Taken together, our findings demonstrated that plasma CRP levels were substantially associated with common genetic variants in the CRP gene and could predict the development of hypertension.
Association of MCP-1 -2518 A/G single nucleotide polymorphism with the serum level of CRP in Slovak patients with ischemic heart disease, angina pectoris, and hypertension.
Having two or all three risk factors (smoking actively, body mass index over 25 kg/m<sup>2</sup>, high-sensitive C-reactive protein (hsCRP) level over 3 mg/L) indicates a 4-fold risk for incident hypertension within 21-year follow-up.
The findings of this study support that CRP gene polymorphisms have significant association with genetic susceptibility of HT and quantitative traits of blood pressure.
Deceased patients had a significantly higher age (mean 64.4 vs. 51.1 years); frequency of male sex (31.5% vs. 16.7%), hypertension (40.4 vs. 18.5%), and diabetes mellitus (25.8% vs. 7.7%); ESR (mean 57.1 vs. 43.0 mm/h); CRP (mean 16.9 vs. 8.7 mg/L); and FIB-4 (mean 1.5 vs. 1.0) (all P < 0.05) than the survivors.
There were no significant differences between subjects with wild-type (677CC) and with mutant (677CT+677TT) alleles in terms of diabetes duration, visceral fat area, total cholesterol, triglyceride, fasting plasma glucose, systolic blood pressure, diastolic blood pressure, high-sensitivity C-reactive protein, homocysteine (Hcy), and carotid intima-media thickness values.
We evaluated the effect of four SNPs in the CRP gene on serum levels of protein and body mass index (BMI) in 150 unrelated Mexican subjects from 18 to 25 years old, without hypertension, non-overweight, and without inflammatory diseases, non-smoking and non-consumers of alcohol.
When we evaluated the associations between the CRP-related SNPs with cardiovascular disease phenotypes, rs9375813 (ARG1) showed a marginal association with hypertension (P = 0.0440).
In this study, men homozygous with the ApoE epsilon4 allele had thicker CCA-IMT, independently of Apo E epsilon2 and epsilon3 alleles, CRP, lipid variables (TG, LDL, HDL) and other CVD risk factors (smoking, hypertension, body mass index, diabetes), suggesting CCA-IMT to be modified by the ApoE epsilon4 genotype in a recessive pattern.
Prospective and retrospective cohort studies evaluating the association of circulating C reactive protein (CRP), high-sensitive CRP (hs-CRP), interleukin 6 (IL-6) and IL-1β to the risk of developing hypertension in the general population were included.
After adjustment for age, body mass index, fibrinogen level and high sensitivity C-reactive protein level, rs4673 was found to be an independent risk factor for AH in subjects with type 2 diabetes, whereas rs1001179 and rs1050450 were not.
Here, we evaluated the impact of serum C-reactive protein (CRP) and the white blood cell (WBC) count on the risk of hypertension in middle-aged Japanese men at a work site.
The results of our study suggest a synergistic effect of CRP C allele with classical risk factors such as hypertension, obesity, dyslipidemia and MetS.
Notably, the associations of rs2274700 (A473A) with DBP (P = 2.1×10(-3)), SBP (P = 8×10(-5)) and hypertension risk (P = 7.9×10(-3)) were significant only in the individuals with low CRP levels (<2.0 mg/l), but not in those with CRP levels ≥2.0 mg/l (P≥0.0807) (P for interaction ≤0.0467).
In comparison to controls, PE/E significantly increased systolic BP (MD = 8.3 mmHg, 95%CI 6.8 to 9.7), diastolic BP (MD = 6.8 mmHg, 95%CI 5.6 to 8.0), BMI (MD = 2.0 kg/m<sup>2</sup>; 95%CI 1.6 to 2.4), waist (MD = 4.3 cm, 95%CI 3.1 to 5.5), waist-to-hip ratio (MD = 0.02, 95%CI 0.01 to 0.03), weight (MD = 5.1 kg, 95%CI 2.2 to 7.9), total cholesterol (MD = 4.6 mg/dL, CI 1.5 to 7.7), LDL (MD = 4.6 mg/dL; 95%CI 0.2 to 8.9), triglycerides (MD = 7.7 mg/dL, 95%CI 3.6 to 11.7), glucose (MD = 2.6 mg/dL, 95%CI 1.2 to 4.0), insulin (MD = 19.1 pmol/L, 95%CI 11.9 to 26.2), HOMA-IR index (MD = 0.7, 95%CI 0.2 to 1.2), C reactive protein (MD = 0.05 mg/dL, 95%CI 0.01 to 0.09), and the risks of hypertension (RD = 0.24, 95%CI 0.15 to 0.33) and MetS (RD = 0.11, 95%CI 0.08 to 0.15).
In conclusion, age, male gender, BMI, smoking and T2DM history, serum IL‑6, TNF‑α and CRP were positively correlated with CIH combined with hypertension, while NO and NOS were negatively correlated with CIH.
It is assumed that the major components of MS - obesity, insulin resistance, dyslipidemia, and hypertension - are linked to renal damage through the systemic release of several pro-inflammatory mediators, such as uric acid (UA), C-reactive protein (CRP), and generalized oxidative stress.
In univariate analysis, renal impairment was associated with age (p < 0.001), HLA-B27 positivity (p = 0.003), several cardiovascular (CV) risk factors (history of hypertension, p < 0.001; systolic blood pressure, p = 0.009; diabetes, p = 0.005; and Framingham risk score, p < 0.001), disease activity scores [BASDAI, p = 0.001; Ankylosing Spondylitis Disease Activity Score-C-reactive protein (ASDAS-CRP), p < 0.001], functional variables (Bath Ankylosing Spondylitis Functional Index, p < 0.001), inflammatory biomarkers (erythrocyte and CRP, both p < 0.001), and NSAID intake since onset of disease (percentage of days, p = 0.008).
Outcomes included markers of insulin resistance (change in homeostasis model assessment of insulin resistance (HOMA-IR) at 6 months = primary outcome), hypertension (24-hour ambulatory/blood pressure) and inflammation (high-sensitivity C-reactive protein: hs-CRP).
Significant associations with CRP were seen in women, but not men; with current and former (but not non-) smokers; participants younger (but not older) than 65 y; those without diabetes (but not with), and those with (but not without), hypertension.
Stress-induced hypertension in rats produced altered serum sodium, potassium, immunoglobins, C-reactive protein, vitamin D, and calcium level which is restored by atenolol.