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Antihypertensive Medications, Bone Mineral Density, and Fractures: a Review of Old Cardiac Drugs That Provides New Insights Into Osteoporosis

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Antihypertensive Medications, Bone Mineral Density, and Fractures: a Review of Old Cardiac Drugs That Provides New Insights Into Osteoporosis Endocrine DOI 10.1007/s12020-014-0167-4 REVIEW Antihypertensive medications, bone mineral density, and fractures: a review of old cardiac drugs that provides new insights into osteoporosis Mahua Ghosh • Sumit R. Majumdar Received: 16 November 2013 / Accepted: 4 January 2014 Ó Springer Science+Business Media New York 2014 Abstract Osteoporosis is increasing in prevalence and fractures of the upper extremity, spine, and hip. Nearly 50 importance as society’s age, with the clinical consequence million Americans (26 % of women aged C 65 years and of fractures of the hip, spine, and upper extremity, leading to over 50 % of women aged C 85 years) are affected by impaired quality of life, loss of function and independence, osteoporosis, with total direct health care costs estimated to and increased morbidity and mortality. A major risk factor $US 12–18 billion [1]. Therefore, osteoporosis creates a for osteoporosis is older age, and cardiovascular diseases major burden for the individual as well as huge cost to the also share this risk factor; therefore, osteoporosis and car- health care system. diovascular disease often coexist and share risk factors. Recent studies have indicated the existence of a poten- Medications used for the treatment of cardiovascular dis- tial relationship between bone health and cardiovascular eases, in particular antihypertensive drugs, have been shown health [2, 3]. Both bone health and cardiovascular health in a variety of studies of varying designs to modulate bone share common etiological factors such as older age, post- health in both a positive or negative manner. In this article, menopausal status, diabetes, and lifestyle factors such as we reviewed the pharmacology, potential mechanisms, and smoking, diet, and physical activity [4]. Several studies possible effects on bone mineral density and fracture risk of suggest that vascular calcification is an actively regulated commonly prescribed antihypertensive medications, process and shares many features with bone development including thiazide and non-thiazide diuretics, beta-blockers, and metabolism [5], and women with hypertension have calcium channel blockers, renin–angiotensin–aldosterone significantly lower bone mineral density (BMD) at the system agents, and nitrates. femoral neck than those without [6]. Indeed, independent of BMD, hypertension is an independent risk factor for Keywords Osteoporosis Bone health Fractures fragility fracture [adjusted hazard ratio (HR), 1.49; 95% CI, Hypertension CardiovascularÁ medicationsÁ Á 1.13–1.96] [7], and it is associated with accelerated bone Á loss in elderly white women [8]. We recently showed that heart failure, independent of BMD and cardiovascular risk Introduction factors, is associated with 30 % increased risk of major osteoporotic fractures [9]. Although observational in nat- Osteoporosis is a common and chronic condition, and the ure, in aggregate, studies such as these suggest a potential major clinical consequences of this disease are osteoporotic link between cardiovascular disease (particularly hyper- tension) and bone health. Cardiovascular medications used for hypertension, such M. Ghosh S. R. Majumdar Division ofÁ General Internal Medicine, Department of Medicine, as thiazide and non-thiazide diuretics, beta-blockers, and University of Alberta, Edmonton, AB, Canada calcium channel blockers, are also the most commonly prescribed medications in the developed and developing S. R. Majumdar (&) world [10–12], and the question arises then whether or not 5-134B Clinical Science Building, 11350—83rd Avenue, Edmonton, AB T6G 2G3, Canada therapy for one condition can modulate the other in either e-mail: [email protected] positive or negative manner. In this article, we review the 123 Endocrine currently available evidence on the pharmacology, poten- among long-term thiazide users compared with nonusers; tial mechanisms, and possible effects on bone mineral there were no trials [25]. density and fracture risk of commonly prescribed antihy- In summary, thiazide diuretics increase (or prevent pertensive medications, including thiazide and non-thiazide decreases) in BMD in both men and women and, in obser- diuretics, beta-blockers, calcium channel blockers, renin– vational studies, are associated with a reduction in fracture angiotensin–aldosterone system agents, and nitrates. risk. Loop diuretics Literature review Pharmacology Thiazide diuretics Loop diuretics increase the urinary excretion of sodium Pharmacology chloride by selective inhibition of the Na?,K?, 2Cl co- transporters in the loop of Henle and distal nephron [26]. Thiazide diuretics can affect kidney, intestine, and bone Loop diuretics promote sodium and water excretion via the and thereby modulate calcium homeostasis. In the kidney, kidney and mitigate excessive sodium and water retention. thiazides inhibit the thiazide-sensitive sodium chloride co- Therefore, loop diuretics are used for heart failure as well transporter (NCC) in the distal tubule and exert natriuretic as a part of combination therapy for difficult-to-treat and calcium-sparing effects [13]. In the intestine, thiazides hypertension [27]. enhance calcium uptake and suppress parathyroid hormone secretion [14]. Overall, thiazides reduce urinary excretion Potential mechanisms affecting bone health of calcium by about 40 % [15, 16]. Treatment with loop diuretics is associated with signifi- Potential mechanisms affecting bone health cantly increased urinary calcium excretion, and increased levels of PTH and 1,25-dihydroxyvitamin D [28]. Long- Thiazides exert direct effects on bone by stimulating term treatment with furosemide causes hypocalcaemia, osteoblast differentiation and bone mineral formation resulting in elevation of PTH and increased levels of bone- through osteoblast differentiation markers runt-related specific alkaline phosphatase, an indication of accelerated transcription factor 2 and osteopontin [17]. The NCC is also bone remodeling [29]. expressed in human osteoblast and osteoblast-like cells, which, when blocked by a thiazides, enhances bone calcium Clinical evidence uptake [18]. These mechanisms could explain why, inde- pendent of their renal and intestinal effects, thiazides are able A prospective study in older women indicated that loop to exert a direct positive homeostatic effect on bones [19]. In diuretic users had greater loss of total hip BMD than non- studies of bendroflumethiazide, there were dose-dependent users (mean annualized % BMD -0.87 vs -0.71, P = 0.03) decreases in urinary calcium excretion, no change in PTH after a mean of 4.4 ± 0.6 years [30]. The risks of neither levels, a dose-dependent increase in plasma 1,25(OH)2D falls nor fractures were greater in loop diuretic users than in levels and concomitant increases in osteocalcin (a marker of nonusers [30], findings that were replicated in older men bone formation), and decreases in bone-specific alkaline [31]. In a randomized-controlled trial, one-year treatment of phosphatase (a marker of bone resorption) [20, 21]. bumetanide decreased BMD, and subjects treated with bumetanide had increased markers of bone turnover com- Clinical evidence pared with placebo [32]. Given that the placebo group was treated with calcium and vitamin D supplements, in this trial In a longitudinal, observational study in elderly men with bumetanide at the least antagonized the positive effects of mean follow-up for 5 years, thiazides reduced the rate of calcium and vitamin D supplements. In another study, bone loss at the calcaneus and radius [22]. Similar result bumetanide dose-dependently increased renal calcium loss was seen in post-menopausal women [23]. In a population- with a concomitant increase in plasma PTH and based cohort of 248 older women, the mean BMD was 1,25(OH)2D levels [20]. A recent study indicated the clin- 9.6 % greater in the lumbar spine (P \ 0.01) and 5.4 % ical association of hyponatremia during the use of loop greater in the whole skeleton (P \ 0.01) among thiazide diuretics with an increased risk of osteoporosis associated users than in controls [24]. A Cochrane review, including fractures, and the authors suggested that a moderate but twenty-one observational studies with nearly 400,000 par- persistent loss of both bone sodium and calcium could be ticipants, reported reduction in risk of hip fracture by 24 % exerted by loop diuretics [33]. Finally, in a large cohort 123 Endocrine study with 376,061 subjects, falls were more common been subdivided into three types: beta-1 (heart and vessels), among loop diuretic users than with other antihypertensive beta-2 (pulmonary tissues), and beta-3 (adipose tissue) agents although there was no difference in fracture risk [34]. [41–43]. Bone cells express beta-2 adrenoceptors, although In summary, via direct (loss of BMD) and indirect low levels of beta-1 and beta-3 adrenoceptors are also (increased falls) mechanisms, it seems loop diuretics have a present [44]. Beta-blockers (BB) exert their effect by negative effect on bone health and are associated with inhibition of beta-adrenergic receptors and are widely used increased risk of fractures. in the treatment of hypertension and heart failure. These agents are often described in terms of their ‘‘cardio-selec- Spironolactone tivity’’ depending on their selective action of beta-1 receptor-blocking properties [45]. Nonselective BB have Pharmacology action on beta-2 and beta-3 receptors and thus tend to exert their effects beyond heart. Like many other receptor Spironolactone is a potassium-sparing
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