Decrease In C-reactive Protein Levels Research Articles

Pre-diabetes, insulin resistance, inflammation and CVD risk

There is accumulating evidence that insulin resistance in the pre-diabetic state is associated with the presence of additional cardiovascular risk factors and increased incidence of cardiovascular disease (CVD). There is also accumulating evidence indicating that chronic sub-clinical inflammation as measured by such inflammatory markers as C-reactive protein (CRP) is associated with insulin resistance and other features of the insulin resistance syndrome, increased risk of development of type 2 diabetes and increased cardiovascular event risk. Insulin-sensitizing agents may have greater effects in reducing cardiovascular risk than secretagogues in the pre-diabetic state, and glitazones have been found to decrease CRP levels in patients with diabetes. Statins also reduce CRP levels. Efforts to reduce CVD should include increased emphasis on improving glycaemic control, preventing development of diabetes and addressing cardiovascular risk factors in the pre-diabetic state.

C-Reactive Protein Levels Correlate With Mortality and Organ Failure in Critically Ill Patients

C-reactive protein (CRP) is an acute-phase protein, the blood levels of which increase rapidly in response to infection, trauma, ischemia, burns, and other inflammatory conditions. Although used frequently in the ICU as a sepsis marker, the relation of CRP levels to organ damage is not well known. This study assessed the association between early serum CRP concentrations and the development of organ failure and mortality in ICU patients. A prospective cohort study. A 31-bed ICU in a university hospital. All 313 patients admitted to the ICU during the 4-month study period. None. Patients with high CRP levels at ICU admission had more severe organ dysfunction (higher sequential organ failure assessment scores, days of renal extracorporeal support therapy), longer ICU stays, and higher mortality rates than patients with normal ICU admission CRP levels. CRP concentrations were correlated with the presence and number of organ failures. ICU admission serum CRP levels > 10 mg/dL were associated with a significantly higher incidence of respiratory (65% vs 28.8%, p < 0.05), renal (16.6% vs 3.6%, p < 0.05), and coagulation (6.4% vs 0.9%, p < 0.05) failures, and with higher mortality rates (36% vs 21%, p < 0.05) than CRP levels < 1 mg/dL. In patients with CRP concentrations > 10 mg/dL on ICU admission, a decrease in CRP level after 48 h was associated with a mortality rate of 15.4%, while an increased CRP level was associated with a mortality rate of 60.9% (relative risk, 0.25; 95% confidence interval, 0.07 to 0.91; p < 0.05). In a heterogeneous ICU population, elevated concentrations of serum CRP on ICU admission are correlated with an increased risk of organ failure and death. Moreover, persistently high CRP concentrations are associated with a poor outcome. Serial measurements may be helpful to identify those patients who require more aggressive interventions to prevent complications.

Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

Studies in animals and humans indicate a pivotal role for adhesion molecules (AMs) in the pathogenesis of atherosclerosis. Whereas an association between hypercholesterolaemia and AM expression has been suggested, it is unclear whether lowering cholesterol decreases AM expression and release. We compared the effects of a 3-month treatment with standard doses of three different statins (atorvastatin, simvastatin and pravastatin) on plasma levels of circulating AM (cAM) in 75 hypercholesterolaemic patients in a randomized clinical trial. Plasma levels of circulating (c)E-selectin, circulating intercellular adhesion molecule-1 (cICAM-1) and circulating vascular cell adhesion molecule-1 (cVCAM-1) were measured before and after 3 months of therapy. None of the statins lowered plasma cAM levels and pooled analyses of all patients showed a 1.7% [95% confidence interval (CI), -1.4–4.9%] increase in cE-selectin, a 2.1% (95% CI, -0.2–4.4%) increase in cICAM-1, and a 2.7% (95% CI, -0.6–6.1%) increase in cVCAM-1 levels. cAM levels did not decrease, even in patients with a &gt;50% decrease (n = 19) in low-density lipoprotein cholesterol levels. This study provides strong evidence that 3 months of therapy with three different statins does not decrease cAM levels, despite normalization of cholesterol levels, and a minor decrease in C-reactive protein levels in patients with moderate hypercholesterolaemia.

Atorvastatin affects C-reactive protein levels in patients with coronary artery disease

SUMMARYBackground: Elevated levels of C-reactive protein (CRP) are considered to be one of the indicators of poor prognosis in coronary artery disease (CAD). The aim of this study was to evaluate anti-inflammatory effects of atorvastatin in patients with CAD by measuring serum CRP levels.Methods: After measuring the baseline levels of CRP and lipid fractions, the patients were divided into two groups. In Group A (n = 46), atorvastatin (20 mg/day) was administered in addition to classic antianginal treatment (beta-blocker, nitrate and aspirin). In Group B (n = 32), the usual antianginal treatment was continued. Following 4 weeks of treatment the same measurements were repeated.Results: In Group A, CRP decreased from 20.3 mg/dl (95% CI, 9-31.8) to 10.8 mg/dl (95% CI, 2.7-18.9) (p < 0.001). In Group B, CRP decreased from 17 mg/dl (95% CI, 13.1-21) to 12.8 mg/dl (95% CI, 9.7-15.9) (p < 0.01). The decrease in group A was more than in group B (p = 0.003).Conclusions: In patients with CAD, atorvastatin exerted an anti-inflammatory effect represented by decreasing CRP levels. This effect was independent of the change in low density lipoprotein cholesterol (LDL-C) or high density lipoprotein cholesterol (HDL-C) levels.

Effect of treating periodontitis on C-reactive protein levels: a pilot study.

BackgroundPeriodontitis is associated with elevated levels of C-reactive protein and fibrinogen and it may be a coronary heart disease risk factor. We wanted to study if treatment of periodontitis can decrease the levels of these inflammatory markers.MethodsC-reactive protein and fibrinogen levels were measured in 35 patients (21 M, 14 F, mean age 50 years) with adult periodontitis, before and after treatment.ResultsThe median baseline C-reactive protein level in the patients was 1.05 mg/l and it decreased to 0.7 mg/l (p = 0.05) after periodontal treatment. Of the 30 patients who could be included in the analyses, 24 patients had a baseline level below 2 mg/l (the 95th percentile limit in Finland); 6 patients had levels higher than this. Elevation of the baseline C-reactive protein level or the magnitude of its decrease were not associated with severe form of periodontitis. The decrease in C-reactive protein levels was at least 50 % in 4/6 of those with elevated baseline levels, as compared with 3/24 of the rest of the patients (p = 0.016). No corresponding effect was observed in fibrinogen levels.ConclusionsPeriodontitis seems to increase C-reactive protein only in some individuals, presumably the ones reacting to it with a systemic inflammatory reaction. Periodontal treatment decreases C-reactive protein levels in these individuals and it may thus decrease their risk of coronary heart disease.

Sensitive markers of inflammation make it possible to study the chronic process: the rise of interest in low levels of C-reactive protein

Increases in baseline levels of C-reactive protein (CRP) have been consistently identified as an independent risk indicator of cardiovascular events. The measurement of the low level is robust and well established. Increases in low levels of CRP can mark low-grade continuous inflammation and hyperresponse in acute situations. In addition, CRP can exert various actions on vascular cells and activates complement thus participating in infarction pathogenesis. Various cardiovascular drugs, notably statins, can induce a marked decrease in low levels of CRP, which is indicative of their beneficial effect on inflammation. Future studies need to demonstrate whether increases in baseline levels of CRP can become a useful practical addition to risk recognition strategies and possibly may also serve as an additional surrogate end-point in cardiovascular disease treatments.

C-reactive protein (CRP), a comparison of pre- and post-mortem blood levels

During autopsy of 26 inpatients with elevated CRP levels (14–536mg/l) blood was taken from the femoral vessels and analysed for the content of CRP. The post-mortem CRP values were compared with the results of CRP analysis performed within the last 24h before death. This showed that the post-mortem values of CRP in average were reduced with 35% compared to the ante-mortem values. The decrease in CRP levels was not significantly influenced by the time interval from death until blood was drawn for analysis, at least up to 6 days. When blood taken from healthy individuals killed in accidents was analysed, no elevated CRP values were observed, indicating that there is negligible risk for false positive results. It is also shown that frozen blood can be used for CRP analysis if an immunometric kit assay based on whole blood is applied. The results demonstrate that an elevated level of CRP in post-mortem blood is a good marker for an ongoing inflammatory process prior to death. CRP analysis may therefore be a helpful tool in post-mortem examinations, especially in non-hospitalised individuals without medical records.

Helicobacter Pylori Infection: A New Cause of Anorexia in Peritoneal Dialysis Patients

Helicobacter pylori (HP) infection has frequently been found in dialysis patients. Chronic infections induce overproduction of pro-inflammatory substances. Inflammation has been associated with cachexia and anorexia. We explored the relationship between HP infection, anorexia, and malnutrition in peritoneal dialysis (PD) patients. The study included 48 clinically stable PD patients divided into four groups: HP+ with anorexia (group I, n = 12); HP+ without anorexia (group II, n = 4); HP- with anorexia (group III, n = 5); and HP- without anorexia (group IV, n = 27). Infection with HP was diagnosed by breath test. Anorexia was evaluated using a personal interview and an eating motivation scale (VAS). The VAS included five questions that are answered before and after eating. The questions concern desire to eat, hunger, feeling of fullness, prospective consumption, and palatability. Biochemical markers of nutrition and inflammation were also determined. At baseline, group I showed lower scores for desire to eat, hunger sensation, prospective consumption, and palatability. They also showed lower lymphocyte counts, prealbumin, transferrin, serum albumin, normalized equivalent of protein-nitrogen appearance (nPNA), and residual renal function (RRF). In addition, the same group showed higher levels of C-reactive protein (CRP) and more sensation of fullness than the remaining groups. In the entire series, we found significant linear correlations between the following markers of nutrition and certain questions on the VAS: albumin with before-lunch desire to eat (r = 0.38, p < 0.05), and prealbumin with before-lunch hunger (r = 0.41, p < 0.05) and after-lunch hunger (r = -0.35, p < 0.05). Negative linear correlations were found between albumin and fullness before lunch (r = -0.45, p < 0.01), and between prealbumin and before-lunch desire to eat (r = -0.39, p < 0.05). Negative linear correlations were also seen between CRP and albumin (r = -0.35, p < 0.05) and between CRP and prealbumin (r = -0.36, p < 0.05). Similarly, CRP showed a negative correlation with before-lunch desire to eat (r = -0.38, p < 0.05) and afterlunch desire to eat (r = -0.45, p < 0.01). After HP eradication, group I showed a significant increase in markers of nutrition and in VAS scores for almost all questions. Simultaneously, they showed a decrease in CRP level. Significant differences were also found in lymphocyte count (1105 +/- 259.4 cells/mm3 vs 1330.8 +/- 316 cells/mm3, p < 0.05), nPNA (0.9 +/- 0.16 g/kg/day vs 1.07 +/- 0.3 g/kg/day, p < 0.05), prealbumin (26.7 +/- 6.5 mg/dL vs 33.9 +/- 56.6 mg/dL, p < 0.01), albumin (3.48 +/- 0.3 g/dL vs 3.67 +/- 0.35 g/dL, p < 0.05), CRP (1.16 +/- 1.14 mg/dL vs 0.88 +/- 1.2 mg/dL, p < 0.054), before-lunch desire to eat (56.6 +/- 6.8 vs 72.2 +/- 4, p < 0.001), after-lunch desire to eat (5.4 +/- 2.6 vs 12.3 +/- 2, p < 0.01), hunger before lunch (55.4 +/- 5.4 vs 73.1 +/- 4.6, p < 0.001), hunger after lunch (5.8 +/- 2.9 vs 11 +/- 4, p < 0.01), fullness before lunch (36.6 +/- 10.3 vs 18.7 +/- 8.8, p < 0.001), consumption after lunch (5 +/- 4.7 vs 17.5 +/- 18, p < 0.05), and palatability (61 +/- 5.3 vs 74.1 +/- 4.1, p < 0.001). Infection with HP is associated with anorexia, inflammation, and malnutrition in PD patients. Eradication of HP significantly improves this syndrome. Residual renal function seem to have a protective effect on appetite preservation. The present study supports the hypothesis of the involvement of inflammation in the pathogenesis of malnutrition in PD patients.

C-reactive protein in patients with familial hypercholesterolemia: no effect of simvastatin therapy

Patients with familial hypercholesterolemia (FH) are especially at risk for premature cardiovascular disease (CVD). Recent studies revealed C-reactive protein (CRP) as a strong predictor of future first or recurrent CVD events, suggesting that CRP plays an important role in the development of atherosclerosis. The aim of this study was to evaluate the effect of one year of simvastatin treatment on serum levels of CRP and to assess the influence of risk factors for CVD on CRP concentrations in patients with FH. We measured baseline CRP levels in 337 patients with FH. A second blood sample, collected after one year of treatment with simvastatin (20–40 mg once daily) was measured in a subgroup of 129 patients. Patients with CVD present at baseline had significantly higher serum levels of CRP (2.26 mg/l versus 1.55 mg/l, P<0.001). CRP levels were associated with smoking, body mass index, age, levels of triglycerides (TG), and the use of NSAIDs or anticoagulation drugs. Simvastatin therapy significantly improved lipid profiles in the intervention group. There was a small, but non-significant decrease of CRP levels upon treatment. CRP decreased from 1.51 mg/l median (interquartile range (IQR) 0.76–3.41) at baseline to 1.24 mg/l median (IQR 0.72–2.92) after treatment, ( P=0.328). In conclusion, CRP levels were associated with the presence of CVD in FH patients. Simvastatin therapy had no significant effect on CRP levels in these patients.

Exacerbation of Acute Pancreatitis in the Presence of Chronic Liver Injury in Rats, with Special Reference to Therapeutic Efficacy of Prostaglandin E1

The pathophysiology of acute pancreatitis accompanied by chronic liver injury, and the therapeutic efficacy of prostaglandin (PG)E1 were studied experimentally in rats. Chronic liver injury was produced by subcutaneous administration of CCl4. Acute pancreatitis was induced by the closed duodenal loop (CDL) method, immediately after which PGE1 (60 ng/kg/min) was infused intravenously via the jugular vein. Serum levels of amylase, alpha2-macroglobulin-trypsin complex (alpha2M-TRY), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were determined before and at 3 and 6 h after the onset of acute pancreatitis. Rats without administration of CCl4 served as controls. Serum amylase levels were lower in the liver injury (LI) group than in the normal liver (NL) group at 3 and 6 h. PGE1 had no effect on amylase levels in either group. Serum alpha2M-TRY levels were similar in the two groups at 3 h, but significantly higher in LI than in NL at 6 h. PGE1 tended to decrease alpha2M-TRY levels only in LI. Serum CRP levels were significantly more elevated in LI than in NL at 0, 3, and 6 h. PGE1 decreased CRP levels only in LI. Serum TNF-alpha concentrations were higher in LI, especially at 6 h. PGE1 reduced TNF-alpha levels in LI. Pancreatitis severity scores were significantly higher in LI. PGE1 significantly decreased the severity scores only in LI. Fat necrosis scores were significantly lower in LI. Histologically, interstitial edema was much more prominent in NL than in LI, whereas interstitial hemorrhage was more severe in LI at 3 and 6 h. PGE1 lessened the hemorrhage in LI. The extent of both vacuolization and necrosis of acinar cells was similar for both groups and tended to be improved by PGE1. It is concluded that acute pancreatitis becomes much more serious in the presence of chronic liver injury, and that PGE1 can ameliorate the exacerbated lesions, probably by improvements in blood flow through the pancreatic tissue.

P-4-517 - The role of the aseptic technique of craniostomy procedure in infection of diversional CSF surgery

Endothelin (ET) is involved in the etiopathogenesis of peripheral arterial disease (PAD). We hypothesized that ET antagonism might improve the endothelial function, inflammatory status, and symptoms in PAD. This pilot randomized clinical trial was designed to determine the clinical efficacy, pleiotropic effects, and safety of dual ET-receptor antagonist bosentan in Hispanic patients with PAD presenting intermittent claudication. The Bosentan Population-Based Randomized Trial for Clinical and Endothelial Function Assessment on Endothelin Antagonism Therapy was a 12-month, randomized, controlled, parallel-group, double-blind, proof-of-concept pilot study evaluating the effect of bosentan on absolute claudication distance (primary efficacy end point), flow-mediated arterial dilation, and C-reactive protein levels (primary pleiotropic end points) in patients with PAD with Rutherford category 1 to 2 of recent diagnosis. Secondary end points included ankle-brachial index, subjective claudication distance, and safety. Of the 629 screened subjects, 56 patients were randomized 1:1 to receive bosentan for 12 weeks (n = 27) or placebo (n = 29). Six months after the initiation, a significant treatment effect in flow-mediated arterial dilation of 2.43 ± 0.3% (95% CI 1.75 to 3.12; p = 0.001), absolute claudication distance of 283 ± 23 m (95% CI 202 to 366; p = 0.01), ankle-brachial index of 0.16 ± 0.03 (95% CI 0.09 to 0.23; p = 0.001), and a decrease in C-reactive protein levels of −2.0 ± 0.5 mg/L (95% CI −2.8 to −1.1; p = 0.02) were observed in the bosentan-treated group compared to the control group. No severe adverse effects were found in the bosentan group. In conclusion, in Hispanic patients with intermittent claudication, bosentan was well tolerated and improved endothelial function and claudication distance as well as inflammatory and hemodynamic states.

Assessment of vitamin and trace elementsupplementation in severely burned patients undergoing long-term parenteral and enteral nutrition

The efficacy of an oral supplement of vitamins and trace elements during a long-termartificial parenteral and enteral nutrition was investigated for 3 months in patients with extensive burns. Thirty severely burned patients (22 male, 8 female, age 41 ± 18 years, range 23–59 years, 33 ± 12% total body surface area burn, 22% ± 8 full thickness burn surface area) were included. Every 10 days, from day 10 until day 90, we determined serum levels of: u • vitamins B1, B12, A, E • folic acid • copper, zinc, iron • transferrin, albumin, prealbumin, total proteins • fibronectin, retinol binding protein (RBP) • calcium • phosphorus • triglycerides • total cholesterol • C reactive protein (CRP) • erythrocyte folic acid The mean daily nutritional support was 60 Kcals and 0.4 g N per kg of body weight, 70% enterally and 30% parenterally administered, with enteral vitamin and trace element supplementation. On day 10, there was a decrease of the serum level of 19/20 parameters. For 8 parameters (vitamin A, total cholesterol, iron, transferrin, fibronectin, phosphorus, RBP, total proteins), the level was lower than usual. Between day 10 and day 20, a significant normalization of 6 of them was noted, the average levels of transferrin and iron remaining below normal values until day 50. There was a significant decrease in C-reactive protein levels, however above normal limits. No deficiency in vitamins or trace elements was found. Cyclic variations of serum levels occurred which may be more related to volemic, hydroelectrolytic, endocrine and inflammatory disorders than to nutritional problems.