Treated Hypertension has No Influence on the Efficacy of Alendronate in the Therapy of Postmenopausal Osteoporosis: A Non-Randomized, Non-Blind, Controlled Prospective Study

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Abstract

Changes in hormone metabolism during menopause are involved in the development of osteoporosis and arterial hypertension. A mutual influence of these two clinical pictures is evident on the basis of pathophysiological factors.

In this study, we investigated whether a drug therapy of hypertension influences the efficacy of a bisphosphonate (alendronate) in the treatment of postmenopausal osteoporosis. For this purpose, 60 female patients were enrolled in the study, 30 of them on drug treatment for hypertension in addition to requiring treatment for osteoporosis, while the control group was only suffering from osteoporosis.

Bone density was measured at the start of the study and 6 months after therapy (QCT).

A significant increase in bone density was demonstrated in both groups, while a difference between the groups could not be seen.

Treated arterial hypertension does not have a negative influence on the treatment of postmenopausal osteoporosis with alendronate. Rather, the concomitant treatment of these two clinical pictures would appear to make sense, in order to reduce morbidity and mortality.

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Most cited references 24

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Effects of estrogen plus progestin on risk of fracture and bone mineral density: the Women's Health Initiative randomized trial.

Zhao Chen, Simon J McGowan, Andrea LaCroix … (2003)

In the Women's Health Initiative trial of estrogen-plus-progestin therapy, women assigned to active treatment had fewer fractures. To test the hypothesis that the relative risk reduction of estrogen plus progestin on fractures differs according to risk factors for fractures. Randomized controlled trial (September 1993-July 2002) in which 16 608 postmenopausal women aged 50 to 79 years with an intact uterus at baseline were recruited at 40 US clinical centers and followed up for an average of 5.6 years. Women were randomly assigned to receive conjugated equine estrogen, 0.625 mg/d, plus medroxyprogesterone acetate, 2.5 mg/d, in 1 tablet (n = 8506) or placebo (n = 8102). All confirmed osteoporotic fracture events that occurred from enrollment to discontinuation of the trial (July 7, 2002); bone mineral density (BMD), measured in a subset of women (n = 1024) at baseline and years 1 and 3; and a global index, developed to summarize the balance of risks and benefits to test whether the risk-benefit profile differed across tertiles of fracture risk. Seven hundred thirty-three women (8.6%) in the estrogen-plus-progestin group and 896 women (11.1%) in the placebo group experienced a fracture (hazard ratio [HR], 0.76; 95% confidence interval [CI], 0.69-0.83). The effect did not differ in women stratified by age, body mass index, smoking status, history of falls, personal and family history of fracture, total calcium intake, past use of hormone therapy, BMD, or summary fracture risk score. Total hip BMD increased 3.7% after 3 years of treatment with estrogen plus progestin compared with 0.14% in the placebo group (P<.001). The HR for the global index was similar across tertiles of the fracture risk scale (lowest fracture risk tertile, HR, 1.20; 95% CI, 0.93-1.58; middle tertile, HR, 1.23; 95% CI, 1.04-1.46; highest tertile, HR, 1.03; 95% CI, 0.88-1.24) (P for interaction =.54). This study demonstrates that estrogen plus progestin increases BMD and reduces the risk of fracture in healthy postmenopausal women. The decreased risk of fracture attributed to estrogen plus progestin appeared to be present in all subgroups of women examined. When considering the effects of hormone therapy on other important disease outcomes in a global model, there was no net benefit, even in women considered to be at high risk of fracture.

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Relationship between osteoporosis and cardiovascular disease in postmenopausal women.

László Tankó, Claus Christiansen, David A. Cox … (2005)

In the placebo group of the MORE study, including 2576 postmenopausal women (mean age, 66.5 years), the authors describe a strong linear association between the severity grade of osteoporosis (from low BMD to presence of severe vertebral fractures) and the future risk of cardiovascular events. Accordingly, treatment of postmenopausal osteoporosis should include consideration of measures to prevent adverse cardiovascular outcomes. Observations indicate an inverse association between BMD and the severity of peripheral atherosclerosis in postmenopausal women. The predictive value of osteoporosis and its different severity stages for the risk of acute cardiovascular events remains unknown. Participants were 2576 women (mean age, 66.5 years) assigned to placebo and followed for 4 years in an osteoporosis treatment trial. Those with at least one vertebral fracture or total hip BMD T score < or = -2.5 at baseline were defined as having osteoporosis, whereas those without vertebral fracture and total hip BMD T score between -2.5 and -1 were defined as having low bone mass. The primary outcome for these posthoc analyses was the incidence of adjudicated fatal or nonfatal cardiovascular events. After adjustment for potential confounders, women with osteoporosis had a 3.9-fold (95% CI, 2.0-7.7; p < 0.001) increased risk for cardiovascular events compared with women with low bone mass. Under the same boundaries, a total hip BMD T score < or = -2.5 versus a T score between -2.5 and -1 was associated with a 2.1-fold (95% CI, 1.2-3.6; p < 0.01) increase in risk, whereas presence of at least one vertebral fracture versus no vertebral fracture at baseline was associated with a 3.0-fold (95% CI, 1.8-5.1; p < 0.001) increase in risk. The risk of cardiovascular events increased incrementally with the number and increasing severity of baseline vertebral fractures (both p < 0.001). Postmenopausal women with osteoporosis are at an increased risk for cardiovascular events that is proportional to the severity of osteoporosis at the time of the diagnosis. Treatment of postmenopausal osteoporosis should include consideration of measures to prevent cardiovascular outcomes.

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Regulation of vascular calcification by osteoclast regulatory factors RANKL and osteoprotegerin.

Shaun P. Collin (2004)

Vascular calcification often occurs with advancing age, atherosclerosis, various metabolic disorders such as diabetes mellitus and end-stage renal disease, or in rare genetic diseases, leading to serious clinical consequences. Such mineralization can occur at various sites (cardiac valves, arterial intima or media, capillaries), involve localized or diffuse widespread calcification, and result from numerous causes that provoke active inflammatory and osteogenic processes or disordered mineral homeostasis. Although valuable research has defined many key factors and cell types involved, surprising new insights continue to arise that deepen our understanding and suggest novel research directions or strategies for clinical intervention in calcific vasculopathies. One emerging area in vascular biology involves the RANKL/RANK/OPG system, molecules of the tumor necrosis factor-related family recently discovered to be critical regulators of immune and skeletal biology. Evidence is accumulating that such signals may be expressed, regulated, and function in vascular physiology and pathology in unique ways to promote endothelial cell survival, angiogenesis, monocyte or endothelial cell recruitment, and smooth muscle cell osteogenesis and calcification. Concerted research efforts are greatly needed to understand these potential roles, clarify whether RANKL (receptor activator of nuclear factor kappaB ligand) promotes and osteoprotegerin (OPG) protects against vascular calcification, define how OPG genetic polymorphisms relate to cardiovascular disease, and learn whether elevated serum OPG levels reflect endothelial dysfunction in patients. Overall, the RANKL/RANK/OPG system may mediate important and complex links between the vascular, skeletal, and immune systems. Thus, these molecules may play a central role in regulating the development of vascular calcification coincident with declines in skeletal mineralization with age, osteoporosis, or disease.

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Author and article information

Journal

Journal ID (nlm-ta): Open Orthop J

Journal ID (publisher-id): TOORTHJ

Title: The Open Orthopaedics Journal

Publisher: Bentham Open

ISSN (Electronic): 1874-3250

Publication date (Electronic): 7 January 2011

Publication date Collection: 2011

Volume: 5

Pages: 27-31

Affiliations

[1 ]Orthopaedic Department, Center for Musculoskeletal Surgery, Charité – University Medicine Berlin, Charitéplatz 1, D-10117 Berlin, Germany

[2 ]General Medical Practice, Lindenstr. 39, D-15848 Friedland/Beeskow, Germany

Author notes

[* ]Address correspondence to this author at the Center for Musculoskeletal Surgery, Charité – University Medicine Berlin, Charitéplatz 1, D-10117 Berlin, Germany; Tel: +49 30 450 652 206; Fax: +49 30 450 515 922; E-mail: doerte.matziolis@ 123456charite.de

Article

Publisher ID: TOORTHJ-5-27

DOI: 10.2174/1874325001105010027

PMC ID: 3027189

PubMed ID: 21270954

SO-VID: b0081ce5-47fb-4053-bda0-c8f70652b45d

License:

This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

History

Date received : 22 April 2010

Date revision received : 12 July 2010

Date accepted : 25 November 2010

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Treated Hypertension has No Influence on the Efficacy of Alendronate in the Therapy of Postmenopausal Osteoporosis: A Non-Randomized, Non-Blind, Controlled Prospective Study

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Most cited references 24

Effects of estrogen plus progestin on risk of fracture and bone mineral density: the Women's Health Initiative randomized trial.

Relationship between osteoporosis and cardiovascular disease in postmenopausal women.

Regulation of vascular calcification by osteoclast regulatory factors RANKL and osteoprotegerin.

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