001) without change in the CT scan scores. In parenterally fed patients these parameters did not change but there was an increase in EndoCAb antibody levels and a fall in TAC.Enterally fed patients showed no change in the level of EndoCAb antibodies and an increase in TAC. Conclusion—TEN moderates the acute phase response, and improves disease severity and clinical outcome despite unchanged pancreatic injury on CT scan. Reduced systemic exposure to endotoxin and reduced oxidant stress also occurred in the TEN group. Enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial. (Gut 1998;42:431‐435)
627 citations
TL;DR: The data suggest that CRP may promote atherosclerotic lesion formation by activating the complement system and being involved in foam cell formation as well as in the deep fibroelastic layer and in the fibromuscular layer of the intima adjacent to the media.
Abstract: There is increasing evidence that complement activation may play a role in atherogenesis. Complement proteins have been demonstrated to be present in early atherosclerotic lesions of animals and humans, and cholesterol-induced atherosclerotic lesion formation is reduced in complement-deficient animals. Potential complement activators in atherosclerotic lesions are now a subject matter of debate. C-reactive protein (CRP) is an acute-phase protein that is involved in inflammatory processes in numerous ways. It binds to lipoproteins and activates the complement system via the classic pathway. In this study we have investigated early atherosclerotic lesions of human coronary arteries by means of immunohistochemical staining. We demonstrate here that CRP deposits in the arterial wall in early atherosclerotic lesions with 2 predominant manifestations. First, there is a diffuse rather than a focal deposition in the deep fibroelastic layer and in the fibromuscular layer of the intima adjacent to the media. In this location, CRP frequently colocalizes with the terminal complement complex. Second, the majority of foam cells below the endothelium show positive staining for CRP. In this location, no colocalization with the terminal complement proteins can be observed. Our data suggest that CRP may promote atherosclerotic lesion formation by activating the complement system and being involved in foam cell formation.
568 citations
TL;DR: The data suggest that dysregulation of some inflammatory cytokines occurs with age, but the role of inflammation in aging remains unclear.
Abstract: Objective. To determine the association among aging, inflammation, and cytokine production by peripheral blood mononuclear cells. Population and Methods. We examined production of interleukin-1 (J (IL-1 (J), tumor necrosis factor-a (TNF-a), IL1 receptor antagonist (IL-IRa), and IL-6 in 711 elderly participants in the Framingham Heart Study (mean age, 79 y) and 21 young healthy volunteers (mean age, 39 y). The elderly subjects were categorized by serum C-reactive protein (CRP) concentration, a marker of systemic inflammation. Results. Production of IL-6 (p < .00001) and IL-IRa {p < .00001) was higher in the elderly subjects than in the control group. IL-6 production increased with increasing CRP, whereas IL-IRA was uniformly elevated in elderly subjects regardless of CRP. However, we found no difference in the production of IL-1 fj or TNF-a between the young and elderly groups, regardless of CRP status. IL-6 population correlated with IL-1 (3 {r = .36, p < .0001) and TNF-a production (r = .25, p < .0001), but IL-1 Ra production did not. Conclusion. Production of IL-6 and IL-IRa — but not IL-1 (} or TNF-a — was increased in the elderly compared to healthy, young subjects. The increase in IL-6 also correlated with increased production of CRP, a marker of inflammation. However, IL-IRa was increased in the elderly independently of CRP production. Although limited by the small control group, these data suggest that dysregulation of some inflammatory cytokines occurs with age, but the role of inflammation in aging remains unclear.
398 citations
TL;DR: Low-grade infections may be one of the causes of the inflammatory reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein, and warrant further studies in this field.
Abstract: An increasing body of evidence has linked infections to atherosclerosis and thrombosis. Herpesviruses cause atherosclerosis in experimental animals. Herpesviruses can also be detected in atherosclerotic lesions in humans. Cytomegalovirus may play a role in arteriosclerosis in transplanted hearts, and this virus, together with tumor suppressor protein p53, can be found in restenosis lesions following angioplasty. Chlamydia pneumoniae and dental infections are associated with coronary heart disease in cross-sectional and longitudinal studies, and preceding respiratory infections are associated with ischemic stroke. Infections may favor formation of atherosclerosis and thrombosis by elevation of blood levels of fibrinogen, leukocytes, clotting factor, and cytokines and by alteration of the metabolism and functions of endothelial cells and monocyte macrophages. Low-grade infections may also be one of the causes of the inflammatory reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein. These observations warrant further studies in this field.
289 citations
TL;DR: Plasma levels of C-reactive protein were measured 72 hours after successful coronary artery stenting in 76 patients with stable angina pectoris and at 12-month follow-up, the cumulative event rate was higher in patients with abnormal levels ofC-re active protein than that observed in patients who were event free.
Abstract: Plasma levels of C-reactive protein were measured 72 hours after successful coronary artery stenting in 76 patients with stable angina pectoris. At 12-month follow-up, the cumulative event rate was higher in patients with abnormal levels of C-reactive protein than that observed in patients with normal C-reactive protein who were event free.
209 citations
TL;DR: It is concluded that experimental Ap-infection by the aerosol route induces a typical acute phase reaction in the pig, and that pig Hp, CRP, MAP, and SAA are major acute phase reactants.
Abstract: In an experimental infection model mimicking acute Actinobacillus pleuropneumoniae (Ap) infection in swine (Sus scrofa) by aerosol inoculation, the development of a number of typical clinical signs was accompanied by a prototypic acute phase reaction encompassing fever and an acute phase protein response peaking at around 2 days after infection. Haptoglobin, C-reactive protein (CRP), and major acute phase protein (MAP) responded with large increases in serum levels, preceding the development of specific antibodies by 4–5 days. Serum amyloid A protein (SAA) was also strongly induced. The increase, kinetics of induction and normalization were different between these proteins. It is concluded that experimental Ap-infection by the aerosol route induces a typical acute phase reaction in the pig, and that pig Hp, CRP, MAP, and SAA are major acute phase reactants. These findings indicate the possibility of using one or more of these reactants for the nonspecific surveillance of pig health status.
199 citations
TL;DR: TEN moderates the acute phase response, and improves disease severity and clinical outcome despite unchanged pancreatic injury on CT scan, and is clinically beneficial in enterally fed patients.
Abstract: Background—In patients with major trauma and burns, total enteral nutrition (TEN) significantly decreases the acute phase response and incidence of septic complications when compared with total parenteral nutrition (TPN).Poor outcome in acute pancreatitis is associated with a high incidence of systemic inflammatory response syndrome (SIRS) and sepsis. Aims—To determine whether TEN can attenuate the acute phase response and improve clinical disease severity in patients with acute pancreatitis. Methods—Glasgow score, Apache II, computed tomography (CT) scan score, C reactive protein (CRP), serum IgM antiendotoxin antibodies (EndoCAb), and total antioxidant capacity (TAC) were determined on admission in 34 patients with acute pancreatitis. Patients were stratified according to disease severity and randomised to receive either TPN or TEN for seven days and then re-evaluated. Results—SIRS, sepsis, organ failure, and ITU stay, were globally improved in the enterally fed patients. The acute phase response and disease severity scores were significantly improved following enteral nutrition (CRP: 156 (117‐222) to 84 (50‐ 141), p<0.005; APACHE II scores 8 (6‐10) to 6 (4‐8), p<0.0001) without change in the CT scan scores. In parenterally fed patients these parameters did not change but there was an increase in EndoCAb antibody levels and a fall in TAC.Enterally fed patients showed no change in the level of EndoCAb antibodies and an increase in TAC. Conclusion—TEN moderates the acute phase response, and improves disease severity and clinical outcome despite unchanged pancreatic injury on CT scan. Reduced systemic exposure to endotoxin and reduced oxidant stress also occurred in the TEN group. Enteral feeding modulates the inflammatory and sepsis response in acute pancreatitis and is clinically beneficial. (Gut 1998;42:431‐435)
159 citations
TL;DR: Both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome.
Abstract: This study assessed the prognostic value of cardiac troponin I (cTnI) and C-reactive protein (CRP) in unstable angina, and specifically in patients with angiographically proven coronary artery disease. These biochemical parameters, which are related to myocardial injury or to systemic inflammation, may help in short-term risk stratification of unstable angina. We prospectively studied 195 patients with unstable angina, 100 of whom had angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/ml) and CRP (N < 3 mg/L) were measured at admission, 12, and 24 hours later. The rate of in-hospital major adverse cardiac events (death, myocardial infarction, or emergency revascularization) was higher in patients with increased cTnI within the first 24 hours, regardless of the results of coronary angiography (23% vs 7%; p < 0.001). Conversely, events occurred at similar rates in patients with or without increased CRP. In patients with angiographic evidence of coronary artery disease, multivariate analysis showed that increased cTnI within 24 hours of admission (35 patients) was an independent predictor of major adverse cardiac events (odds ratio 6.7, range 1.7 to 27.3), but not cTnI levels at admission and CRP at 0, 12, and 24 hours. Thus, both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome. We also found a temporal link between cTnI increase and late elevation of CRP, suggesting that systemic inflammation may partially be a consequence of myocardial injury.
117 citations
TL;DR: Results demonstrate that part of the complement activation in patients with sepsis is independent from a direct interaction with microorganisms but rather results from an endogenous mechanism involving CRP.
Abstract: The involvement of C-reactive protein (CRP) in the activation of complement in patients with sepsis was investigated. In 104 patients with infections of varying severity, circulating levels of CRPcomplement complexes, which are specific indicators for CRP-mediated complement activation, were assessed. Complement-CRP complexes were increased in almost all patients and correlated significantly with levels of C3a (r A .59; P o .001) and C-reactive protein (r A .76; P o .001). In addition, they correlated with levels of secretory phospholipase A2 (r A .59; P o .001). Levels of complement-CRP complexes in patients with a pneumococcal type of infection were similar to those in patients with other types of infections. Complement-CRP complexes were significantly higher in patients with shock (P A .01) and in patients who died (P A .03). These results demonstrate that part of the complement activation in patients with sepsis is independent from a direct interaction with microorganisms but rather results from an endogenous mechanism involving CRP. Excessive activation of inflammatory mediators in patients protein (CRP) may be involved: First, in vitro CRP is able to activate the classical complement pathway on binding to an with sepsis may lead to life-threatening complications such as shock and multiple organ failure. One of the mediator systems appropriate ligand [6]; second, we have observed a biphasic activation of complement in a baboon model of septic shock, activated during sepsis is the complement system. Patients with sepsis have decreased plasma levels of complement proteins the later phase coinciding with increases of circulating CRP [7]; and finally, lymphocytes from patients with an IL-2 ‐ induced
Journal Article•
TL;DR: Increased serum C-reactive protein has been reported to be a marker for subclinical infection during pregnancy in various situations including premature labour and premature rupture of membranes and for complications occurring during puerperium such as thrombophlebitis, thromboembolism or endometritis.
Abstract: OBJECTIVES To record maternal serum C-reactive protein levels during normal onset of labour and normal puerperium and to evaluate if inflammation or infection could be predicted during these two periods when serum C-reactive protein is increased. METHODS Eighty-five pregnant women were enrolled in a longitudinal prospective study and had a blood sample to assess serum C-reactive protein levels on admission to the labour ward for normal onset of labour and at day three post-partum. Inclusion criteria were no previous history, a normal single pregnancy, normal vaginal delivery and an uneventful post-partum course. Twelve non-pregnant women of the same age constitued a control group. An automatic Behring Nephelometer was used to measure serum C-reactive protein concentrations. The Student's t-test (significance p < 0.05) was used for statistical analysis. FINDINGS C-reactive protein was significantly increased during the onset of labour (4.10 +/- 2.79 mg/L) and reached very high levels during the post-partum period (24.07 +/- 18.28 mg/L) compared to the standard normal serum C-reactive protein level in a population of non-pregnant women of the same age (2.39 +/- 0.07 mg/L). INTERPRETATION Increased serum C-reactive protein has been reported to be a marker for subclinical infection during pregnancy in various situations including premature labour and premature rupture of membranes and for complications occurring during puerperium such as thrombophlebitis, thromboembolism or endometritis. This interpretation depends on which upper limit is considered as abnormal. Because serum C-reactive protein was raised during the onset of labour, values of less than 10 mg/L could not be considered as a marker for infection during this period. Elevated serum concentrations of estrogen, progestogen and prostaglandins during labour might be one explanation for those physiological changes. Normal vaginal delivery could be compared to a surgical procedure and tissue injury consecutive to vaginal birth as reflected by a dramatic increase in C-reactive protein. More studies using nephelometry are needed to determine normal and upper values of C-reactive protein during pregnancy.
TL;DR: It is suggested that albumin, cholesterol, prealbumin, and transferrin be used with caution when assessing the nutritional status of older hospitalized patients, and soluble IL-2 receptor levels might be used to correct for the impact of inflammation on these markers of malnutrition.
Abstract: BACKGROUND Many researchers have speculated that markers of malnutrition such as albumin, prealbumin, cholesterol, and transferrin are influenced by inflammation. The mechanism of this interaction has not been well understood. METHODS This was a prospective cross-sectional study. We evaluated 72 male patients older than 60 years admitted to a geriatric rehabilitation unit. Subjects with severe hepatic or renal diseases were excluded. We measured body mass index, caloric intake, serum albumin, prealbumin, cholesterol, transferrin, hemoglobin, and total lymphocyte count. To detect inflammation, we measured C-reactive protein, Westergren sedimentation rate, fibrinogen, and cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, IL-2, and the soluble IL-2 receptor. RESULTS Soluble IL-2 receptor was negatively associated with albumin (r = -.479, p < .0001), prealbumin (r = -.520, p = < .0001), cholesterol (r = -.487, p = .0001), transferrin (r = -.455, p = .0002), and hemoglobin (r = -.371, p = .002). TNF-alpha, IL-1 beta, IL-6, and IL-2 were not associated with these measures. CONCLUSIONS Inflammation increases the incidence of hypoalbuminemia and hypocholesterolemia, potentially leading to overdiagnosis of malnutrition. We suggest that albumin, cholesterol, prealbumin, and transferrin be used with caution when assessing the nutritional status of older hospitalized patients. In the future, soluble IL-2 receptor levels might be used to correct for the impact of inflammation on these markers of malnutrition.
Journal Article•
TL;DR: The results show that plasma endothelin-1 levels increase in chronic inflammatory bowel disease and mainly in Crohn's disease, leading us on to believe that endotheli-1 has a important role in inflammatory bowel Disease.
Abstract: AIM The purpose of this study was to investigate the behavior of circulating endothelin-1, a vasoconstrictor and mitogenic peptide, in patients with inflammatory bowel disease. PATIENTS We investigated plasma endothelin-1 levels in 29 patients with Crohn's disease, 13 with ulcerative colitis and 26 healthy subjects as controls. METHODS Erythrocyte sedimentation and C-reactive protein were also measured in all patients. Plasma endothelin-1 was measured by specific radioimmunoassay and expressed as pg/ml. RESULTS Both Crohn's disease and ulcerative colitis patients showed a significant increase in plasma endothelin-1 concentration (22.3 +/- 8.2 pg/ml and 11.2 +/- 2.7 pg/ml, respectively) when compared to healthy subjects (6.2 +/- 1.5 pg/ml). Moreover, plasma endothelin-1 levels were significantly higher in Crohn's disease patients than those in ulcerative colitis patients (22.3 +/- 8.2 pg/ml vs 11.2 +/- 2.7 pg/ml; p < 0.001, respectively). A weak correlation (r = 0.645; p < 0.013) between erythrocyte sedimentation and endothelin-1 levels was observed in Crohn's disease patients. Age, sex, clinical activity of the disease, duration of history, anatomical localization of disease and therapy had no influence on plasma endothelin-1 levels. CONCLUSION Our results show that plasma endothelin-1 levels increase in chronic inflammatory bowel disease and mainly in Crohn's disease. This observation leads us on to believe that endothelin-1 has a important role in inflammatory bowel disease.
Journal Article•
TL;DR: Serum determination of interleukin-6 in the first 24 hours of the disease is a better marker of the severity of acute biliary pancreatitis than C-reactive protein.
Abstract: BACKGROUND: Data concerning the interleukin 6 pattern in acute biliary pancreatitis are lacking. AIM: To define the best cut-off point of this molecule in differentiating the severe form of acute biliary pancreatitis from the mild form and to evaluate its sensitivity, specificity and diagnostic accuracy in the prognosis of acute biliary pancreatitis in comparison with those of serum C-reactive protein. PATIENTS: Forty-four patients with acute biliary pancreatitis: 27 patients with mild pancreatitis and 17 with the severe form of the disease. METHODS: Serum interleukin-6 and C-reactive protein concentrations were assessed in all patients on admission and for the following 5 days. RESULTS: Serum interleukin-6 levels were significantly higher (p < 0.02) in patients with severe acute biliary pancreatitis than in those with the mild form of the disease. No significant difference in serum C-reactive protein levels was found in the first 2 days in patients with mild biliary pancreatitis when compared to those with the severe form of the disease. Using a cut-off point of 2.7 pg/ml for serum interleukin-6 and 11 mg/dl for serum C-reactive protein, the sensitivity of the two molecules in assessing the severity of acute pancreatitis on the first day of the study was 87.5% for interleukin-6 and 6.3% for C-reactive protein, the specificity, 83.3% for interleukin-6 and 91.7% for C-reactive protein, and the accuracy 85.0% for interleukin-6 and 57.5% for C-reactive protein. CONCLUSIONS: Serum determination of interleukin-6 in the first 24 hours of the disease is a better marker of the severity of acute biliary pancreatitis than C-reactive protein.
TL;DR: A defined rise in C-reactive protein serum levels can predict sepsis sooner in burned children, and this level can be predicted 82% of the time.
Abstract: C-Reactive protein serum levels were measured in 57 pediatric patients with 3% to 92% total body surface area burns to determine whether a defined rise in C-reactive protein serum levels could indicate sepsis earlier in burn patients. A rise in C-reactive protein serum levels was defined as an increase of at least 3 mg/dL for 2 days or 10 mg for 1 day. Increases the first 2 days after the burn or the day after surgery were excluded, since these injuries increase C-reactive protein serum levels. Patients were defined as septic when they were on systemic antibiotics and exhibited at least two of 16 specific clinical parameters. C-Reactive protein serum levels correctly predicted sepsis 82% of the time (efficiency = 82%). Nonseptic patients generally did not show increased C-reactive protein serum levels (specificity = 69%). When sepsis did occur, it always was preceded by increased C-reactive protein (sensitivity = 100%), and the increased C-reactive protein occurred 2.3 ± 0.5 days before the patient was deemed septic clinically. Hence, a defined rise in C-reactive protein serum levels can predict sepsis sooner in burned children.
TL;DR: In SLE, serum and urinary nitrate levels do not parallel lupus activity, and other variables, related or not to Sle, seem to affect these levels.
Abstract: SUMMARY Objective. To study prospectively whether serum and urinary nitrate levels are related to lupus activity. Methods. Fifty patients with systemic lupus erythematosus (SLE ) were studied prospectively for 2 yr. Every 4 months, the SLE Disease Activity Index (SLEDAI ) was administered to the patients, and blood and 24 h urine samples were obtained; 88 healthy controls were also studied. Nitrate levels were measured by the Greiss method. Statistical analyses were performed using standard parametric and non-parametric tests, and analysis of serial measurements. Results. Twelve patients suVered infections, 12 active nephritis and 17 episodes of non-renal activity. By analysis of serial measurements, serum and urinary nitrate levels did not correlate with SLEDAI. C-Reactive protein (CRP) levels, presence of infection and creatinine clearance weakly influenced nitrate levels. Conclusions. In SLE, serum and urinary nitrate levels do not parallel lupus activity. Other variables, related or not to SLE, seem to aVect these levels. Nitric oxide (NO) is a biological messenger that when indicated by their clinical condition. At each visit, clinical evaluation was peformed. Special attenregulates physiological functions and participates in pathological processes. NO is synthesized from l- tion was paid to disease activity, selected organ involvement, presence of infection, and therapy. The SLE arginine, by constitutive NO synthases (cNOS) and inducible NO synthases (iNOS ), and is readily trans- Disease Activity Index (SLEDAI ) [15] was administered by the same investigator (MRG-C ) to all formed into nitrite and nitrate which are excreted into the urine. cNOS produce small amounts of NO which patients. When indicated, additional laboratory and radiological tests were carried out. The number of regulate blood vessel tone, platelet aggregation and neurotransmission. iNOS are stimulated by endotoxins accumulated ARA criteria, delay from diagnosis to study, tobacco use, history of hypertension and previ
TL;DR: SLE patients with increased systemic inflammation had an activated HANS axis which can be measured by a parasympathetic pupillary reflex test, and patients with latency time hyperreflexia had more severe systemic inflammation.
Abstract: In chronic inflammatory diseases, cytokines stimulate the hypothalamus pituitary adrenal axis and the hypothalamus autonomic nervous system (HANS) axis. The present study was performed to find autonomic nervous function parameters in patients with systemic lupus erythematosus (SLE) which are suitable to demonstrate the activation of the HANS axis during systemic inflammation. Thirty-four patients with SLE (age 35.3 +/- 1.9 yr) were investigated by seven standardized autonomic nervous function tests. The SLEDAI and laboratory parameters of systemic inflammation were assessed by standard techniques. Pupillary latency time hyperreflexia was found in 29.4%, whereas maximal pupillary area was hyperresponsive in only 2.9%. A total of 12% had overall cardiovascular autonomic nervous hyperreflexia. Patients with latency time hyperreflexia had more severe systemic inflammation [erythrocyte sedimentation rate (ESR): P < 0.001; C-reactive protein (CRP): P = 0.0094; fibrinogen: P < 0.001; albumin: P = 0.003; antinuclear antibodies: P = 0.020]. The longitudinal study of 13 patients during 4 yr demonstrated a parallel increase and decrease in latency time percentile and ESR. SLE patients with increased systemic inflammation had an activated HANS axis which can be measured by a parasympathetic pupillary reflex test.
TL;DR: It is reported that an increase in circulating C reactive protein concentrations is associated with increased recurrence of tumour in patients who have undergone curative surgery for colorectal cancer and there is also evidence that an increased C reactiveprotein concentration is an independent predictive factor of survival in patients with gastrointestinal cancer.
Abstract: Measuring C reactive protein concentrations may be more useful
EDITOR—Nielsen et al reported an association between circulating concentrations of plasminogen activator inhibitor-1 and survival in patients with colorectal cancer.1 They suggest that this reflects the specific role of plasminogen activator inhibitor-1 in tumour progression.
It has been known for some time that disease progression in colorectal cancer is associated with an increase in the acute phase response as evidenced by the prototypical acute phase protein (C reactive protein).2 We have reported that an increase in circulating C reactive protein concentrations is associated with increased recurrence of tumour in patients who have undergone curative surgery for colorectal cancer.3 There is also evidence that an increased C reactive protein concentration is an independent predictive factor of survival in patients with gastrointestinal cancer.4 Therefore the association between increased plasminogen …
TL;DR: Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis compared with Crohn’s disease and healthy donors and its sensitivity and specificity to discriminate ulceratives colitis from Crohn's disease was 75% and 71%, respectively.
Abstract: Background—Increased expression of CD44v6 on colonic crypt epithelial cells in ulcerative colitis has been suggested as a diagnostic tool to distinguish ulcerative colitis from colonic Crohn's disease.
Aims—To investigate colonic CD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6) in patients with ulcerative colitis and Crohn's disease.
Methods—Colonic biopsy samples were obtained from 16 patients with ulcerative colitis, 13 with ileocolonic Crohn's disease, and 10 undergoing polypectomy. Serum samples were obtained from 15 patients with active ulcerative colitis, 20 with active Crohn's disease, and 20 healthy donors. Colonic CD44v6 expression was evaluated immunohistochemically by monoclonal antibody 2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6 concentrations were measured by ELISA.
Results—2F10 stained colonic epithelium of inflamed ulcerative colitis and Crohn's disease samples in 80% and 40% of cases, respectively, and VFF18 in 95% and 87%, respectively. Both monoclonal antibodies displayed a sensitivity and specificity of 60% and 87% to differentiate ulcerative colitis from colonic Crohn's disease. Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis (median 153 ng/ml; interquartile range (IQR) 122-211) compared with Crohn's disease (219; IQR 180-243) and healthy donors (221; IQR 197-241 (p=0.002)). Its sensitivity and specificity to discriminate ulcerative colitis from Crohn's disease was 75% and 71%, respectively.
Conclusion—Colonic CD44v6 and serum sCD44v6 concentrations do not facilitate reliable differential diagnosis between ulcerative colitis and Crohn's disease.
Keywords: CD44 variant 6; differential diagnosis; immunohistochemistry; soluble CD44v6
Journal Article•
TL;DR: It is shown that the majority of sickle hemoglobinopathy patients have elevated sHLA-I levels during the steady state and after recent crisis, suggesting the presence of chronic inflammation during the Steady state.
Abstract: This study examined the presence of a persistent state of low-grade inflammation in sickle cell anemia patients by measuring circulating sHLA-I heterodimers and C-reactive protein during the steady state and after recent crises Thirty-nine pediatric sickle hemoglobinopathy patients were studied during the steady state and 11 patients were evaluated within 1 month of a painful crisis A disease severity score was generated for each patient, and soluble HLA-I (sHLA-I) and C-reactive protein levels were determined Soluble HLA-I was significantly elevated in 55% of the steady-state group and in 36% of the recent-crisis group The percentage of patients with elevated sHLA-I differed in the various disease subgroups in the steady state: 46% of Hb SS patients, 70% of Hb SC patients, 75% of Hb S beta-thal patients, and 20% of Hb SSF patients Steady-state and recent-crisis sHLA-I levels were not significantly different C-reactive protein levels were elevated in 11% of steady-state patients and in 9% of recent-crisis patients Soluble HLA-I levels did not correlate with C-reactive protein levels or disease severity score, age, hemoglobin, reticulocyte count, platelet count, or white cell count These results show that the majority of sickle hemoglobinopathy patients have elevated sHLA-I levels during the steady state and after recent crisis, suggesting the presence of chronic inflammation during the steady state
TL;DR: Low levels of mononuclear leukocyte-associated β-endorphin in acute myocardial infarction may be due to the release of endogenous opioid after stimulation by stress and acute-phase reactants and play a role in inflammation and pain.
Abstract: Lymphocytes can be activated to produce and release opioid peptides. We investigated the levels of immunoreactive β-endorphin in peripheral blood mononuclear cells from 11 patients with acute myocardi
Journal Article•
TL;DR: The reactivity and sensitivity of SAA was clearly higher than those of CRP in patients with viral infections, on steroid therapy and undergoing chronic allograft rejection, suggesting that monitoring SAA levels provides more useful information than monitoring CRP.
Abstract: Serum amyloid A (SAA) is an inflammation-reactive protein, like C-reactive protein (CRP). In this study, we examined SAA levels in the sera of kidney transplant patients with acute rejection (N = 12), chronic rejection (N = 60) and cytomegalovirus (CMV) infection complications and compared them with serum CRP levels in terms of sensitivity and reactivity. The SAA and CRP showed almost similar kinetics in 10 patients within 2 months of kidney transplantation. However, in 2 patients SAA responded more sensitively to CMV infection and acute rejection. SAA increased significantly 10-fold relative to its baseline levels. The SAA levels also increased along with those of serum creatinine levels. Our experiments clearly showed that SAA and CRP responded sensitively to several stimuli with elevated serum levels including surgical trauma, acute allograft rejection and infection. However, the reactivity and sensitivity of SAA was clearly higher than those of CRP in patients with viral infections, on steroid therapy and undergoing chronic allograft rejection, suggesting that monitoring SAA levels provides more useful information than monitoring CRP.
TL;DR: Recurrent urinary infection, raised serum levels of C-reactive protein, and the risk of cardiovascular disease in patients with spinal cord injury are studied.
Abstract: Recurrent urinary infection, raised serum levels of C-reactive protein, and the risk of cardiovascular disease in patients with spinal cord injury: a hypothesis
TL;DR: The plasma concentration of C-reactive protein and risk of developing peripheral vascular disease is associated with an increased risk of adverse events and death in women.
Abstract: Source Citation Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation. 1998 Feb 10; 9...
Journal Article•
TL;DR: In this article, a prospective study was undertaken to assess the differences between the levels of the main plasma components of complement in allergic subjects and in those with pseudo-allergic clinical manifestations.
Abstract: BACKGROUND This prospective study was undertaken to assess the differences between the levels of the main plasma components of complement in allergic subjects and in those with pseudoallergic clinical manifestations METHODS Plasma C3 and C4 were evaluated in a total of 256 subjects examined consecutively at the allergology outpatients clinic of the Internal Medicine Division B, University of Turin Total IgE and C1-inhibitor levels were also determined in 128 and 44 subjects respectively RESULTS C3 and C4 levels were not significantly different (p = 0398 and p = 0497) in 123 subjects with a positive and 133 with a negative prick test, nor in allergic subjects with respiratory as opposed to skin symptoms (p = 0293 and p = 0462), whereas the C-1 inhibitor was significantly lower (p = 0046) in the respiratory subgroup Total IgE was positively correlated with the C3 level (p = 0036) in 75 allergic subjects CONCLUSIONS These findings suggest that plasma C3 and C4 values are not sufficient to discriminate IgE inflammation (positive prick test) and pseudoallergy (negative prick test) in the assessment of subjects with clinically suspected allergy The positive correlation between IgE synthesis and C3 also points to an interaction between IgE synthesis and C3 regulation proteins in patients with IgE mediated diseases Further investigation of other acute phase proteins (C reactive protein, fibrinogen) and the cytokines regulating their synthesis (IL-6) in such patients will help to clarify this correlation
TL;DR: The role of inflammation in atherosclerosis development is gaining substantial attention and in men, elevated levels of C-reactive protein, a marker for inflammation, are associated with a twofold increase in the risk for stroke, a threefold increase for myocardial infarction, and a fourfold increase with age.
Abstract: The role of inflammation in atherosclerosis development is gaining substantial attention. In men, elevated levels of C-reactive protein, a marker for inflammation, are associated with a twofold increase in the risk for stroke, a threefold increase in the risk for myocardial infarction …
TL;DR: C-reactive protein (CRP) is an acute-phase reactant associated with adverse clinical outcome in patients with acute coronary syndromes and its use in clinical practice is still under investigation.
Abstract: C-reactive protein (CRP) is an acute-phase reactant associated with adverse clinical outcome in patients with acute coronary syndromes. This study