Original Contributions |
From the Departments of Medicine and Pathology (M.C.) and the Department of Pathology (R.P.T.), University of Vermont, Burlington; the London School of Hygiene and Tropical Medicine, Department of Public Health, London, UK (E.N.M.); the Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle (B.M.P.); the Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pa (L.H.K.) and the Department of Medicine, The Johns Hopkins University, Baltimore, Md (A.S.D.).
Correspondence to Mary Cushman, MD, MSc, Assistant Professor of Medicine, University of Vermont, 55A South Park Drive, Colchester, VT 05446. E-mail mcushman{at}salus.uvm.edu
| Abstract |
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65 years of age.
Subjects were selected from 3393 participants in the fourth year
examination of the Cardiovascular Health Study, an
observational study of vascular disease risk factors. After excluding
women with vascular disease, we compared levels of inflammation and
hemostasis variables in the 230 women using unopposed estrogen and
60 using estrogen/progestin, with those of 196 nonusers
selected as controls. Compared with nonusers, unopposed
estrogen use was associated with 59% higher mean C-reactive protein
(P<0.001), but with modestly lower levels of other
inflammation indicators, fibrinogen, and alpha-1 acid
glycoprotein (P<0.001). Factor VIIc was
16% higher among estrogen users (P<0.001), but this
was not associated with higher thrombin production (prothrombin
fragment 1-2), or increased fibrin breakdown (D-dimer). Concentration
of plasminogen activator
inhibitor-1 was 50% lower in both using groups
(P<0.001) compared with nonusers, and this was
associated with higher plasmin-antiplasmin complex: 8% higher in
estrogen and 18% higher in estrogen/progestin users
(P<0.05). Relationships between the markers and hormone
use were less pronounced in estrogen/progestin users, with no
association for C-reactive protein except in women in upper 2 tertiles
of body mass index (P for interaction, 0.02). The
direction and strength of the associations of HRT use with inflammation
markers differed depending on the protein, so it is not clear whether
HRT confers coronary risk reduction through an
inflammation-sensitive mechanism. Associations with hemostasis markers
indicated no association with evidence of procoagulation and a possible
association with increased fibrinolytic activity.
Key Words: blood coagulation inflammation hormone replacement therapy elderly women
| Introduction |
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C-reactive protein, fibrinogen, albumin, and alpha-1 acid glycoprotein are hepatically-derived acute phase reactant proteins.10 At concentrations below those indicative of clinical inflammation, C-reactive protein was associated with future coronary events in studies of those with unstable or stable angina,11 healthy middle-aged men and women,12 13 and healthy elderly men and women.14 Fibrinogen, a marker of inflammation and coagulation, predicted coronary events,15 and levels declined with HRT.9 Low albumin predicted coronary risk in several studies,16 17 18 19 and this was more prominent in women in 2 studies.17 19 Potential biological roles for albumin include enhanced fibrinolytic function,20 vasodilation, antioxidant effects, and reduced platelet aggregability.21 Alpha-1 acid glycoprotein has not been widely studied, and was not associated with increased coronary risk in the all-male MRFIT study.18 However, because alpha-1 acid glycoprotein is regulated by similar cytokines as C-reactive protein during the acute phase response, its relationship to HRT is of interest. The relationship between inflammation markers and atherosclerosis is not understood at this time. The association may be related to arterial wall inflammation due to preclinical atherosclerosis, low grade infections, genetic, or unknown environmental factors. Defining the relationship between HRT and these markers may provide useful information concerning modification of cardiovascular disease (CVD) risk by HRT.
We studied cross-sectional associations of estrogen use with markers of inflammation in female participants of the Cardiovascular Health Study, a cohort study of risk factors for CVD in 5888 free-living men and women age 65 and over. Women with clinical vascular disease were excluded to minimize confounding by disease on the markers.22 Coagulation and fibrinolysis markers, some which have been previously reported in prospective studies of hormone use,23 24 25 were also studied to (1) extend previous findings to an older age group and (2) simultaneously study a number of related markers.
| Methods |
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Women were excluded from analysis if they had a history of clinical vascular disease, were taking warfarin or transdermal estrogen, or did not have a plasma sample available from the 1992 to 1993 examination. All hormone users remaining were studied. History of clinical vascular disease was defined in the following 3 ways: (1) baseline presence of cardiovascular, cerebrovascular, or peripheral vascular disease using previously published criteria28 ; (2) incident vascular disease events identified between the baseline and 1992 to 1993 examination years, and adjudicated by committee29 ; and (3) discovery, during adjudication of incident events, of the presence of previously unknown prestudy vascular diagnoses. Women were divided into the following 3 exposure groups: 230 taking unopposed estrogen, 60 taking estrogen with progestin, and a comparison group of 196 women randomly selected from the remaining women not currently using hormones and frequency matched with estrogen-takers on 5-year age strata, clinic site, and race.
Definitions
Hormone use was established by medication inventory. Past use
and duration of current or past use, hysterectomy and oophorectomy
status, pregnancy history, smoking status, and alcohol use (drinks per
week) were established by interview. Osteoporosis was defined by the
question, "Has a doctor told you that you currently have
osteoporosis?" Blood pressure, ankle-brachial index, waist-hip ratio,
and body mass index were measured as previously
reported.26 Hypertension was defined as absent, borderline
(systolic pressure 140 to 160 mm Hg or
diastolic pressure 90 to 95 mm Hg), or definite
(systolic pressure >160 mm Hg or diastolic
>95 mm Hg, or self-reported hypertension in association with use
of antihypertensive medication). Diabetes was defined as fasting
glucose >140 mg/dL or use of insulin or oral hypoglycemic agents.
Physical activity was defined as the weekly kilocalories of energy
expenditure as measured by questionnaire.26
Laboratory Analyses
A fasting morning blood sample was collected with minimal stasis
as previously described.30 C-reactive protein and alpha-1
acid glycoprotein were measured by
colorimetric competitive immunoassays (C-reactive
protein antibodies and antigens from Calbiochem) with respective
coefficients of variation (CVs) of 4.8% and 14.2%.31
Plasminogen activator inhibitor-1
(PAI-1) antigen was measured by a sandwich immunoassay.32
Prothrombin fragment 1-2 (Baxter-Dade), fibrin fragment D-dimer, and
plasmin-antiplasmin complex (PAP) were measured by enzyme-linked
immunosorbent assays.33 34 The respective CVs for values
in the range of our results were 11.8%, 10.1%, 18.5%, and 4.2%.
Lipid levels, blood cell counts, albumin, fibrinogen, and
factor VIIc were measured as previously described.30
Statistical Analysis
SPSS 6.1.3 was used for data analysis, using the CHS
database from the 1992 to 1993 examination, updated October 3, 1996.
Baseline characteristics between study groups were compared using
2 tests or Fisher's exact test for
categorical data and t tests for continuous data. Log
transformation was done when necessary to achieve gaussian
distributions. Because many biomarkers had skewed distributions, crude
associations between hormone use and the markers were determined by the
Wilcoxon rank sum test. To assess the independence of
relationships between hormone use and the markers, multivariable
linear models were developed using each marker (untransformed for
simplicity of interpretation) as the dependent variable, with
hormone use status forced into the model and covariates entered in
stepwise fashion (P value for entry 0.10, for removal 0.15).
Including only blacks and whites, interaction by race was assessed
(there were too few subjects of other races). Because it has been
suggested that relationships between HRT and hemostasis are explained
in large part by obesity,35 interaction by body mass
index was assessed. In this hypothesis-generating analysis, we
set the statistical significance level for all analyses at
0.05.
| Results |
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Characteristics of the HRT use groups are shown in Table 1
, and were similar to results from the
baseline CHS examination.27 There were 17 estrogen users
and 2 combined therapy users (mean age 73.9) without available blood
samples; 2 of 19 (11%) had diabetes and 9 of 19 (47%) had
hypertension. Characteristics of unopposed estrogen versus combined
estrogen-progestin users were similar, but estrogen users had a longer
duration of use, and a much higher prevalence of hysterectomy and
oophorectomy. Compared with nonusers, users of either estrogen
or combined therapy had lower body size, higher income, younger age at
menopause, and were more likely to have had hysterectomy, oophorectomy,
and osteoporosis. Lipid levels were more favorable in users, with HDL
levels similar in estrogen compared with combined therapy users. There
were 10 users and 5 nonusers taking regular aspirin, and there
were 19 users and 18 nonusers taking lipid-lowering drugs. More
women in both using groups reported hormone use for osteoporosis
prevention (206 of 285, 72%) than for coronary disease
prevention (50 of 271, 19%). There were no differences between users
and nonusers in the other factors shown in Table 1
.
|
Table 2
shows levels of the study
variables in the 3 exposure groups. The largest difference between
users and nonusers was for C-reactive protein, with 59% higher
median C-reactive protein levels in estrogen users than
nonusers (3.49 mg/L versus 2.20 mg/L). Median C-reactive
protein in estrogen/progestin users was similar to nonusers
(2.41 mg/L). For albumin the difference also suggested
increased inflammation in users. Fibrinogen and alpha 1-acid
glycoprotein were lower in both groups of users compared
with nonusers, but the fibrinogen difference was not
significant in combined therapy users. For all 3 latter analytes
representing inflammation, the magnitudes of the
differences between users and nonusers were much smaller (3%
to 17%) than for C-reactive protein.
|
In unopposed estrogen and combined therapy users, median PAI-1 levels were lower than nonusers by 48% and 56% respectively, with respective values of 14 ng/mL and 12 ng/mL, compared with 27 ng/mL in nonusers. This was associated with less PAI-1-mediated plasmin suppression, measured as higher PAP, by 8% and 18%, respectively, in estrogen and combined therapy users (5.4 nmol/L nonusers, 5.9 nmol/L estrogen, 6.4 nmol/L combined therapy). A marker of procoagulant activity and fibrinolytic response, D-dimer, did not differ among the groups. In assessment of procoagulation, estrogen users had 16% higher factor VIIc levels than nonusers (137% versus 118%), and this was not observed in estrogen-progestin users. This difference did not translate to higher thrombin production, as measured by fragment 1-2.
Because preanalytical factors and variability due to minor illness may affect the values of some markers, unusually high values were excluded for all analyses, resulting in no substantial difference in bivariate relationships with hormone use status (data not shown). Additionally, exclusion of women using either regular aspirin or nonsteroidal anti-inflammatory drugs had no effect on results with the exception that the statistical significance of the difference in fibrinogen between combined therapy users and nonusers was improved (P=0.03; data not shown).
In the control group, 67 of 196 (34%) women reported past use of
estrogen for a median duration of 3 years (range 1 month to 34 years).
These past users had lower body mass index and waist-hip ratio, and
higher prevalence of osteoporosis, hysterectomy, and oophorectomy
compared with never users, with levels intermediate between
current and never users (data not shown). Lipid levels and the other
variables in Table 1
were similar between past and never
users (data not shown). Most variables in Table 2
were
similar between past and never users. Levels of C-reactive protein were
slightly higher and PAI-1 slightly lower in past versus never users,
but these differences were not statistically significant. D-dimer level
was lower in past users compared with never users (121 versus 164
µg/L, P=0.01). Exclusion of past users from the control
group did not alter the differences between nonusers and users
for any of the hemostasis and inflammation markers.
For both groups of current hormone users there were no significant relationships between age-adjusted duration of use and levels of the study variables, except for factor VIIc, with a 1.8% absolute increase for every 5 years of current use of unopposed estrogen (P<0.05). For past users in the control group there were no associations of current level of any study analyte to age-adjusted past duration of use.
Comparing women using hormones for
5 years (36 estrogen/16
estrogen/progestin) with the 196 nonusers, relationships were
similar to those in Table 2
with a nonsignificantly lower
C-reactive protein in estrogen/progestin users compared with
nonusers (1.77 versus 2.30 mg/L, P=0.27). Although
PAP was higher in these short-term users, the difference was not
statistically significant. In analysis of the 77 women
reporting unopposed estrogen use for >20 years, there were similar
relationships of study variables compared with nonusers.
These long-term users had higher levels of C-reactive protein (4.20
mg/L), factor VIIc (142%), PAP (6.2 nmol/L), and lower fibrinogen
(2.93 g/L) and alpha-1 acid glycoprotein (571 mg/L) than
the entire group of current estrogen users (see Table 2
for
values).
There were 30 estrogen users and 23 nonusers who were black. Relationships of study variables to use were similar to those in whites, except that black users had higher fibrinogen levels than nonusers (3.62 versus 3.02 g/L, P=0.003), a relationship opposite to that in whites (2.97 g/L users versus 3.17 g/L nonusers, P<0.001; P for race interaction=0.03). Adjusting for confounders (hypertension, LDLc), values were similar but the interaction term was no longer statistically significant (P=0.23). Overall, C-reactive protein concentration was higher in blacks than whites (4.06 versus 2.90 mg/L, P=0.02), with black estrogen users having the highest values: 4.52 mg/L black users versus 3.40 mg/L black nonusers (P=0.41); 3.92 mg/L white users versus 2.18 mg/L white nonusers (P<0.001, P for interaction by race >0.05).
Associations between estrogen use and the study variables, with and
without adjustment for confounders, are shown in Table 3
. The covariates that entered each model
generally reflected lipid status and obesity. Comparing estrogen users
with nonusers, for C-reactive protein and fibrinogen, income
level also remained in the final model. There was mild attenuation of
most relationships after adjustment, but use of unopposed estrogen
remained associated with higher C-reactive protein and factor VIIc and
lower fibrinogen, alpha-1 acid glycoprotein,
albumin, and PAI-1 concentrations. Comparing combined hormone
therapy users to nonusers, relationships between study
variables also persisted after adjustment, except for loss of
statistical significance for lower PAI-1, adjusted for HDLc and body
mass index.
|
In analyses stratified by body mass index, C-reactive protein
was higher with unopposed estrogen in all 3 body mass index tertiles
(Figure 1
). For combined users,
C-reactive protein was higher than nonusers among those in the
second and third BMI tertiles, even though C-reactive protein was not
higher in the overall combined therapy group (P for
interaction=0.02 adjusted for LDL and income). Women in the lowest body
mass index tertile, who were nonusers or on combined therapy,
had the lowest C-reactive protein levels.
|
Figure 2
shows that PAI-1 level also
differed by use status and body mass index (P for
interaction=0.0003 for combined use; 0.04 for estrogen, adjusted for
HDL). Within body mass index tertiles, all using groups had lower PAI-1
levels than nonusers. Nonusers in the highest body mass
index tertile had the highest PAI-1 concentration, and unopposed
estrogen users in the highest tertile had lower PAI-1 level, but only
with a concentration similar to nonusing women in the lowest
tertile.
|
| Discussion |
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Associations of HRT with inflammation differed among the markers with respect to direction, suggesting complexity in inflammation regulation. These differing relationships may be related to differential influences of HRT on transcriptional control, clearance, or cytokine regulation of these proteins. Our results agree with an experimental study of 15 women, where an 18% decline in alpha-1 acid glycoprotein over 4 weeks,36 was observed. Alpha-1 acid glycoprotein and albumin are also lower in pregnancy,37 suggesting decreased synthesis or increased clearance by estrogen.
Our data indicate that hormone use was associated with higher C-reactive protein, a recently recognized vascular risk marker. To our knowledge no other study has assessed C-reactive protein in relation to HRT, using a sensitive assay. Because C-reactive protein is a powerful risk marker, and might influence progression of atherosclerosis, confirmation of our findings is necessary.
Our results suggest any increase of factor VIIc observed with HRT does not translate to a procoagulant tendency, as assessed by the thrombin marker prothrombin 1-2. We previously reported in healthy subjects that factor VIIc level was not cross-sectionally associated with prothrombin 1-2 or fibrinopeptide A, another marker of thrombin.38 Two small prospective crossover studies showed short-term increase of fragment 1-2 on HRT,23 24 and a larger prospective study is indicated.
The relationship between fibrinolysis markers and coronary risk has not been clarified, and few data specific to older women are available. Our results suggest that the large decline of PAI-1 observed experimentally,25 and confirmed here cross-sectionally, translates to a modestly higher plasmin-antiplasmin complex. In different settings, increased plasmin-antiplasmin may be a response to either decreased PAI-1 inhibition, or increased fibrin formation. The differences in PAI-1 and plasmin-antiplasmin by hormone use were not associated with higher D-dimer, suggesting the higher plasmin-antiplasmin reflects the lower PAI-1 concentration. One small randomized study showed a nonsignificant increase of D-dimer with HRT25 and larger studies are warranted to fully understand the significance of fibrinolytic effects of HRT.
Our data support a hypothesis that body mass index, as a measure of obesity, may modify the associations of HRT with PAI-135 and C-reactive protein. Women with the highest body mass index had the greatest difference in PAI-1 between users and nonusers, with lower concentration in users. However, this same group had the highest C-reactive protein level with use. One explanation for these findings relates to evidence that adipocytes synthesize and secrete inflammatory cytokines and PAI-1, and that this secretion is upregulated in obesity.39 In the setting of obesity, it is possible that hormone therapy has effects on both inflammation and fibrinolysis through adipocyte function. Prospective clinical studies and animal model research may clarify these relationships.
The primary limitation of the study is the cross-sectional design. The study shares other limitations with the majority of observational research on HRT; it is possible that healthier women, at lowest risk for CHD, were prescribed estrogen, which might influence results.40 The women studied were long-term users on average, so other health-conscious behaviors were probably more likely in users, although not all our findings suggested beneficial health effects. Multivariate methods were used to attempt to adjust for confounding factors that may relate to these sources of bias. The CHS cohort is healthier than the general elderly population, possibly limiting generalizability. Results are limited by the relatively small number of combined hormone users and the small number of black users, so cautious interpretation of results for those groups is indicated. Findings related to fibrinogen and PAI-1 agree with other prospective studies,9 25 supporting the validity of the remaining new findings; however, prospective randomized trials are required to confirm these findings.
In conclusion, HRT use in older women was associated with differences in newer risk markers that might translate to increased as well as reduced risk of arterial occlusion. Taken together, the findings related to procoagulation and fibrinolysis suggest overall beneficial effects of HRT on hemostatic balance, at doses usually used by older women. Use of HRT may have differential effects on components of the inflammatory response. The influence on vascular disease risk of these differences in relationships of HRT to inflammation markers, especially in light of recent reports,8 13 requires further study. Before specific treatment recommendations may be made on the basis of these new risk markers, effects of therapy on the markers need to be confirmed in ongoing clinical trials. Any effects observed should include assessment of effect modification by obesity and race, and the relationship between changes in markers with therapy and subsequent ischemic events.
| Acknowledgments |
|---|
Received June 25, 1998; accepted October 13, 1998.
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E. Wong, M. Freiberg, R. Tracy, and L. Kuller Epidemiology of Cytokines: The Women On the Move through Activity and Nutrition (WOMAN) Study Am. J. Epidemiol., August 15, 2008; 168(4): 443 - 453. [Abstract] [Full Text] [PDF] |
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J. H. Ix, M. A. Allison, J. O. Denenberg, M. Cushman, and M. H. Criqui Novel cardiovascular risk factors do not completely explain the higher prevalence of peripheral arterial disease among African Americans. The San Diego Population Study. J. Am. Coll. Cardiol., June 17, 2008; 51(24): 2347 - 2354. [Abstract] [Full Text] [PDF] |
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M. E. Wierman and W. M. Kohrt Review Article: Vascular and Metabolic Effects of Sex Steroids: New Insights Into Clinical Trials Reproductive Sciences, May 1, 2007; 14(4): 300 - 314. [Abstract] [PDF] |
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J. I. Barzilay, C. Blaum, T. Moore, Q. Li Xue, C. H. Hirsch, J. D. Walston, and L. P. Fried Insulin Resistance and Inflammation as Precursors of Frailty: The Cardiovascular Health Study Arch Intern Med, April 9, 2007; 167(7): 635 - 641. [Abstract] [Full Text] [PDF] |
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N. S. Jenny, N. D. Yanez, B. M. Psaty, L. H. Kuller, C. H. Hirsch, and R. P. Tracy Inflammation Biomarkers and Near-Term Death in Older Men Am. J. Epidemiol., March 15, 2007; 165(6): 684 - 695. [Abstract] [Full Text] [PDF] |
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C. D. Bushnell, P. Hurn, C. Colton, V. M. Miller, G. del Zoppo, M. S.V. Elkind, B. Stern, D. Herrington, G. Ford-Lynch, P. Gorelick, et al. Advancing the Study of Stroke in Women: Summary and Recommendations for Future Research From an NINDS-Sponsored Multidisciplinary Working Group Stroke, September 1, 2006; 37(9): 2387 - 2399. [Abstract] [Full Text] [PDF] |
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M. A. Albert and P. M Ridker C-Reactive Protein as a Risk Predictor: Do Race/Ethnicity and Gender Make a Difference? Circulation, August 1, 2006; 114(5): e67 - e74. [Full Text] [PDF] |
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K. K. Koh and B.-K. Yoon Controversies regarding hormone therapy: Insights from inflammation and hemostasis Cardiovasc Res, April 1, 2006; 70(1): 22 - 30. [Abstract] [Full Text] [PDF] |
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S. Kathiresan, M. G. Larson, R. S. Vasan, C.-Y. Guo, P. Gona, J. F. Keaney Jr, P. W.F. Wilson, C. Newton-Cheh, S. L. Musone, A. L. Camargo, et al. Contribution of Clinical Correlates and 13 C-Reactive Protein Gene Polymorphisms to Interindividual Variability in Serum C-Reactive Protein Level Circulation, March 21, 2006; 113(11): 1415 - 1423. [Abstract] [Full Text] [PDF] |
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P. W. F. Wilson, B.-H. Nam, M. Pencina, R. B. D'Agostino Sr, E. J. Benjamin, and C. J. O'Donnell C-Reactive Protein and Risk of Cardiovascular Disease in Men and Women From the Framingham Heart Study Arch Intern Med, November 28, 2005; 165(21): 2473 - 2478. [Abstract] [Full Text] [PDF] |
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L. G. Best, Y. Zhang, E. T. Lee, J.-L. Yeh, L. Cowan, V. Palmieri, M. Roman, R. B. Devereux, R. R. Fabsitz, R. P. Tracy, et al. C-Reactive Protein as a Predictor of Cardiovascular Risk in a Population With a High Prevalence of Diabetes: The Strong Heart Study Circulation, August 30, 2005; 112(9): 1289 - 1295. [Abstract] [Full Text] [PDF] |
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S. B. Kritchevsky, M. Cesari, and M. Pahor Inflammatory markers and cardiovascular health in older adults Cardiovasc Res, May 1, 2005; 66(2): 265 - 275. [Abstract] [Full Text] [PDF] |
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L. M. Szymanski, C. M. Kessler, and B. Fernhall Relationship of physical fitness, hormone replacement therapy, and hemostatic risk factors in postmenopausal women J Appl Physiol, April 1, 2005; 98(4): 1341 - 1348. [Abstract] [Full Text] [PDF] |
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P. W.F. Wilson CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Ability of Inflammatory Markers to Predict Disease in Asymptomatic Patients: A Background Paper Circulation, December 21, 2004; 110(25): e568 - e571. [Abstract] [Full Text] [PDF] |
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H. Alexander, A. L. Stegner, C. Wagner-Mann, G. C. Du Bois, S. Alexander, and E. R. Sauter Proteomic Analysis to Identify Breast Cancer Biomarkers in Nipple Aspirate Fluid Clin. Cancer Res., November 15, 2004; 10(22): 7500 - 7510. [Abstract] [Full Text] [PDF] |
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K.-C. Leung, G. Johannsson, G. M. Leong, and K. K. Y. Ho Estrogen Regulation of Growth Hormone Action Endocr. Rev., October 1, 2004; 25(5): 693 - 721. [Abstract] [Full Text] [PDF] |
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K. M. Prestwood, C. Unson, M. Kulldorff, and M. Cushman The Effect of Different Doses of Micronized 17{beta}-Estradiol on C-Reactive Protein, Interleukin-6, and Lipids in Older Women J. Gerontol. A Biol. Sci. Med. Sci., August 1, 2004; 59(8): M827 - M832. [Abstract] [Full Text] [PDF] |
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K. K. Koh, M.-S. Shin, I. Sakuma, J. Y. Ahn, D. K. Jin, H. S. Kim, D. S. Kim, S. H. Han, W.-J. Chung, and E. K. Shin Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women Arterioscler Thromb Vasc Biol, August 1, 2004; 24(8): 1516 - 1521. [Abstract] [Full Text] [PDF] |
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A. D. Pradhan, A. Z. LaCroix, R. D. Langer, M. Trevisan, C. E. Lewis, J. A. Hsia, A. Oberman, J. M. Kotchen, and P. M Ridker Tissue Plasminogen Activator Antigen and D-Dimer as Markers for Atherothrombotic Risk Among Healthy Postmenopausal Women Circulation, July 20, 2004; 110(3): 292 - 300. [Abstract] [Full Text] [PDF] |
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K. K. Koh and I. Sakuma Should Progestins Be Blamed for the Failure of Hormone Replacement Therapy to Reduce Cardiovascular Events in Randomized Controlled Trials? Arterioscler Thromb Vasc Biol, July 1, 2004; 24(7): 1171 - 1179. [Abstract] [Full Text] [PDF] |
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R. V. Milani, C. J. Lavie, and M. R. Mehra Reduction in C-reactive protein through cardiac rehabilitation and exercise training J. Am. Coll. Cardiol., March 17, 2004; 43(6): 1056 - 1061. [Abstract] [Full Text] [PDF] |
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B. L. Stauffer, G. L. Hoetzer, D. T. Smith, and C. A. DeSouza Plasma C-reactive protein is not elevated in physically active postmenopausal women taking hormone replacement therapy J Appl Physiol, January 1, 2004; 96(1): 143 - 148. [Abstract] [Full Text] [PDF] |
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J. E. Manson, J. Hsia, K. C. Johnson, J. E. Rossouw, A. R. Assaf, N. L. Lasser, M. Trevisan, H. R. Black, S. R. Heckbert, R. Detrano, et al. Estrogen plus Progestin and the Risk of Coronary Heart Disease N. Engl. J. Med., August 7, 2003; 349(6): 523 - 534. [Abstract] [Full Text] [PDF] |
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T. B. Ledue and N. Rifai Preanalytic and Analytic Sources of Variations in C-reactive Protein Measurement: Implications for Cardiovascular Disease Risk Assessment Clin. Chem., August 1, 2003; 49(8): 1258 - 1271. [Abstract] [Full Text] [PDF] |
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M. A. Albert, R. J. Glynn, and P. M Ridker Plasma Concentration of C-Reactive Protein and the Calculated Framingham Coronary Heart Disease Risk Score Circulation, July 15, 2003; 108(2): 161 - 165. [Abstract] [Full Text] [PDF] |
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M. Yilmazer, V. Fenkci, S. Fenkci, O. Aktepe, M. Sonmezer, and G. Kurtay Association of serum complement (C3, C4) and immunoglobulin (IgG, IgM) levels with hormone replacement therapy in healthy post-menopausal women Hum. Reprod., July 1, 2003; 18(7): 1531 - 1535. [Abstract] [Full Text] [PDF] |
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S. Fenkci, V. Fenkci, M. Yilmazer, M. Serteser, and T. Koken Effects of short-term transdermal hormone replacement therapy on glycaemic control, lipid metabolism, C-reactive protein and proteinuria in postmenopausal women with type 2 diabetes or hypertension Hum. Reprod., April 1, 2003; 18(4): 866 - 870. [Abstract] [Full Text] [PDF] |
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P. D. Hurn and L. M. Brass Estrogen and Stroke: A Balanced Analysis Stroke, February 1, 2003; 34(2): 338 - 341. [Full Text] [PDF] |
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C. R. Isasi, R. J. Deckelbaum, R. P. Tracy, T. J. Starc, L. Berglund, and S. Shea Physical Fitness and C-Reactive Protein Level in Children and Young Adults: The Columbia University BioMarkers Study Pediatrics, February 1, 2003; 111(2): 332 - 338. [Abstract] [Full Text] [PDF] |
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L. E. Rabbani, N. A. Seminario, R. R. Sciacca, H. J. Chen, and E.-G. V. Giardina Oral conjugated equine estrogen increases plasma von Willebrand factor in postmenopausal women J. Am. Coll. Cardiol., December 4, 2002; 40(11): 1991 - 1999. [Abstract] [Full Text] [PDF] |
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E.M. Bladbjerg, S.O. Skouby, L.F. Andersen, and J. Jespersen Effects of different progestin regimens in hormone replacement therapy on blood coagulation factor VII and tissue factor pathway inhibitor Hum. Reprod., December 1, 2002; 17(12): 3235 - 3241. [Abstract] [Full Text] [PDF] |
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J. Walston, M. A. McBurnie, A. Newman, R. P. Tracy, W. J. Kop, C. H. Hirsch, J. Gottdiener, L. P. Fried, and for the Cardiovascular Health Study Investigators Frailty and Activation of the Inflammation and Coagulation Systems With and Without Clinical Comorbidities: Results From the Cardiovascular Health Study Arch Intern Med, November 11, 2002; 162(20): 2333 - 2341. [Abstract] [Full Text] [PDF] |
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P. Garnero, C. Jamin, C.-L. Benhamou, C. Pelissier, and C. Roux Effects of tibolone and combined 17{beta}-estradiol and norethisterone acetate on serum C-reactive protein in healthy post-menopausal women: a randomized trial Hum. Reprod., October 1, 2002; 17(10): 2748 - 2753. [Abstract] [Full Text] [PDF] |
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K. K. Koh Effects of estrogen on the vascular wall: vasomotor function and inflammation Cardiovasc Res, September 1, 2002; 55(4): 714 - 726. [Full Text] [PDF] |
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A. D. Pradhan, J. E. Manson, J. E. Rossouw, D. S. Siscovick, C. P. Mouton, N. Rifai, R. B. Wallace, R. D. Jackson, M. B. Pettinger, and P. M Ridker Inflammatory Biomarkers, Hormone Replacement Therapy, and Incident Coronary Heart Disease: Prospective Analysis From the Women's Health Initiative Observational Study JAMA, August 28, 2002; 288(8): 980 - 987. [Abstract] [Full Text] [PDF] |
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M. K.C. Ng, P. Y. Liu, A. J. Williams, S. Nakhla, L. P. Ly, D. J. Handelsman, and D. S. Celermajer Prospective Study of Effect of Androgens on Serum Inflammatory Markers in Men Arterioscler Thromb Vasc Biol, July 1, 2002; 22(7): 1136 - 1141. [Abstract] [Full Text] [PDF] |
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M. Jayachandran and V. M. Miller Ovariectomy upregulates expression of estrogen receptors, NOS, and HSPs in porcine platelets Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H220 - H226. [Abstract] [Full Text] [PDF] |
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D. M. Herrington, E. Vittinghoff, F. Lin, J. Fong, F. Harris, D. Hunninghake, V. Bittner, H. G. Schrott, R. S. Blumenthal, R. Levy, et al. Statin Therapy, Cardiovascular Events, and Total Mortality in the Heart and Estrogen/Progestin Replacement Study (HERS) Circulation, June 25, 2002; 105(25): 2962 - 2967. [Abstract] [Full Text] [PDF] |
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J. B. Braunstein, D. W. Kershner, P. Bray, G. Gerstenblith, S. P. Schulman, W. S. Post, and R. S. Blumenthal Interaction of Hemostatic Genetics With Hormone Therapy : New Insights To Explain Arterial Thrombosis in Postmenopausal Women Chest, March 1, 2002; 121(3): 906 - 920. [Abstract] [Full Text] [PDF] |
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R. S. Eidelman, G. A. Lamas, C. H. Hennekens, and P. M. Ridker Aspirin, Postmenopausal Hormones, and C-Reactive Protein Arch Intern Med, February 25, 2002; 162(4): 480 - 481. [Full Text] [PDF] |
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T. S Mikkola and T. B Clarkson Estrogen replacement therapy, atherosclerosis, and vascular function Cardiovasc Res, February 15, 2002; 53(3): 605 - 619. [Abstract] [Full Text] [PDF] |
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H. N. Hodis, W. J. Mack, R. A. Lobo, D. Shoupe, A. Sevanian, P. R. Mahrer, R. H. Selzer, C.-r. Liu, C.-h. Liu, S. P. Azen, et al. Estrogen in the Prevention of Atherosclerosis: A Randomized, Double-Blind, Placebo-Controlled Trial Ann Intern Med, December 4, 2001; 135(11): 939 - 953. [Abstract] [Full Text] [PDF] |
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D. A. Lewis, M. P. Bracamonte, K. S. Rud, and V. M. Miller Genome and Hormones: Gender Differences in Physiology: Selected Contribution: Effects of sex and ovariectomy on responses to platelets in porcine femoral veins J Appl Physiol, December 1, 2001; 91(6): 2823 - 2830. [Abstract] [Full Text] [PDF] |
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D. M. Herrington, K. B. Brosnihan, B. E. Pusser, E. W. Seely, P. M. Ridker, N. Rifai, and D. B. MacLean Differential Effects of E and Droloxifene on C-Reactive Protein and Other Markers of Inflammation in Healthy Postmenopausal Women J. Clin. Endocrinol. Metab., September 1, 2001; 86(9): 4216 - 4222. [Abstract] [Full Text] [PDF] |
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M. D. P. Luyer, S. Khosla, W. G. Owen, and V. M. Miller Prospective Randomized Study of Effects of Unopposed Estrogen Replacement Therapy on Markers of Coagulation and Inflammation in Postmenopausal Women J. Clin. Endocrinol. Metab., August 1, 2001; 86(8): 3629 - 3634. [Abstract] [Full Text] [PDF] |
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S. Yamada, T. Gotoh, Y. Nakashima, K. Kayaba, S. Ishikawa, N. Nago, Y. Nakamura, Y. Itoh, and E. Kajii Distribution of Serum C-Reactive Protein and Its Association with Atherosclerotic Risk Factors in a Japanese Population : Jichi Medical School Cohort Study Am. J. Epidemiol., June 15, 2001; 153(12): 1183 - 1190. [Abstract] [Full Text] [PDF] |
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R. P. Tracy Is Visceral Adiposity the "Enemy Within"? Arterioscler Thromb Vasc Biol, June 1, 2001; 21(6): 881 - 883. [Full Text] [PDF] |
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E. Barinas-Mitchell, M. Cushman, E. N. Meilahn, R. P. Tracy, and L. H. Kuller Serum Levels of C-reactive Protein Are Associated with Obesity, Weight Gain, and Hormone Replacement Therapy in Healthy Postmenopausal Women Am. J. Epidemiol., June 1, 2001; 153(11): 1094 - 1101. [Abstract] [Full Text] [PDF] |
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P. M. Ridker High-Sensitivity C-Reactive Protein : Potential Adjunct for Global Risk Assessment in the Primary Prevention of Cardiovascular Disease Circulation, April 3, 2001; 103(13): 1813 - 1818. [Abstract] [Full Text] [PDF] |
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F. K. Welty Cardiovascular Disease and Dyslipidemia in Women Arch Intern Med, February 26, 2001; 161(4): 514 - 522. [Abstract] [Full Text] [PDF] |
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T. Tolbert and S. Oparil Hormone Replacement Therapy and Stroke: Are the Results Surprising? Circulation, February 6, 2001; 103(5): 620 - 622. [Full Text] [PDF] |
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M. Cushman, J. P. Costantino, R. P. Tracy, K. Song, L. Buckley, J. D. Roberts, and D. N. Krag Tamoxifen and Cardiac Risk Factors in Healthy Women : Suggestion of an Anti-inflammatory Effect Arterioscler Thromb Vasc Biol, February 1, 2001; 21(2): 255 - 261. [Abstract] [Full Text] [PDF] |
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D. Zanger, B. K. Yang, J. Ardans, M. A. Waclawiw, G. Csako, L. M. Wahl, and R. O. Cannon III Divergent effects of hormone therapy on serum markers of inflammation in postmenopausal women with coronary artery disease on appropriate medical management J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1797 - 1802. [Abstract] [Full Text] [PDF] |
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N. Sattar, N. G. Forouhi, R. A. Wild, M. Cushman, P. A. Sakkinen, R. P. Tracy, C. Legault, E. Barrett-Connor, M. L. Stefanick, C. M. Kessler, et al. C-Reactive Protein and Hormone Replacement Therapy Response Circulation, September 26, 2000; 102 (13): e96 - e97. [Full Text] [PDF] |
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D. M. Herrington, D. M. Reboussin, K. B. Brosnihan, P. C. Sharp, S. A. Shumaker, T. E. Snyder, C. D. Furberg, G. J. Kowalchuk, T. D. Stuckey, W. J. Rogers, et al. Effects of Estrogen Replacement on the Progression of Coronary-Artery Atherosclerosis N. Engl. J. Med., August 24, 2000; 343(8): 522 - 529. [Abstract] [Full Text] [PDF] |
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R. F. Redberg, N. Rifai, L. Gee, and P. M. Ridker Lack of association of C-reactive protein and coronary calcium by electron beam computed tomography in postmenopausal women: implications for coronary artery disease screening J. Am. Coll. Cardiol., July 1, 2000; 36(1): 39 - 43. [Abstract] [Full Text] [PDF] |
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Postmenopausal estrogen replacement therapy and increased rates of cholecystectomy and appendectomy Can. Med. Assoc. J., May 1, 2000; 162(10): 1421 - 1424. |
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X. Zhu, B. Bonet, H. Gillenwater, and R. H. Knopp Opposing Effects of Estrogen and Progestins on LDL Oxidation and Vascular Wall Cytotoxicity: Implications for Atherogenesis Experimental Biology and Medicine, December 1, 1999; 222(3): 214 - 221. [Abstract] [Full Text] |
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D.M. Herrington and C.D. Furberg Hormone therapy: time for replacement? Eur. Heart J., September 2, 1999; 20(18): 1285 - 1286. [PDF] |
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P. M. Ridker, C. H. Hennekens, N. Rifai, J. E. Buring, and J. E. Manson Hormone Replacement Therapy and Increased Plasma Concentration of C-Reactive Protein Circulation, August 17, 1999; 100(7): 713 - 716. [Abstract] [Full Text] [PDF] |
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M. Cushman, C. Legault, E. Barrett-Connor, M. L. Stefanick, C. Kessler, H. L. Judd, P. A. Sakkinen, and R. P. Tracy Effect of Postmenopausal Hormones on Inflammation-Sensitive Proteins : The Postmenopausal Estrogen/Progestin Interventions (PEPI) Study Circulation, August 17, 1999; 100(7): 717 - 722. [Abstract] [Full Text] [PDF] |
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D. M. Herrington, T. D. Howard, K. B. Brosnihan, D. P. McDonnell, X. Li, G. A. Hawkins, D. M. Reboussin, J. Xu, S. L. Zheng, D. A. Meyers, et al. Common Estrogen Receptor Polymorphism Augments Effects of Hormone Replacement Therapy on E-Selectin but Not C-Reactive Protein Circulation, April 23, 2002; 105(16): 1879 - 1882. [Abstract] [Full Text] [PDF] |
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