PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 621279-7 1978 One subject exhibited a second rise in SAA and CRP concentrations after acute over-indulgence with alcohol, suggesting that acute liver damage may have caused an acute phase reaction. Alcohols 99-106 C-reactive protein Homo sapiens 47-50 30721633-7 2019 Alcohol risk category was roughly linearly related with the occurrence of elevated values for GGT, ALT and CRP. Alcohols 0-7 C-reactive protein Homo sapiens 107-110 33154657-5 2020 Results: There was a negative correlation between serum retinol and hs-CRP in alcohol drinking men. Alcohols 78-85 C-reactive protein Homo sapiens 71-74 33154657-6 2020 There was a negative correlation between serum retinol and hs-CRP in the alcohol-nonsmoking female group. Alcohols 73-80 C-reactive protein Homo sapiens 62-65 33154657-7 2020 There was a positive correlation between alpha-tocopherol and hs-CRP in the nonsmoking and alcohol-drinking group. Alcohols 91-98 C-reactive protein Homo sapiens 65-68 33154657-8 2020 There was a positive correlation between alpha-tocopherol and hs-CRP in the nonsmoking and alcohol-drinking female group. Alcohols 91-98 C-reactive protein Homo sapiens 65-68 32447974-9 2020 Maladaptive coping behaviours were apparent, notably hazardous alcohol consumption, which was associated with a clinically significant elevation in C-reactive protein levels (> 3 mg/L). Alcohols 63-70 C-reactive protein Homo sapiens 148-166 31483873-8 2019 Multivariate linear regression was performed to test the relationships between alcohol consumption and systemic oxidative stress (4-hydroxynonenal; 4-HNE) and inflammation (c-reactive protein; CRP). Alcohols 79-86 C-reactive protein Homo sapiens 173-191 30878797-4 2019 At baseline, median levels of serum CRP significantly differed by demographics (sex, age category, marital status, and education levels) and health behaviors (cigarette smoking status, alcohol drinking status, BMI category, and physical activity levels). Alcohols 185-192 C-reactive protein Homo sapiens 36-39 30878797-5 2019 In the multivariable analysis, the study participants who were women, older, never drinking alcohol, overweight or obese, and physically inactive had increased likelihood of having high CRP levels (>= median levels among all study participants) compared to their counterparts. Alcohols 92-99 C-reactive protein Homo sapiens 186-189 33740951-11 2021 The only independent variables for CRP/alb changes were CCI and heavy alcohol use. Alcohols 70-77 C-reactive protein Homo sapiens 35-38 33740951-12 2021 The CRP/alb ratio was significantly lower in non-heavy alcohol users (odds ratio [OR] 0.114, 95% confidence interval [CI] 0.024-0.541; adjusted p = 0.006) than in other patients. Alcohols 55-62 C-reactive protein Homo sapiens 4-11 33740951-15 2021 CONCLUSIONS: The CRP/alb ratio was high in OSCC patients with combined comorbities of age and disease history and in patients with heavy alcohol use. Alcohols 137-144 C-reactive protein Homo sapiens 17-24 32976314-6 2020 [ZERO WIDTH SPACE] RESULTS: Cox regression analyses revealed that parental alcohol problems (HR 3.09, 95% CI: 1.38-6.88) were associated with an increased risk of type II diabetes during the follow-up, even after adjustment for age, marital status, education, Human Population Laboratory (HPL) Depression Scale scores, smoking, alcohol consumption, body mass index, and serum high-sensitivity C-reactive protein. Alcohols 75-82 C-reactive protein Homo sapiens 393-411 33356789-14 2020 Hs-CRP has statistically significant associations between alcohol use, dementia, white blood cell count, and HDL levels. Alcohols 58-65 C-reactive protein Homo sapiens 3-6 27496931-0 2016 C-reactive protein level partially mediates the relationship between moderate alcohol use and frailty: the Health and Retirement Study. Alcohols 78-85 C-reactive protein Homo sapiens 0-18 29628291-13 2018 CRP can be consumed with tea, food, alcohol, and medicine. Alcohols 36-43 C-reactive protein Homo sapiens 0-3 28612359-0 2018 The relationship between moderate alcohol consumption, depressive symptomatology, and C-reactive protein: the Health and Retirement Study. Alcohols 34-41 C-reactive protein Homo sapiens 86-104 28612359-10 2018 Further, moderate drinkers had lower CRP levels suggesting that inflammation partially mediates the relationship between moderate alcohol use and depressive symptomatology. Alcohols 130-137 C-reactive protein Homo sapiens 37-40 29479472-0 2018 Moderate use of alcohol is associated with lower levels of C reactive protein but not with less severe joint inflammation: a cross-sectional study in early RA and healthy volunteers. Alcohols 16-23 C-reactive protein Homo sapiens 59-77 29479472-7 2018 Association between C reactive protein (CRP) level and alcohol was studied in 1070 newly presenting patients with RA. Alcohols 55-62 C-reactive protein Homo sapiens 20-38 29479472-7 2018 Association between C reactive protein (CRP) level and alcohol was studied in 1070 newly presenting patients with RA. Alcohols 55-62 C-reactive protein Homo sapiens 40-43 29479472-9 2018 A J-shaped curve was observed in the association between alcohol consumption and CRP level, with the lowest levels in patients consuming 1-7 drinks/week (P=0.037). Alcohols 57-64 C-reactive protein Homo sapiens 81-84 29479472-10 2018 Conclusion: Despite the fact that moderate alcohol consumption has been shown protective against RA, and our data confirm a J-shaped association of alcohol consumption with CRP levels in RA, alcohol was not associated with the severity of joint inflammation. Alcohols 148-155 C-reactive protein Homo sapiens 173-176 29479472-10 2018 Conclusion: Despite the fact that moderate alcohol consumption has been shown protective against RA, and our data confirm a J-shaped association of alcohol consumption with CRP levels in RA, alcohol was not associated with the severity of joint inflammation. Alcohols 148-155 C-reactive protein Homo sapiens 173-176 27496931-4 2016 OBJECTIVE: this study aims to elucidate a possible mechanism - CRP modulation - by which moderate alcohol consumption may protect against frailty. Alcohols 98-105 C-reactive protein Homo sapiens 63-66 27496931-11 2016 RESULTS: results from structural equation modelling support the hypothesised model that moderate alcohol use is associated with less frailty and lower CRP levels. Alcohols 97-104 C-reactive protein Homo sapiens 151-154 27496931-12 2016 Furthermore, the indirect relationship from moderate alcohol use to frailty through CRP was statistically significant. Alcohols 53-60 C-reactive protein Homo sapiens 84-87 27496931-13 2016 CONCLUSIONS: overall findings suggest that inflammation measured by CRP is one mechanism by which moderate alcohol use may confer protective effects for frailty. Alcohols 107-114 C-reactive protein Homo sapiens 68-71 24099969-2 2013 OBJECTIVE: To test the concurrent and predictive relations between C-reactive protein (CRP) and use and abuse of alcohol, nicotine and cannabis in a longitudinal, population sample of adolescents and young adults, at the period of highest increase in drug use. Alcohols 113-120 C-reactive protein Homo sapiens 67-85 26969644-0 2016 Associations of cigarette smoking, betel quid chewing and alcohol consumption with high-sensitivity C-reactive protein in early radiographic knee osteoarthritis: a cross-sectional study. Alcohols 58-65 C-reactive protein Homo sapiens 100-118 25712819-9 2015 RESULTS: In men, CRP levels had significant associations with depressive symptoms before (beta=0.420, p=0.010) and after (beta=0.336, p=0.025) adjusting for age, body mass index, systolic blood pressure, number of comorbidities, smoking status, alcohol intake, marital status, education and sleep duration. Alcohols 245-252 C-reactive protein Homo sapiens 17-20 23607539-1 2014 We describe a case of serum amyloid A (SAA) and C-reactive protein (CRP) positive nodule detected by immunohistochemical analysis in a 37-year-old woman with alcohol-related cirrhosis. Alcohols 158-165 C-reactive protein Homo sapiens 48-66 23607539-1 2014 We describe a case of serum amyloid A (SAA) and C-reactive protein (CRP) positive nodule detected by immunohistochemical analysis in a 37-year-old woman with alcohol-related cirrhosis. Alcohols 158-165 C-reactive protein Homo sapiens 68-71 26209440-6 2015 RESULTS: Hemoglobin, hematocrit, and serum C-reactive protein level measured after admission for 24 h were significantly higher in the alcohol group than in the biliary group. Alcohols 135-142 C-reactive protein Homo sapiens 43-61 26339617-5 2015 Additionally CRP and Alb levels were found significantly associated with overall survival in univariate analysis (log-rank test, P < 0.001 and P = 0.002, resp.) and CRP remained significant after controlling for age, alcohol, performance status, and TNM stage, whereas albumin showed a borderline effect on the hazard rate (P = 0.052). Alcohols 220-227 C-reactive protein Homo sapiens 13-16 26339617-5 2015 Additionally CRP and Alb levels were found significantly associated with overall survival in univariate analysis (log-rank test, P < 0.001 and P = 0.002, resp.) and CRP remained significant after controlling for age, alcohol, performance status, and TNM stage, whereas albumin showed a borderline effect on the hazard rate (P = 0.052). Alcohols 220-227 C-reactive protein Homo sapiens 168-171 24827394-0 2014 Acute alcohol exposure has an independent impact on C-reactive protein levels, neutrophil CD64 expression, and subsets of circulating white blood cells differentiated by flow cytometry in nontrauma patients. Alcohols 6-13 C-reactive protein Homo sapiens 52-70 24827394-4 2014 After multiple regression analysis, alcohol exposure remained independently associated with values of CRP, neutrophils CD4 indexes, cytotoxic and noncytotoxic T lymphocytes, and CD16-negative and -positive monocytes. Alcohols 36-43 C-reactive protein Homo sapiens 102-105 24099969-2 2013 OBJECTIVE: To test the concurrent and predictive relations between C-reactive protein (CRP) and use and abuse of alcohol, nicotine and cannabis in a longitudinal, population sample of adolescents and young adults, at the period of highest increase in drug use. Alcohols 113-120 C-reactive protein Homo sapiens 87-90 24099969-6 2013 RESULTS: CRP levels were higher in the presence of nicotine, alcohol, and cannabis use and nicotine dependence. Alcohols 61-68 C-reactive protein Homo sapiens 9-12 24099969-9 2013 CONCLUSIONS: The inter-relationship of CRP and substance abuse has implications for the later health risks associated with early drug and alcohol use and abuse. Alcohols 138-145 C-reactive protein Homo sapiens 39-42 23541381-1 2013 Light to moderate alcohol consumption and leisure time physical activity (LTPA) are independently associated with lower levels of high sensitivity C-reactive protein (CRP), a predictor of cardiometabolic risk. Alcohols 18-25 C-reactive protein Homo sapiens 147-165 24378001-4 2013 RESULTS: After adjusting for sex, age, blood pressure, cigarette smoking, alcohol drinking and so on, data showed that both rs1800206 and rs9794 were associated with the changes along with the levels of CRP (P < 0.05). Alcohols 74-81 C-reactive protein Homo sapiens 203-206 22831953-6 2013 Multiple linear regression models were used to predict CRP change based on other risk factor changes, controlling for age, race, alcohol intake, and hormone replacement therapy. Alcohols 129-136 C-reactive protein Homo sapiens 55-58 23793744-7 2013 A higher degree of systemic inflammation, reflected by the ESR and CRP level, was associated with a smaller proportion of patients consuming alcohol. Alcohols 141-148 C-reactive protein Homo sapiens 67-70 24044608-6 2013 RESULTS: Observed results indicated that the CRP and SAA levels in HIV-positive subjects who are METH, cocaine and alcohol users were significantly higher when compared with either drugs of abuse or HIV-positive alone. Alcohols 115-122 C-reactive protein Homo sapiens 45-48 23541381-1 2013 Light to moderate alcohol consumption and leisure time physical activity (LTPA) are independently associated with lower levels of high sensitivity C-reactive protein (CRP), a predictor of cardiometabolic risk. Alcohols 18-25 C-reactive protein Homo sapiens 167-170 23541381-10 2013 Similarly, depression interacted with alcohol consumption in predicting CRP in men but not women (F=5.03, p<.008) such that for men light to moderate alcohol consumption was associated with lower CRP but only among those with decreased depressive symptoms. Alcohols 38-45 C-reactive protein Homo sapiens 72-75 23541381-10 2013 Similarly, depression interacted with alcohol consumption in predicting CRP in men but not women (F=5.03, p<.008) such that for men light to moderate alcohol consumption was associated with lower CRP but only among those with decreased depressive symptoms. Alcohols 153-160 C-reactive protein Homo sapiens 72-75 23541381-10 2013 Similarly, depression interacted with alcohol consumption in predicting CRP in men but not women (F=5.03, p<.008) such that for men light to moderate alcohol consumption was associated with lower CRP but only among those with decreased depressive symptoms. Alcohols 153-160 C-reactive protein Homo sapiens 199-202 21111583-7 2012 Obesity, weight gain, cigarette smoking and alcohol intake were positively associated with high CRP levels, while physical activity and a dietary pattern with high consumption of fruit were inversely related to high CRP levels. Alcohols 44-51 C-reactive protein Homo sapiens 96-99 21769439-8 2012 CRP level was significantly higher in subjects with T2D than those without (p = 0.023), and this result persisted even after adjustment for age, gender, BMI, smoking, and alcohol consumption. Alcohols 171-178 C-reactive protein Homo sapiens 0-3 23456822-6 2013 In analyses adjusted for age, race/ethnicity, diabetes, menopause transition stage, body mass index, smoking, alcohol use, physical activity, medications, prior fracture, and study site, CRP was associated inversely with each composite strength index (0.035-0.041 SD decrement per doubling of CRP, all p < 0.001), but not associated with femoral neck or lumbar spine BMD. Alcohols 110-117 C-reactive protein Homo sapiens 187-190 23727640-8 2013 After adjustment for age, BMI, smoking status, and alcohol intake, dose-response relationships were observed between gamma-GTP and CRP levels in both overweight and non-overweight men. Alcohols 51-58 C-reactive protein Homo sapiens 131-134 22614460-2 2012 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. Alcohols 271-278 C-reactive protein Homo sapiens 44-47 22824238-11 2012 Alcohol consumption was associated with lower CRP (P = 0.05) and ESR (P = 0.003) but did not influence IR or Ig levels. Alcohols 0-7 C-reactive protein Homo sapiens 46-49 21111583-11 2012 Obesity, smoking and alcohol intake were associated with high CRP, a biomarker of low-grade inflammation in middle-aged men, while a dietary pattern rich in fruit and high physical activity were inversely associated with the prevalence of high CRP. Alcohols 21-28 C-reactive protein Homo sapiens 62-65 22868815-7 2012 High-sensitivity C-reactive protein concentrations were lowest in men with a moderate intake of alcohol (<30 mL/day). Alcohols 96-103 C-reactive protein Homo sapiens 17-35 21726166-5 2011 Negative relations of CRP with both total and direct bilirubin were found after adjustment of age, body mass index, hypertension, diabetes, hypercholesterolemia, cardiovascular disease, taking aspirin, smoking, alcohol drinking and regular exercise and total bilirubin or direct bilirubin. Alcohols 211-218 C-reactive protein Homo sapiens 22-25 22153549-6 2012 For both sexes, CRP increased as the number of MS components increased (p=0.015 for men and p<0.001) after adjustment for age, smoking, alcohol intake and, for women, menopause. Alcohols 139-146 C-reactive protein Homo sapiens 16-19 19803417-3 2009 Epidemiological studies have revealed demographic and socioeconomic factors that associate with CRP concentration; these include age, sex, birth weight, ethnicity, socioeconomic status, body mass index (BMI), fiber consumption, alcohol intake, and dietary fatty acids. Alcohols 228-235 C-reactive protein Homo sapiens 96-99 21267537-6 2011 RESULTS: Elevated high sensitivity CRP (hsCRP) levels were found to be associated with prediabetes after adjusting for age, sex, race-ethnicity, education, smoking, alcohol consumption, hypertension, BMI and total cholesterol. Alcohols 165-172 C-reactive protein Homo sapiens 35-38 20011938-10 2009 Moderate alcohol consumption appeared as a protective factor for CRP elevation (p =0.029). Alcohols 9-16 C-reactive protein Homo sapiens 65-68 19486653-6 2009 The relationship of parental education with CRP in women persisted on multivariable adjustment for both lifestyle risk factors (smoking, alcohol consumption, sleep, exercise, body mass index) and individual SES. Alcohols 137-144 C-reactive protein Homo sapiens 44-47 19318443-7 2009 This positive association between CRP and diabetes risk did not change when participants were stratified by age group, smoking status, level of obesity, alcohol drinking habit, or family history of diabetes. Alcohols 153-160 C-reactive protein Homo sapiens 34-37 19116941-6 2009 After adjustment for sex, age, BMI, education, alcohol consumption, smoking, hypertension status, recreational physical activity and occupational physical activity, the ORs across quartiles of CRP were 1.00, 1.43, 2.14 and 2.29 for IFG (P for trend: 0.025) and 1.00, 1.85, 2.32 and 2.79 for IGT (P for trend: 0.012). Alcohols 47-54 C-reactive protein Homo sapiens 193-196 19339014-6 2009 After adjustments for age, sex, acute infection and chronic inflammatory conditions, very high CRP was associated with lower social position, depressive symptoms, physical inactivity, smoking, and alcohol abstinence. Alcohols 197-204 C-reactive protein Homo sapiens 95-98 19138871-4 2009 METHODS: In cross-sectional analysis, multivariable linear regression with adjustment for age, BMI, smoking status, alcohol intake, and nutritional factors was used to relate log CRP, the independent variable, to IGF-I and IGFBP-3 in a sample of black (n=364) and white men (n=486) separately by race. Alcohols 116-123 C-reactive protein Homo sapiens 179-182 19032692-6 2008 There was a positive association between CRP levels and AMS scores over time (r = 0.22; P < 0.001), while adjusting for smoking, alcohol use, age, and body mass index. Alcohols 132-139 C-reactive protein Homo sapiens 41-44 17392546-5 2007 RESULTS: After adjustment for age and survey and lifestyle factors including smoking, alcohol intake, and physical activity, elevated concentrations of CRP showed a considerably stronger association with risk of type 2 diabetes in women (hazard ratio comparing tertile extremes 7.60 [95% CI 4.43-13.04]) than in men (1.84 [1.27-2.67]). Alcohols 86-93 C-reactive protein Homo sapiens 152-155 18372583-4 2008 METHODS AND RESULTS: The association between alcohol consumption and concentrations of high sensitivity C-reactive protein (hs-CRP) and fibrinogen were investigated. Alcohols 45-52 C-reactive protein Homo sapiens 104-122 18545810-9 2008 Significant associations between C-reactive protein levels were observed with age, socioeconomic indicators, obesity status, smoking, fat and alcohol intake, and minor psychiatric disorder. Alcohols 142-149 C-reactive protein Homo sapiens 33-51 17980786-6 2007 Alcohol-induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, endothelin-1, adhesion molecules, tumor necrosis factor alpha, interleukin-6, C-reactive protein, and haemostatic factors. Alcohols 0-7 C-reactive protein Homo sapiens 221-239 17137657-1 2007 The association between alcohol consumption and CRP was evaluated in a longitudinal study among 72 middle aged adults for whom 572 repeated measurements of CRP were obtained. Alcohols 24-31 C-reactive protein Homo sapiens 48-51 17137657-4 2007 Average alcohol consumption during the last 12 months showed a clear U-shaped relationship with CRP-levels, with lowest levels found for moderate alcohol consumption of less than 16 g/day. Alcohols 8-15 C-reactive protein Homo sapiens 96-99 17137657-4 2007 Average alcohol consumption during the last 12 months showed a clear U-shaped relationship with CRP-levels, with lowest levels found for moderate alcohol consumption of less than 16 g/day. Alcohols 146-153 C-reactive protein Homo sapiens 96-99 17696726-4 2007 Moderate alcohol consumption and high physical activity have been associated with low levels of hs-CRP, but the evidence in these cases is not conclusive. Alcohols 9-16 C-reactive protein Homo sapiens 99-102 16952410-7 2007 After adjusting for age, sex, BMI, baseline glucose regulation status, total cholesterol, urine albumin to creatinine ratio, systolic blood pressure, smoking and alcohol drinking, the association between diabetes and CRP remained significant, with a hazard ratio of 1.23 (95% confidence interval (CI) 1.05, 1.45) corresponding to a doubling in CRP values. Alcohols 162-169 C-reactive protein Homo sapiens 217-220 16614110-6 2006 The odds ratio of colorectal cancer for plasma C-reactive protein was estimated using a conditional logistic regression model adjusted for pack-years of smoking, body mass index, alcohol consumption, physical exercise, and family history of colorectal cancer. Alcohols 179-186 C-reactive protein Homo sapiens 47-65 16678922-7 2007 RESULTS: In both genders, we observed inverse associations between estimated VO2max and levels of CRP after controlling for age, race, body mass index category, hypertension, diabetes, smoking status, alcohol consumption, and use of medications including aspirin, non-steroidal anti-inflammatory drugs, steroid, lipid-lowering agents, antimicrobials, or estrogen/progesterone (in women). Alcohols 201-208 C-reactive protein Homo sapiens 98-101 17477779-3 2007 Thus we conducted a population-based cross-sectional study to examine the associations of CRP levels with CRP C1444T polymorphism and two cytokine polymorphisms (IL-1B C-31T and TNF-A T-1031C), according to sex, age, smoking, alcohol, and BMI, in a total of 489 Japanese health checkup examinees (156 males and 333 females). Alcohols 226-233 C-reactive protein Homo sapiens 90-93 17116715-6 2006 Men who consumed >or=15.2 g of alcohol/d (4th quartile of the distribution) were younger (P < 0.001), had elevated plasma HDL-C concentrations (P < 0.001), and lower plasma concentrations of insulin (P = 0.01), CRP (P = 0.01), and fibrinogen (P < 0.001) than men in the 1st quartile (<1.3 g of alcohol/d). Alcohols 34-41 C-reactive protein Homo sapiens 220-223 16386256-0 2006 C-reactive protein and alcohol consumption: Is there a U-shaped association? Alcohols 23-30 C-reactive protein Homo sapiens 0-18 16671874-5 2006 RESULTS: The mean (+/- SE) CRP level was 65% higher (95% confidence interval: -2%, 180%; P = 0.06) in women with periodontitis (2.46 +/- 0.52 mg/l) than in controls (1.49 +/- 0.22 mg/l), adjusting for factors related to CRP levels, including age, race/ethnicity, pre-pregnancy body mass index, alcohol intake, education, income, and gestational age at blood collection. Alcohols 294-301 C-reactive protein Homo sapiens 27-30 16563907-6 2006 Multivariate adjusted analyses indicated that social integration was significantly inversely associated with CRP concentration in men after adjusting for age, race/ethnicity, smoking, alcohol consumption, physical activity, body mass index, cardiovascular disease, other major or chronic conditions, physical functioning, socioeconomic status, and depression (odds ratio 2.23, 95% confidence interval 1.05 to 4.76, for elevated CRP [>3.19 mg/L] in the least socially integrated quartile vs the most socially integrated quartile). Alcohols 184-191 C-reactive protein Homo sapiens 109-112 17110470-10 2007 These associations were also apparent in participants who consumed < or = 20 g/day of alcohol and those with normal weight, with values of alanine aminotransferase within reference intervals, or with C-reactive protein < 3.0 mg/L, and participants without metabolic syndrome. Alcohols 89-96 C-reactive protein Homo sapiens 203-221 16020877-6 2005 Although the adjustment for body mass index in addition to age, cigarette smoking, and alcohol consumption attenuated the associations between CRP and fasting insulin, fasting glucose, and HOMA-IR, elevated CRP levels were associated with increased insulin levels and HOMA-IR in both sexes. Alcohols 87-94 C-reactive protein Homo sapiens 143-146 15883967-8 2005 Higher CRP levels, correlated to smoking and, inversely, to alcohol intake, identify a further 12% of the cohort at higher cardiovascular risk. Alcohols 60-67 C-reactive protein Homo sapiens 7-10 16257350-11 2005 Alcohol intake-related reduced risk for restriction was associated with lower risk of CHF, diabetes, obesity, and lower markers of inflammation (white blood cell, fibrinogen, and C-reactive protein) consistent with less lung congestion, external restriction, and/or lung inflammation. Alcohols 0-7 C-reactive protein Homo sapiens 179-197 15184288-8 2004 Light-to-moderate alcohol consumers and nonusers of hormone replacement therapy (HRT) had lower CRP levels than abstainers and HRT users, respectively. Alcohols 18-25 C-reactive protein Homo sapiens 96-99 15780504-7 2005 Moderate alcohol intake is associated with reduced serum PTH as well as decreased levels of CRP and fibrinogen; conceivably, modulation of PTH mediates, at least in part, the favorable impact of moderate drinking on the acute phase reactants. Alcohols 9-16 C-reactive protein Homo sapiens 92-95 15571824-6 2004 Self-reported moderate daily alcohol intake up to 40 g was associated with lower concentrations of CRP, fibrinogen, PV and WBC count, compared to non-drinking and heavy drinking, even after adjustment for various potential confounders. Alcohols 29-36 C-reactive protein Homo sapiens 99-102 15208162-0 2004 Alcohol misuse increases serum antibodies to oxidized LDL and C-reactive protein. Alcohols 0-7 C-reactive protein Homo sapiens 62-80 15208162-1 2004 AIMS: To clarify the relationship of alcohol consumption with serum antibodies to oxidized low-density lipoprotein (oxLDL) and the inflammation marker C-reactive protein (CRP). Alcohols 37-44 C-reactive protein Homo sapiens 171-174 15521602-5 2004 In the above mentioned groups, alcohol and CNS acting agents increased CRP values in over 33% of the patients, whereas in the case of patients under the influence of cardiac drugs or carbon monoxide, the same effect was observed in more than 16% of the cases. Alcohols 31-38 C-reactive protein Homo sapiens 71-74 15117839-9 2004 The association between leptin and CRP was significant even after adjustment for age, BMI, waist-to-hip ratio, smoking, and alcohol consumption in women (F=7.13, P=0.01) and men (F=5.69, P=0.02). Alcohols 124-131 C-reactive protein Homo sapiens 35-38 15177126-6 2004 The relation of alcohol use and CRP levels was significantly modified by apoE genotype (P interaction 0.03), with a positive association among participants with an apoE4 allele (P = 0.05), but a trend toward an inverse association among those without an apoE4 allele (P = 0.15). Alcohols 16-23 C-reactive protein Homo sapiens 32-35 14769682-6 2004 After adjustment for age, race, smoking status, history of diabetes, history of cardiovascular disease, physical activity, high-density lipoprotein cholesterol, antiinflammatory medications, statins, and total fat mass, alcohol intake showed a J-shaped relationship with mean IL-6 (P for quadratic term <0.001) and CRP (P=0.014) levels. Alcohols 220-227 C-reactive protein Homo sapiens 318-321 14769682-10 2004 CONCLUSIONS: In well-functioning older persons, light alcohol consumption is associated with lower levels of IL-6 and CRP. Alcohols 54-61 C-reactive protein Homo sapiens 118-121 14525675-7 2003 Alcohol lowers CRP, but the mechanism is unknown. Alcohols 0-7 C-reactive protein Homo sapiens 15-18 14669152-8 2003 Gender significantly interacted with WC to predict CRP after adjusting for age, smoking status, alcohol, and BMI (P <.05). Alcohols 96-103 C-reactive protein Homo sapiens 51-54 14663297-6 2003 RESULTS: Multivariate analysis, after controlling for several potential confounders, revealed a J-shaped association between alcohol intake (none, 1-2, 3-4, 5+ wine glasses/day) and uric acid, C-reactive protein, homocysteine, fibrinogen, triglycerides, apolipoproteins A1 and B, HDL and total cholesterols, blood glucose levels, leucocyte count and arterial blood pressure levels (only in males). Alcohols 125-132 C-reactive protein Homo sapiens 193-278 12551869-2 2003 However, data evaluating the relationship between C-reactive protein (CRP), a predictor of cardiovascular risk, and alcohol consumption are sparse. Alcohols 116-123 C-reactive protein Homo sapiens 50-68 12831831-4 2003 CRP concentration was greater in lower compared with higher SES participants (1.18+/-0.75 vs. 0.75+/-0.8 mg/l,p=.002) independently of sex, age, body mass, waist/hip ratio, smoking, alcohol, and season of the year. Alcohols 182-189 C-reactive protein Homo sapiens 0-3 12551869-2 2003 However, data evaluating the relationship between C-reactive protein (CRP), a predictor of cardiovascular risk, and alcohol consumption are sparse. Alcohols 116-123 C-reactive protein Homo sapiens 70-73 12551869-3 2003 METHODS AND RESULTS: The relationship between alcohol consumption and CRP was evaluated in a cross-sectional survey and over time among 1732 men and 1101 women participating in the Pravastatin Inflammation/CRP Evaluation Study. Alcohols 46-53 C-reactive protein Homo sapiens 70-73 12551869-6 2003 In multivariate analysis, the relationship between alcohol consumption and CRP remained significant after controlling for multiple traditional cardiovascular risk factors. Alcohols 51-58 C-reactive protein Homo sapiens 75-78 12551869-8 2003 CONCLUSION: Moderate alcohol consumption was associated with lower CRP concentrations than no or occasional alcohol intake, an effect that was independent of alcohol-related effects on lipids. Alcohols 21-28 C-reactive protein Homo sapiens 67-70 12428180-0 2002 Moderate alcohol consumption reduces plasma C-reactive protein and fibrinogen levels; a randomized, diet-controlled intervention study. Alcohols 9-16 C-reactive protein Homo sapiens 44-62 12589876-8 2003 After adjusting for age, cigarette smoking, alcohol consumption, heart rate, and puberty development, children in the fourth quartile CRP subgroups were heavier and had significantly higher body mass index (BMI) and lower HDL-C levels than children with nondetected CRP. Alcohols 44-51 C-reactive protein Homo sapiens 134-137 12428180-1 2002 OBJECTIVE: To evaluate the effect of moderate alcohol consumption on the acute phase proteins C-reactive protein and fibrinogen. Alcohols 46-53 C-reactive protein Homo sapiens 94-112 12428180-11 2002 CONCLUSIONS: Moderate alcohol consumption significantly decreased plasma C-reactive protein and fibrinogen levels. Alcohols 22-29 C-reactive protein Homo sapiens 73-91 11253971-3 2001 METHODS: We investigated the association between alcohol consumption (assessed by a 7-day food record) and concentrations of C-reactive protein (CRP), alpha1-globulins, alpha2-globulins, albumin, and transferrin, and leucocyte count in a sample of 2006 men and women aged 18-88 years participating in a national health survey carried out in former West Germany in 1987-88. Alcohols 49-56 C-reactive protein Homo sapiens 125-143 12463288-0 2002 Relation between alcohol consumption and C-reactive protein levels in the adult US population. Alcohols 17-24 C-reactive protein Homo sapiens 41-59 12463288-3 2002 METHODS: To evaluate the association of alcohol consumption with C-reactive protein, we analyzed the findings of the Third National Health and Nutrition Examination, a population-based survey representing the noninstitutionalized US population. Alcohols 40-47 C-reactive protein Homo sapiens 65-83 12463288-9 2002 CONCLUSIONS: Alcohol consumption is associated with a decreased probability of elevated C-reactive protein levels. Alcohols 13-20 C-reactive protein Homo sapiens 88-106 11253971-5 2001 FINDINGS: Among men, alcohol consumption showed a U-shaped association with mean values of CRP (p for linear term 0.65, for quadratic term 0.048), alpha1-globulins (p=0.20, 0.0006), alpha2-globulins (p=0.82, 0.31), and leucocyte count (p=0.51, 0.26) even after adjustment for age, smoking, body-mass index, HDL and LDL cholesterol, history of hypertension, education, and income. Alcohols 21-28 C-reactive protein Homo sapiens 91-94 11253971-10 2001 In view of the robust association between markers of inflammation, especially CRP, and risk of coronary heart disease, an anti-inflammatory action of alcohol could contribute to the link between moderate consumption and lower cardiovascular mortality. Alcohols 150-157 C-reactive protein Homo sapiens 78-81 8751208-10 1995 CONCLUSIONS: These results suggest that the expression of c-reactive protein but not haptoglobin is upregulated in alcohol-induced acute liver injury. Alcohols 115-122 C-reactive protein Homo sapiens 58-76 8284758-8 1994 In the same 40 patients the 1-week alcohol consumption correlated with the number of positive Ranson criteria (r = 0.40, p < 0.05) and serum CRP concentration (r = 0.37, p < 0.05). Alcohols 35-42 C-reactive protein Homo sapiens 144-147 35338162-11 2022 The high alcohol pattern was associated with high concentrations of circulating concentrations of pro-inflammatory markers (CRP, IL-6, VEGF). Alcohols 9-16 C-reactive protein Homo sapiens 124-127 10449692-7 1999 In multivariate analysis, the relationship between HRT use and CRP remained significant after control for body mass index, age, diabetes, hypertension, hyperlipidemia, alcohol use, and cigarette consumption (P=0.001). Alcohols 168-175 C-reactive protein Homo sapiens 63-66