Core EvidencePub Date : 2010-06-15DOI: 10.2147/ce.s6011
E Michael Lewiecki
{"title":"Intravenous zoledronic acid for the treatment of osteoporosis: The evidence of its therapeutic effect.","authors":"E Michael Lewiecki","doi":"10.2147/ce.s6011","DOIUrl":"10.2147/ce.s6011","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoporosis is a disease characterized by low bone mineral density and poor bone quality resulting in reduced bone strength and increased risk of fracture. Oral bisphosphonates, first-line therapy for most patients with osteoporosis, are associated with suboptimal adherence to therapy due to factors that include a complex dosing regimen and gastrointestinal intolerance in some patients. Intravenous bisphosphonates address these limitations through infrequent injectable dosing that assures 100% bioavailability. Intravenous zoledronic acid is the newest bisphosphonate to be approved for the treatment of osteoporosis.</p><p><strong>Aims: </strong>This review assesses the evidence for the therapeutic effects of intravenous zoledronic acid for the treatment of osteoporosis.</p><p><strong>Evidence review: </strong>Zoledronic acid 5 mg administered as an annual 15-min intravenous infusion has been shown to reduce the risk of vertebral fractures, hip fractures, and other fractures in a three-year randomized, double-blind, placebo-controlled trial in women with postmenopausal osteoporosis. In a randomized, double-blind, placebo-controlled trial in women and men with a recent surgical repair of low-trauma hip fracture, it reduced the risk of new clinical fractures and improved survival. In both studies, zoledronic acid was associated with a good safety profile and was generally well tolerated. Zoledronic acid has the potential to improve clinical outcomes by reducing the risk of fracture in patients with osteoporosis.</p><p><strong>Clinical value: </strong>Intravenous zoledronic acid 5 mg every 12 months reduces fracture risk in women with postmenopausal osteoporosis and in women and men with recent low-trauma hip fracture.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 ","pages":"13-23"},"PeriodicalIF":0.0,"publicationDate":"2010-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/ce.s6011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29175563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-06-15DOI: 10.2147/ce.s5997
Melissa Li-Ng, Joseph G Verbalis
{"title":"Conivaptan: Evidence supporting its therapeutic use in hyponatremia.","authors":"Melissa Li-Ng, Joseph G Verbalis","doi":"10.2147/ce.s5997","DOIUrl":"10.2147/ce.s5997","url":null,"abstract":"<p><strong>Introduction: </strong>The available treatment options for euvolemic and hypervolemic hyponatremia are limited, and consist mainly of fluid restriction, diuresis, or hypertonic solutions. Most of these therapies are neither well tolerated nor totally effective, and many are associated with significant adverse effects. Vasopressin receptor antagonists, also known as vaptans, are a new class of agents that now offer an additional treatment option for hyponatremic patients. Conivaptan hydrochloride, a competitive antagonist of vasopressin V1a and V2 receptors, is the first agent in this class to be approved for treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.</p><p><strong>Aims: </strong>This review critically assesses the evidence that support the use of conivaptan for the treatment of patients with euvolemic and hypervolemic hyponatremia.</p><p><strong>Evidence review conclusion: </strong>Conivaptan is effective in raising serum sodium levels in a predictable and safe fashion in euvolemic and hypervolemic hyponatremic patients. Conivaptan provides the first molecularly targeted approach for correcting hyponatremia in hospitalized patients.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 ","pages":"83-92"},"PeriodicalIF":0.0,"publicationDate":"2010-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/ce.s5997","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29175472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-06-15DOI: 10.2147/ce.s5998
Daniel Z Lieberman, Suena H Massey
{"title":"Desvenlafaxine in major depressive disorder: an evidence-based review of its place in therapy.","authors":"Daniel Z Lieberman, Suena H Massey","doi":"10.2147/ce.s5998","DOIUrl":"10.2147/ce.s5998","url":null,"abstract":"<p><strong>Introduction: </strong>Desvenlafaxine, the active metabolite of venlafaxine, is a serotonin norepinephrine reuptake inhibitor (SNRI) recently approved for the treatment of major depressive disorder. It is one of only three medications in this class available in the United States.</p><p><strong>Aims: </strong>The objective of this article is to review the published evidence for the safety and efficacy of desvenlafaxine, and to compare it to other antidepressants to delineate its role in the treatment of depression.</p><p><strong>Evidence review: </strong>At the recommended dose of 50 mg per day the rate of response and remission was similar to other SNRIs, as was the adverse effect profile. The rate of discontinuation was no greater than placebo, and a discontinuation syndrome was not observed at this dose. Higher doses were not associated with greater efficacy, but they did lead to more side effects, and the use of a taper prior to discontinuation. The most common side effects reported were insomnia, somnolence, dizziness, and nausea. Some subjects experienced clinically significant blood pressure elevation.</p><p><strong>Place in therapy: </strong>Like duloxetine, desvenlafaxine inhibits the reuptake of both norepinephrine and serotonin at the starting dose. Dual reuptake inhibitors have been shown to have small but statistically significantly greater rates of response and remission compared to selective serotonin reuptake inhibitors, and they have also shown early promise in the treatment of neuropathic pain. Desvenlafaxine may prove to be a valuable treatment option by expanding the limited number of available dual reuptake inhibitors.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 ","pages":"67-82"},"PeriodicalIF":0.0,"publicationDate":"2010-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2899788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29175471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-06-15DOI: 10.2147/ce.s5999
Angelo L Gaffo, Kenneth G Saag
{"title":"Febuxostat: the evidence for its use in the treatment of hyperuricemia and gout.","authors":"Angelo L Gaffo, Kenneth G Saag","doi":"10.2147/ce.s5999","DOIUrl":"https://doi.org/10.2147/ce.s5999","url":null,"abstract":"<p><strong>Introduction: </strong>Gout is a common and disabling cause of arthritis in middle-aged and elderly populations, with its main predisposing factor being hyperuricemia (serum urate > 6.8 mg/dL). Options for treatment of chronic gout until 2008 were allopurinol, a xanthine oxidase inhibitor, and the group of drugs known as uricosurics that stimulate the renal excretion of uric acid. A proportion of patients, including some with chronic kidney disease and solid organ transplantations, could not be treated with the those therapies because of intolerance, drug interactions, or adverse events. Febuxostat is a nonpurine xanthine oxidase inhibitor, recently approved in Europe and the United States for the treatment of chronic gout.</p><p><strong>Aim: </strong>To review the clinical evidence (phase II and III studies) of the effectiveness and safety of febuxostat for treatment of hyperuricemia and gout.</p><p><strong>Evidence review: </strong>Febuxostat, at doses ranging from 40 to 240 mg/day, is efficacious in reducing serum urate in patients with hyperuricemia and gout, comparing favorably with fixed doses of allopurinol in that respect. Early safety signals with respect to liver test abnormalities and cardiovascular outcomes have not been confirmed in recent large prospective trials but need to be further monitored.</p><p><strong>Clinical potential: </strong>Given its low cost and extensive clinical experience, allopurinol will likely remain the first-line drug for management of hyperuricemia and gout. Febuxostat may provide an important option in patients unable to use allopurinol, those with very high serum urate levels, or in the presence of refractory tophi.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 ","pages":"25-36"},"PeriodicalIF":0.0,"publicationDate":"2010-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/ce.s5999","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29175564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-06-15DOI: 10.2147/ce.s5996
Hari A Deshpande, Scott Gettinger, Julie Ann Sosa
{"title":"Axitinib: The evidence of its potential in the treatment of advanced thyroid cancer.","authors":"Hari A Deshpande, Scott Gettinger, Julie Ann Sosa","doi":"10.2147/ce.s5996","DOIUrl":"https://doi.org/10.2147/ce.s5996","url":null,"abstract":"<p><strong>Introduction: </strong>Thyroid cancer is a rare disease with an incidence of around 37,000 cases per year. However, its incidence is rising faster than many other cancers and for men this disease ranks highest overall in the rate of increase (2.4% annual increase) in cancer deaths. As the number of radioactive iodine-resistant thyroid cancers increases, the need for newer treatments has become more important. Axitinib is one of many new small molecule inhibitors of growth factor receptors that have shown promise in the treatment of many cancers. It targets the vascular endothelial growth factor receptors 1, 2 and 3.</p><p><strong>Aims: </strong>The goal of this article is to review the published evidence for the use of axitinib in the treatment of thyroid cancer and define its therapeutic potential.</p><p><strong>Evidence review: </strong>The major evidence of axitinib activity has appeared in meeting report abstracts. One phase II study has been published. This included patients with any histological type of thyroid cancer that was not amenable to treatment with radioactive iodine.</p><p><strong>Clinical potential: </strong>To date, in phase II clinical studies axitinib has demonstrated antitumor activity in advanced refractory thyroid cancer. As a monotherapy it resulted in a 30% response rate with another 38% of patients having stable disease. Axitinib appears to have a good tolerability profile, with hypertension being the most common grade 3 or greater side effect.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 ","pages":"43-8"},"PeriodicalIF":0.0,"publicationDate":"2010-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/ce.s5996","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29175566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-01-01Epub Date: 2010-10-22DOI: 10.2147/CE.S8008
Peter Alagona
{"title":"Pitavastatin: evidence for its place in treatment of hypercholesterolemia.","authors":"Peter Alagona","doi":"10.2147/CE.S8008","DOIUrl":"10.2147/CE.S8008","url":null,"abstract":"<p><p>Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are the most potent pharmacologic agents for lowering total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). They have become an accepted standard of care in the treatment of patients with known atherosclerotic cardiovascular disease (secondary prevention) and also those at increased risk of cardiovascular events. There are currently six statin drugs commercially available in the US. Although they are chemically similar and have the same primary mechanisms of action in lowering TC and LDL-C, there are differences in their efficacy or potency, metabolism, drug-drug interactions, and individual tolerability. Considering the numbers of patients who need LDL-C-lowering therapy and questions of individual tolerance and therapeutic response, having a variety of agents to choose from is beneficial for patient care. This paper presents background information on statin treatment and reviews data regarding a new agent, pitavastatin, which has recently been approved for clinical use.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"5 ","pages":"91-105"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29795529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2010-01-01Epub Date: 2010-12-08DOI: 10.2147/CE.S9046
Douglas R Jeffery, Emily Poole Pharr
{"title":"Dalfampridine sustained-release for symptomatic improvement of walking speed in patients with multiple sclerosis.","authors":"Douglas R Jeffery, Emily Poole Pharr","doi":"10.2147/CE.S9046","DOIUrl":"https://doi.org/10.2147/CE.S9046","url":null,"abstract":"<p><p>Dalfampridine sustained-release (SR) is a time-release formulation of 4-aminopyridine, recently approved by the Food and Drug Administration to improve walking in patients with multiple sclerosis (MS). In Phase II trials, walking speed and lower extremity muscle strength was increased in patients with MS, but the increase in walking speed did not reach statistical significance. A responder analysis revealed that approximately 35% of treated patients had a statistically significant and clinically meaningful increase in walking speed. When treated responders were compared with treated nonresponders, walking speed significantly increased in the responder group, but not in the nonresponder or placebo groups. This result was duplicated in two larger Phase III trials. The optimal dose to maximize the risk-benefit ratio was 10 mg twice daily. Higher doses were associated with a greater risk of seizure, but no further improvement in walking speed or in the proportion of responders. Dalfampridine SR is eliminated by renal clearance and undergoes only limited metabolism (<10%). It is contraindicated in patients with moderate or severe renal insufficiency and in those with a history of seizures or epileptiform activity on electroencephalography. The development of time-released 4-aminopyridine represents a major advance in symptomatic therapy for MS.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"5 ","pages":"107-12"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/CE.S9046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29795528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2009-12-22DOI: 10.2147/CE.S7031
Markos Poulopoulos, C. Waters
{"title":"Carbidopa/levodopa/entacapone: the evidence for its place in the treatment of Parkinson's disease.","authors":"Markos Poulopoulos, C. Waters","doi":"10.2147/CE.S7031","DOIUrl":"https://doi.org/10.2147/CE.S7031","url":null,"abstract":"Introduction: \u0000Parkinson’s disease (PD) is a common neurodegenerative disease. In the 1960s, it was shown that the degeneration of dopamine producing neurons in the substantia nigra (SN) caused the motor features of PD. Dopamine replacement with levodopa, a dopamine precursor, resulted in remarkable benefit. Yet, the intermittent administration of levodopa is a major cause of motor complications, such as “wearing-off” of levodopa’s benefit and involuntary movements, known as dyskinesia. Therefore, agents that prolong levodopa’s half-life were employed, such as carbidopa, an aromatic amino acid decarboxylase (AADC) inhibitor, and entacapone, a catechol-O-methyltransferase (COMT) inhibitor. The combination product carbidopa/levodopa/entacapone (CLE) was approved in 2003 for the treatment of PD patients.","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"5 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2009-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/CE.S7031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68313188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Core EvidencePub Date : 2009-06-17DOI: 10.3355/CE.2008.017
J. Krzesinski, E. Cohen
{"title":"Exforge® (amlodipine/valsartan combination) in hypertension: the evidence of its therapeutic impact","authors":"J. Krzesinski, E. Cohen","doi":"10.3355/CE.2008.017","DOIUrl":"https://doi.org/10.3355/CE.2008.017","url":null,"abstract":"Introduction: Hypertension is an important risk factor for cardiovascular disease and its management requires improvement. New treatment strategies are needed. Aims: This review analyses one of these strategies, which is the development of effective and safe combination therapy. Indeed, at least two antihypertensive agents are often needed to achieve blood pressure control. Exforge® (Novartis) is a new drug combination of the calcium channel blocker, amlodipine, and the angiotensin II receptor blocker, valsartan. Evidence review: The amlodipine/valsartan combination is an association of two well-known antihypertensive products with specific targets in cardiovascular protection, namely calcium channel blockade and antagonism of the renin-angiotensin-aldosterone system. This kind of association, with neutral metabolic properties and significant antihypertensive efficacy, could be a useful new antihypertensive product. Currently available data have shown that this new combination is well-tolerated and effective even in severe hypertension. Clinical value: Clinical trials are ongoing for further assessment of the efficacy, compliance, and safety of this combination and its congeners. No data exist to prove that the amlodipine/valsartan combination is better than other antihypertensive strategies for cardiovascular or renal protection, but some trials with other combination therapies show such potential advantage.","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"4 1","pages":"1 - 11"},"PeriodicalIF":0.0,"publicationDate":"2009-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69448396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anidulafungin: an evidence-based review of its use in invasive fungal infections.","authors":"Susan L Davis, Jose A Vazquez","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Anidulafungin is a new echinocandin antifungal agent with indications for use in esophageal candidiasis and candidemia. The mortality and morbidity associated with fungal infections in healthcare facilities necessitates the development of new treatment options for these diseases.</p><p><strong>Aims: </strong>This review assesses the pharmacology and evidence for the use of anidulafungin in the treatment of serious fungal infections.</p><p><strong>Evidence review: </strong>There is substantial evidence that anidulafungin is a potent antifungal agent with activity against a broad range of fungal species. Likewise, evidence supports that anidulafungin is a well-tolerated antifungal agent. Clinical studies provide sufficient evidence for regulatory approval for esophageal candidiasis and candidemia, and limited evidence suggests that anidulafungin may be superior to fluconazole for candidemia and invasive candidiasis. The introduction of anidulafungin into clinical practice adds a third option for therapy in the echinocandin class. Research into its efficacy in other fungal infections is ongoing, and further studies into the impact of anidulafungin on economic outcomes will be beneficial.</p><p><strong>Place in therapy: </strong>Current evidence supports the use of anidulafungin in the management of candidemia, esophageal candidiasis, and invasive candidiasis, as demonstrated by the successful results in large multicenter clinical trials.</p>","PeriodicalId":10764,"journal":{"name":"Core Evidence","volume":"2 4","pages":"241-9"},"PeriodicalIF":0.0,"publicationDate":"2008-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29588080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}