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Treatment of postmenopausal osteoporosis in women: a systematic review.

Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte, Brasil.
Cadernos de saúde pública / Ministério da Saúde, Fundação Oswaldo Cruz, Escola Nacional de Saúde Pública (Impact Factor: 0.89). 02/2008; 24 Suppl 4:s592-606. DOI: 10.1590/S0102-311X2008001600011
Source: PubMed

ABSTRACT Osteoporosis, a typical disease of the elderly, has become a frequent and relevant public health problem. Several drugs are available for treatment of osteoporosis, some of which are currently dispensed by the Brazilian Unified National Health System. The objective of this study was to present a systematic review of drugs for treatment of osteoporosis, focusing on the adequacy of clinical protocols based on existing evidence in the scientific literature. We conducted a search for randomized clinical trials in PubMed and LILACS that presented results for bone mineral density, incidence of vertebral fractures, and adverse effects. 32 articles met the review's inclusion criteria. Bisphosphonates were reported to have consistently reduced the risk of vertebral fractures. Hormone replacement therapy showed positive outcomes, but its use has been found to increase the risk of cardiovascular disease and breast cancer. Teriparatide and monofluorophosphate also showed efficacy against osteoporosis. Calcium and vitamin D were given to patients as food supplements.

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    • "Sodium nitroprusside (SNP), L-arginine (L-Arg), 1H- [1] [2] [4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), glibenclamide, N G -nitro-Larginine methyl ester (L-NAME), 1400W and alendronate were purchased from Sigma Aldrich (St. Louis, MO). L-N G -iminoethyl-L-ornitine (L-NIO) was purchased from Cayman Chemical (Ann Arbor, MI). "
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    ABSTRACT: Chronic use of alendronate has been linked to gastrointestinal tract problems. Our objective was to evaluate the role of the NO/cGMP/KATP signaling pathway and nitric oxide synthase expression in alendronate-induced gastric damage. Rats were either treated with the NO donor, sodium nitroprusside (SNP; 1, 3, and 10 mg/kg), or the NO synthase (NOS) substrate, l-arginine (l-Arg; 50, 100, and 200 mg/kg). Some rats were pretreated with either ODQ (a guanylate cyclase inhibitor; 10 mg/kg) or glibenclamide (KATP channels blocker; 10 mg/kg). In other experiments, rats were pretreated with l-NAME (non-selective NOS inhibitor; 10 mg/kg), 1400W (selective inducible NOS [iNOS] inhibitor; 10 mg/kg), or l-NIO (a selective endothelial NOS [eNOS] inhibitor; 30 mg/kg). After 1 h, the rats were treated with alendronate (30 mg/kg) by gavage for 4 days. SNP and l-Arg prevented alendronate-induced gastric damage in a dose-dependent manner. Alendronate reduced nitrite/nitrate levels, an effect that was reversed with SNP or l-Arg treatment. Pretreatment with ODQ or glibenclamide reversed the protective effects of SNP and l-Arg. l-NAME, 1400W, or l-NIO aggravated the severity of alendronate-induced lesions. In addition, alendronate reduced the expression of iNOS and eNOS in the gastric mucosa. Gastric ulcerogenic responses induced by alendronate were mediated by a decrease in NO derived from both eNOS and iNOS. In addition, our findings support the hypothesis that activation of the NO/cGMP/KATP pathway is of primary importance for protection against alendronate-induced gastric damage.
    Nitric Oxide 05/2014; 40. DOI:10.1016/j.niox.2014.05.002 · 3.18 Impact Factor
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    • "Sodium nitroprusside (SNP), L-arginine (L-Arg), 1H- [1] [2] [4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), glibenclamide, N G -nitro-Larginine methyl ester (L-NAME), 1400W and alendronate were purchased from Sigma Aldrich (St. Louis, MO). L-N G -iminoethyl-L-ornitine (L-NIO) was purchased from Cayman Chemical (Ann Arbor, MI). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic use of alendronate has been linked to gastrointestinal tract problems. Our objective was to evaluate the role of the NO/cGMP/KATP signaling pathway and nitric oxide synthase expression in alendronate-induced gastric damage. Rats were either treated with the NO donor, sodium nitroprusside (SNP; 1, 3, and 10 mg/kg), or the NO synthase (NOS) substrate, l-arginine (l-Arg; 50, 100, and 200 mg/kg). Some rats were pretreated with either ODQ (a guanylate cyclase inhibitor; 10 mg/kg) or glibenclamide (KATP channels blocker; 10 mg/kg). In other experiments, rats were pretreated with l-NAME (non-selective NOS inhibitor; 10 mg/kg), 1400W (selective inducible NOS [iNOS] inhibitor; 10 mg/kg), or l-NIO (a selective endothelial NOS [eNOS] inhibitor; 30 mg/kg). After 1 h, the rats were treated with alendronate (30 mg/kg) by gavage for 4 days. SNP and l-Arg prevented alendronate-induced gastric damage in a dose-dependent manner. Alendronate reduced nitrite/nitrate levels, an effect that was reversed with SNP or l-Arg treatment. Pretreatment with ODQ or glibenclamide reversed the protective effects of SNP and l-Arg. l-NAME, 1400W, or l-NIO aggravated the severity of alendronate-induced lesions. In addition, alendronate reduced the expression of iNOS and eNOS in the gastric mucosa. Gastric ulcerogenic responses induced by alendronate were mediated by a decrease in NO derived from both eNOS and iNOS. In addition, our findings support the hypothesis that activation of the NO/cGMP/KATP pathway is of primary importance for protection against alendronate-induced gastric damage.
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    • "Clinically, osteoporosis is identified through nontraumatic/minimal fracture in the vertebra, hip, proximal humerus , and femur fracture. Osteoporosis is a disorder specifically found in elderly men and women [3] [4] [5] [6]. Increased economy and aging population will increase the frequency of osteoporosis so that it becomes an essential health issue [5] [7]. "
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    10/2013; 2013:679025. DOI:10.1155/2013/679025
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