Obesity is the major determinant of elevated C-reactive protein in subjects with the metabolic syndrome.

OBJECTIVE: To investigate the relationship between C-reactive protein (CRP) and various characteristics of the metabolic syndrome. DESIGN: Population-based cross-sectional study. SUBJECTS: A total of 1929 subjects undergoing a medical examination in a preventive medicine clinic (age, 50+/-10 y; 63% males). RESULTS: The proportion of subjects with CRP levels above the cut point generally used to indicate an obvious source of infection or inflammation (>10 mg/l) was 3, 7, and 15% in subjects who were normal weight, overweight, and obese, respectively. Subjects with obesity had markedly higher CRP level compared to patients without obesity regardless of whether they had the metabolic syndrome. However, there was no significant difference in CRP levels between nonobese subjects without the metabolic syndrome and subjects in whom the diagnosis of the metabolic syndrome was based on criteria other than obesity (adjusted geometric mean CRP 1.75 vs 2.08 mg/l, P=0.79). Similarly, CRP levels did not differ among obese subjects with and without the metabolic syndrome (adjusted geometric mean CRP 3.22 vs 3.49 mg/l, P=0.99). There was a linear increase in CRP levels with an increase in the number of metabolic disorders (P(trend) <0.0001), which was substantially diminished after controlling for body mass index (BMI) (P(trend)=0.1). Stepwise multivariate linear regression analysis identified BMI, triglyceride levels, HDL cholesterol levels (inversely), and fasting glucose as independently related to CRP levels. However, BMI accounted for 15% of the variability in CRP levels, whereas triglycerides, HDL cholesterol and fasting glucose levels accounted for only approximately 1% of the variability in CRP levels. CONCLUSION: Obesity is the major factor associated with elevated CRP in individuals with the metabolic syndrome. CRP levels in the range suggesting a source of infection or inflammation (>10 mg/l) are more common among obese subjects than in nonobese subjects.

Association between fasting glucose and C-reactive protein in middle-aged subjects.

AIMS: C-reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute-phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects. METHODS: We studied the relation of high-sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population-based cross-sectional study (n = 1000; age 50 +/- 9 years). RESULTS: Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 +/- 0.09, 0.95 +/- 0.12, and 1.11 +/- 0.13, respectively; Ptrend < 0.0001). Increasing CRP with higher fasting glucose levels was apparent even among subjects with fasting glucose in the normal range (Ptrend = 0.039), and subjects with fasting glucose level in the upper quartile of normal fasting glucose had higher CRP levels compared with subjects in the lower quartile (P = 0.035). There was a positive crude correlation between CRP and smoking, post-menopausal hormone use, body mass index, fasting glucose, triglycerides, hypertension, and uric acid (r = 0.11-0.36, P = 0.002-0.0001). A negative correlation was found between CRP and HDL-cholesterol (r = 0.12, P < 0.0001) and physical activity (r = 0.11, P = 0.002). After adjustment for potential confounders in a stepwise multivariate linear regression model, fasting glucose remained significantly and independently related to CRP levels (correlation coefficient 0.06; 95% confidence interval 0.014-0.11, P = 0.011). CONCLUSIONS: Fasting glucose is significantly and positively associated with plasma CRP in middle-aged subjects. CRP levels increase continuously across the spectrum of fasting glucose, beginning in the lowest quartile of normal fasting glucose. This finding suggests that a proinflammatory effect may contribute to the adverse cardiovascular outcome associated with diabetes, impaired fasting glucose, and increasing glucose levels within the normal range.

Plasma antioxidants and lipid peroxidation in acute myocardial infarction and thrombolysis.

OBJECTIVES: The aim of this study was to investigate the balance between prooxidative and protective mechanisms in patients with acute myocardial infarction (AMI) throughout streptokinase (STK) therapy. METHODS: Patients who presented to coronary care unit within 3 hours of infarction were followed. Blood was collected before, 2 and 24 hours post STK. Plasma lipid peroxidation was analyzed by a free radical generating system (AAPH) and malondialdehyde equivalents and conjugated dienes quantitated. Plasma vitamins A, E and beta-carotene, were analyzed by HPLC. Patients' results were compared with those from age-matched, healthy control subjects. RESULTS: In 38 patients with AMI, baseline plasma antioxidant vitamin concentration was reduced compared with a healthy control group. Upon STK therapy, there was a significant drop in plasma vitamin E concentration. Successful reperfusion was followed by an increased plasma oxidizability. Plasma lipids were not significantly different in the AMI patients except for a lower HDL-cholesterol concentration. CONCLUSIONS: Patients with AMI showed a drop in plasma antioxidant vitamins. Upon thrombolysis, there was an enhanced lipid peroxidation. These alterations indicate the significance of free radical generation processes in reperfusion injury in AMI patients, and suggest the potential involvement of antioxidants in the management of AMI treated by thrombolysis.

[The treatment of hypertensive crisis with nifedipine as the basis]. / Tratamentul crizei hipertensive cu nifedipina în teren.

In 48 patients (p) with hypertensive crisis (HC) the effect of nifedipine (N) sublingual 10-20 mg alone (group I, n = 19, mean control AH +/- SD 232 +/- 15.3/132.5 +/- 4.9 mmHg) or associated with furosemide and clonidine (group II, n = 29, AT 249 +/- 21/131.8 +/- 13.6 mmHg). In both groups the AT fell significantly starting five minutes after the administration of N (except diastolic AT in group II); the values measured at 45 min. being 177 +/- 32/105.4 +/- 13 mmHg in group I and 164.6 +/- 44.4/100.1 +/- 16.3 mmHg in group II (the mean proportional difference at 45 min. for systolic AT was 24.6 +/- 11.4% in group I and 28.7 +/- 12.2% in group II; for diastolic AT 20.5 +/- 9.4% in group I, and 27 +/- 12.2% for group II). The good clinical results consisted of lowering of the AT values below critical levels and clinical improvement in 42 p (87.5%). Tolerance to N was good, in a single case was hypotension associated with fainting, both being promptly treated by simple means. CONCLUSIONS. 1. N administered sublingual, 10-20 mg, alone or associated with furosemide has in most patients a rapid hypotensive effect, lowering AT below critical limits within 45 min; 2. the drug is readily administered and without the risk of side effects and can be used in the field in the emergency treatment of hypertension.