PMID- 16842799
OWN - NLM
STAT- MEDLINE
DCOM- 20070806
LR  - 20181201
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 193
IP  - 1
DP  - 2007 Jul
TI  - Circulating chemoattractants RANTES, negatively related to endogenous androgens, 
      and MCP-1 are differentially suppressed by hormone therapy and raloxifene.
PG  - 142-50
AB  - BACKGROUND: The cardinal role of chronic inflammation in the development of 
      atherosclerosis is increasingly being recognized. Estrogens may prevent the 
      evolution of atherosclerosis by suppressing immune response. Furthermore, the 
      conflicting reports on the cardiovascular effects of hormone therapy between 
      observational and clinical trials have triggered interest on the effect of 
      alternative therapies on the cardiovascular system. OBJECTIVE: The aim of this 
      study was to assess the effect of estrogen, estrogen-progestin, tibolone and 
      raloxifene therapy on circulating markers of chemotaxis in healthy postmenopausal 
      women. METHODS: Eighty-eight postmenopausal women aged 44-62 years were randomly 
      allocated to daily: (1) conjugated equine estrogens 0.625 mg (CEE), (2) 
      17beta-estradiol 1mg plus norethisterone acetate 0.5mg (E(2)/NETA), (3) tibolone 
      2.5mg, (4) raloxifene HCl 60 mg or (5) no treatment. Serum monocyte 
      chemoattractant protein-1 (MCP-1) and regulated upon activation, normal T-cell 
      expressed and secreted (RANTES) were measured at baseline and at 3 months. 
      RESULTS: Endogenous testosterone and free androgen index (FAI) correlated 
      negatively, while SHBG correlated positively with serum RANTES (testosterone: 
      r=-0.27, p=0.033; FAI: r=-0.43, p=0.004: SHBG: r=0.34, p=0.026). Serum MCP-1 
      decreased significantly in the CEE group (baseline 125.3+/-51 pg/ml, 3 months 
      84.5+/-36.1 pg/ml, p=0.043), while no difference was detected between baseline 
      and post-treatment levels in the other groups. Furthermore, a significant 
      decrease in serum RANTES was observed at the end of 3 months only in the E2/NETA 
      and the raloxifene group (E2/NETA baseline 8690.6+/-3880.0 pg/ml, 3 months 
      6894.0+/-1720.0 pg/ml, p=0.007; raloxifene baseline 9042.4+/-3765.6 pg/ml, 3 
      months 6718.1+/-2366.2 pg/ml, p=0.011). CONCLUSION: Endogenous androgens may 
      suppress chemotactic response. Postmenopausal hormone therapy and raloxifene may 
      inhibit the expression of chemoattractant molecules and thus attenuate 
      inflammation. The relevance of these findings in terms of clinically established 
      caridoprotection remains to be clarified.
FAU - Christodoulakos, George E
AU  - Christodoulakos GE
AD  - 2nd Department of Obstetrics and Gynecology, University of Athens, Aretaieio 
      Hospital, Athens, Greece.
FAU - Lambrinoudaki, Irene V
AU  - Lambrinoudaki IV
FAU - Economou, Emmanuel V
AU  - Economou EV
FAU - Papadias, Constantinos
AU  - Papadias C
FAU - Vitoratos, Nikolaos
AU  - Vitoratos N
FAU - Panoulis, Constantinos P
AU  - Panoulis CP
FAU - Kouskouni, Evangelia E
AU  - Kouskouni EE
FAU - Vlachou, Sofia A
AU  - Vlachou SA
FAU - Creatsas, George C
AU  - Creatsas GC
LA  - eng
PT  - Journal Article
PT  - Randomized Controlled Trial
DEP - 20060713
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Androgens)
RN  - 0 (Biomarkers)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Estrogens, Conjugated (USP))
RN  - 0 (Norpregnenes)
RN  - 0 (Selective Estrogen Receptor Modulators)
RN  - 4F86W47BR6 (Raloxifene Hydrochloride)
RN  - 4TI98Z838E (Estradiol)
RN  - 9S44LIC7OJ (Norethindrone Acetate)
RN  - FF9X0205V2 (tibolone)
RN  - T18F433X4S (Norethindrone)
SB  - IM
MH  - Adult
MH  - Androgens/*blood
MH  - Atherosclerosis/blood/etiology/prevention & control
MH  - Biomarkers/blood
MH  - Cardiovascular System/drug effects
MH  - Chemokine CCL2/*blood
MH  - Chemokine CCL5/*blood
MH  - Chemotaxis/drug effects
MH  - Estradiol/pharmacology
MH  - *Estrogen Replacement Therapy
MH  - Estrogens, Conjugated (USP)/pharmacology
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - Norethindrone/analogs & derivatives/pharmacology
MH  - Norethindrone Acetate
MH  - Norpregnenes/pharmacology
MH  - Raloxifene Hydrochloride/*pharmacology
MH  - Selective Estrogen Receptor Modulators/*pharmacology
EDAT- 2006/07/18 09:00
MHDA- 2007/08/07 09:00
CRDT- 2006/07/18 09:00
PHST- 2006/02/27 00:00 [received]
PHST- 2006/05/22 00:00 [revised]
PHST- 2006/05/24 00:00 [accepted]
PHST- 2006/07/18 09:00 [pubmed]
PHST- 2007/08/07 09:00 [medline]
PHST- 2006/07/18 09:00 [entrez]
AID - S0021-9150(06)00330-3 [pii]
AID - 10.1016/j.atherosclerosis.2006.05.045 [doi]
PST - ppublish
SO  - Atherosclerosis. 2007 Jul;193(1):142-50. doi: 
      10.1016/j.atherosclerosis.2006.05.045. Epub 2006 Jul 13.