Increased plasma concentrations of TGF‐β<sub>1</sub> after hormone replacement therapy

Djurovic, Srdjan; Os, Ingrid; Hofstad, A. E.; Abdelnoor, Michael; Westheim, Arne; Berg, K.

doi:10.1046/j.1365-2796.2000.00648.x

Cited by 17 publications

(15 citation statements)

References 31 publications

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“…Furthermore, small studies have confirmed the inconsistent effect of menopausal hormones on IL-6 37,43 and have found significant reductions in TNF-␣ 40 and increases in the vasoprotective cytokine TGF-␤ in postmenopausal women treated with hormones. 44 These findings strongly suggest that the effects of menopausal hormones on CRP do not represent a generalized proinflammatory effect mediated through upstream cytokines such as IL-6 but rather are related to a secondary mechanism. 42 The finding that transdermal estradiol, unlike oral conjugated estrogen, does not elevate circulating CRP levels suggests that this secondary mechanism may be a first pass effect of CRP production in the liver after oral estrogen absorption, which is avoided by transdermal delivery.…”

Section: C-reactive Proteinmentioning

confidence: 86%

Hormone Replacement Therapy and Inflammation

et al. 2003

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Abstract-Inflammation plays a central role in the pathogenesis of many forms of vascular disease, including atherosclerosis. Atherogenesis begins with endothelial damage, and the damaged endothelium expresses adhesion molecules, chemokines, and proinflammatory cytokines that direct atherosclerotic plaque formation and spill into the circulation as biomarkers of atherosclerotic disease risk. Menopausal hormone therapy, including a variety of estrogen preparations with or without a progestin, has negative modulatory effects on most of these soluble inflammatory markers, including E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and tumor necrosis factor-␣, inconsistent effects on interleukin-6, and stimulatory effects on transforming growth factor-␤, a vasoprotective cytokine. In contrast, C-reactive protein, a circulating proinflammatory cytokine produced in both liver and atherosclerotic arteries, increases in response to oral conjugated estrogens but not to transdermal estrogen. Although C-reactive protein is clearly linked to increased cardiovascular disease risk in women, the hormone-induced rise in this biomarker is not associated with increased risk and may be related to a first-pass effect of C-reactive protein production in the liver after oral estrogen absorption. Many important questions about the effects of ovarian hormones on vascular inflammation and the pathogenesis of vascular disease cannot be answered in human subjects. Insights from fundamental mechanistic studies in animal models are needed to delineate the cellular/molecular events that determine whether these hormones protect or injure blood vessels.

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Section: C-reactive Proteinmentioning

confidence: 86%

Hormone Replacement Therapy and Inflammation

et al. 2003

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“…Among the six studies on unopposed transdermal E 2 , one reported a significant decrease compared with the untreated control group (Table 2) (31). Among the four studies on transdermal E 2 plus transdermal NETA, one found a significant decrease from baseline (57).…”

Section: Fertility and Sterility âmentioning

confidence: 95%

“…In a few studies, an initial 3-month phase of unopposed E was followed by a 3-or 9-month period of sequentially combined HT. Of these studies, the initial 3-month effect is described in the ''unopposed'' parts of the tables, whereas the end-of-study effect is given in the ''combined'' parts (31,32,36,72,84,95). The same was done for one study describing 4 weeks of unopposed transdermal E 2 followed by 2 weeks of combined HT (49).…”

Section: Trial Flowmentioning

confidence: 99%

“…Among these, five studies included women with CHD (31,32,36,84,95), 12 included women with established risk factors (diabetes, impaired glucose tolerance, or metabolic syndrome in 5 studies) (34,53,55,75,81), hypertension in 3 studies (45,74,78), and (mild) hypercholesterolemia in 4 studies (29,67,85,89), one included women who had undergone a hysterectomy for cervical cancer (27) and the other 52 studies included healthy postmenopausal women (including women hysterectomized for benign reasons).…”

Section: Study Characteristicsmentioning

confidence: 99%

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Effects of non-oral postmenopausal hormone therapy on markers of cardiovascular risk: a systematic review

Hemelaar

Mooren

Rad

et al. 2008

Fertility and Sterility

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“…1,2 Hormone replacement therapy (HRT) may have favorable effects on some cardiovascular risk factors, [3][4][5][6] but not all. 7,8 Randomized, controlled trials with conjugated equine estrogens (CEE) and accompanying gestagens have not shown any beneficial effect on cardiovascular disease or mortality in neither secondary prevention trials or during primary prevention.…”

Section: Introductionmentioning

confidence: 99%