Pub Date : 2019-01-01DOI: 10.1177/2040622319862691
O. Onoviran, Dongming Li, Sarah Toombs Smith, M. Raji
Elderly patients with diabetes are at high risk of polypharmacy because of multiple coexisting diseases and syndromes. Polypharmacy increases the risk of drug–drug and drug–disease interactions in these patients, who may already have age-related sensory and cognitive deficits; such deficits may delay timely communication of early symptoms of adverse drug events. Several glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have been approved for diabetes: liraglutide, exenatide, lixisenatide, dulagluatide, semaglutide, and albiglutide. Some are also approved for treatment of obesity. The current review of literature along with clinical case discussion provides evidence supporting GLP-1 RAs as diabetes medications for polypharmacy reduction in older diabetes patients because of their multiple pleiotropic effects on comorbidities (e.g. hyperlipidemia, hypertension, and fatty liver) and syndromes (e.g. osteoporosis and sleep apnea) that commonly co-occur with diabetes. Using one medication (in this case, GLP-1 RAs) to address multiple conditions may help reduce costs, medication burden, adverse drug events, and medication nonadherence.
{"title":"Effects of glucagon-like peptide 1 receptor agonists on comorbidities in older patients with diabetes mellitus","authors":"O. Onoviran, Dongming Li, Sarah Toombs Smith, M. Raji","doi":"10.1177/2040622319862691","DOIUrl":"https://doi.org/10.1177/2040622319862691","url":null,"abstract":"Elderly patients with diabetes are at high risk of polypharmacy because of multiple coexisting diseases and syndromes. Polypharmacy increases the risk of drug–drug and drug–disease interactions in these patients, who may already have age-related sensory and cognitive deficits; such deficits may delay timely communication of early symptoms of adverse drug events. Several glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have been approved for diabetes: liraglutide, exenatide, lixisenatide, dulagluatide, semaglutide, and albiglutide. Some are also approved for treatment of obesity. The current review of literature along with clinical case discussion provides evidence supporting GLP-1 RAs as diabetes medications for polypharmacy reduction in older diabetes patients because of their multiple pleiotropic effects on comorbidities (e.g. hyperlipidemia, hypertension, and fatty liver) and syndromes (e.g. osteoporosis and sleep apnea) that commonly co-occur with diabetes. Using one medication (in this case, GLP-1 RAs) to address multiple conditions may help reduce costs, medication burden, adverse drug events, and medication nonadherence.","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622319862691","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49001597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-01-01DOI: 10.1177/2040622319862697
X. Lyu, Min Hu, Jieting Peng, Xiangyu Zhang, Y. Sanders
Fibrosis usually results from dysregulated wound repair and is characterized by excessive scar tissue. It is a complex process with unclear mechanisms. Accumulating evidence indicates that epigenetic alterations, including histone acetylation, play a pivotal role in this process. Histone acetylation is governed by histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs are enzymes that remove the acetyl groups from both histone and nonhistone proteins. Aberrant HDAC activities are observed in fibrotic diseases, including cardiac and pulmonary fibrosis. HDAC inhibitors (HDACIs) are molecules that block HDAC functions. HDACIs have been studied extensively in a variety of tumors. Currently, there are four HDACIs approved by the US Food and Drug Administration for cancer treatment yet none for fibrotic diseases. Emerging evidence from in vitro and in vivo preclinical studies has presented beneficial effects of HDACIs in preventing or reversing fibrogenesis. In this review, we summarize the latest findings of the roles of HDACs in the pathogenesis of cardiac and pulmonary fibrosis and highlight the potential applications of HDACIs in these two fibrotic diseases.
{"title":"HDAC inhibitors as antifibrotic drugs in cardiac and pulmonary fibrosis","authors":"X. Lyu, Min Hu, Jieting Peng, Xiangyu Zhang, Y. Sanders","doi":"10.1177/2040622319862697","DOIUrl":"https://doi.org/10.1177/2040622319862697","url":null,"abstract":"Fibrosis usually results from dysregulated wound repair and is characterized by excessive scar tissue. It is a complex process with unclear mechanisms. Accumulating evidence indicates that epigenetic alterations, including histone acetylation, play a pivotal role in this process. Histone acetylation is governed by histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs are enzymes that remove the acetyl groups from both histone and nonhistone proteins. Aberrant HDAC activities are observed in fibrotic diseases, including cardiac and pulmonary fibrosis. HDAC inhibitors (HDACIs) are molecules that block HDAC functions. HDACIs have been studied extensively in a variety of tumors. Currently, there are four HDACIs approved by the US Food and Drug Administration for cancer treatment yet none for fibrotic diseases. Emerging evidence from in vitro and in vivo preclinical studies has presented beneficial effects of HDACIs in preventing or reversing fibrogenesis. In this review, we summarize the latest findings of the roles of HDACs in the pathogenesis of cardiac and pulmonary fibrosis and highlight the potential applications of HDACIs in these two fibrotic diseases.","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622319862697","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48129076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Abdul-Ghani, Muhammad Abdulla, Aza Aiet-Slimane, Tounsia Alavi, Afraneh Anitua, E Ansari, E Antoniu, SA Aşkın, Ayhan Aucella, F Barr, David Beales, Ian Bielefeld, P Bölük, C Bonomini, M Brunner, Patrick Cahoon, William Carrascosa, JM Carrette, Sofie Chang, TP Chiricozzi, Andrea Cohen, D Corbatón Anchuelo, Arturo Crowson, Cynthia Danby, Simon Daugherty, AM Dieter, Brad Dodiuk-Gad, RP Eadie, Mervyn Esposito, P Ferreira Cardoso, Mariana Fisher, Robert Fu, Ping Galimova, Elvira Galluzzo, M Gambazza, S George, Yasmin Gibson, David J Glantz, Stanton A González, Esteban Greenwood, SA Gregory, Darren G Grieshaber, Matthias Harvey, John Huang, L Iannone, Florenzo Jing, ZC Kang, Se-Won Kao, Jia-Horng Kataoka, Yoko Krivoy, A Linnebank, Michael Llamas Velasco, Mar Loughrey, David G Luchesi, KF Macaluso, Fabio Malčić, I Michigami, Toshimi Michopoulos, Spyridon Miller-Ellis, Eydie Mossello, Enrico Müller-Quernheim, Joachim Musiałek, Piotr Nakhostin Ansari, N Nashef, Lina Navas-Acien, Ana Nielsen, Ole Nowakowski, Alexandra Osborn, Katie Panza, Francesco Perry, Sarah Pilz, W Powell, Danielle Puig, Lluís Raina, A Razzaque, Mohammed Ring, Hans Ruan, Qingwei Rudaz, S Ruperto, M Rusu, E Saldaña, SN Sangwan, Virender S Savvas, SM Schofield, P Schröder, N Shah, RC Shrivastava, Vimal Stenager, E TAJ-Reviewer list_2018
{"title":"TAJ-Reviewer list_2018","authors":"Tounsia, Alavi, Afraneh, Anitua, Ansari, Antoniu, Ayhan, Aucella, David, Beales, Ian, Bielefeld, William, Carrascosa, Cynthia, Danby, Mervyn, Espósito, Esteban, Greenwood, G. Darren, Grieshaber, Matthias, Harvey, John, Huang, Florenzo, Jing, Se-Won, Kao, Jia-Horng, Kataoka, Yoko, Krivoy, Linnebank, Michael, Llamas Velasco, Mar, Loughrey, G. David, Luchesi, Kf, Macaluso, Toshimi, Michopoulos, Eydie, Mossello, Joachim, Musiałek, Piotr, Nakhostin Ansari, Ole, Nowakowski, Sarah, Pilz, Danielle, Puig, Sm, Schofield, Rc, Shrivastava, Vimal, Stenager","doi":"10.1177/2040622319829270","DOIUrl":"https://doi.org/10.1177/2040622319829270","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Abdul-Ghani, Muhammad Abdulla, Aza Aiet-Slimane, Tounsia Alavi, Afraneh Anitua, E Ansari, E Antoniu, SA Aşkın, Ayhan Aucella, F Barr, David Beales, Ian Bielefeld, P Bölük, C Bonomini, M Brunner, Patrick Cahoon, William Carrascosa, JM Carrette, Sofie Chang, TP Chiricozzi, Andrea Cohen, D Corbatón Anchuelo, Arturo Crowson, Cynthia Danby, Simon Daugherty, AM Dieter, Brad Dodiuk-Gad, RP Eadie, Mervyn Esposito, P Ferreira Cardoso, Mariana Fisher, Robert Fu, Ping Galimova, Elvira Galluzzo, M Gambazza, S George, Yasmin Gibson, David J Glantz, Stanton A González, Esteban Greenwood, SA Gregory, Darren G Grieshaber, Matthias Harvey, John Huang, L Iannone, Florenzo Jing, ZC Kang, Se-Won Kao, Jia-Horng Kataoka, Yoko Krivoy, A Linnebank, Michael Llamas Velasco, Mar Loughrey, David G Luchesi, KF Macaluso, Fabio Malčić, I Michigami, Toshimi Michopoulos, Spyridon Miller-Ellis, Eydie Mossello, Enrico Müller-Quernheim, Joachim Musiałek, Piotr Nakhostin Ansari, N Nashef, Lina Navas-Acien, Ana Nielsen, Ole Nowakowski, Alexandra Osborn, Katie Panza, Francesco Perry, Sarah Pilz, W Powell, Danielle Puig, Lluís Raina, A Razzaque, Mohammed Ring, Hans Ruan, Qingwei Rudaz, S Ruperto, M Rusu, E Saldaña, SN Sangwan, Virender S Savvas, SM Schofield, P Schröder, N Shah, RC Shrivastava, Vimal Stenager, E TAJ-Reviewer list_2018","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622319829270","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47244715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-01-01DOI: 10.1177/2040622319869116
Dan-Qian Chen, Gang Cao, Hui Zhao, Lin Chen, Tian Yang, Ming Wang, N. Vaziri, Yan Guo, Ying-yong Zhao
Background: Acute kidney injury (AKI) is one of the major risk factors for progression to chronic kidney disease (CKD) and renal fibrosis. However, effective therapies remain poorly understood. Here, we examined the renoprotective effects of melatonin and poricoic acid A (PAA) isolated from the surface layer of Poria cocos, and investigated the effects of combined therapy on the interaction of TGF-β/Smad and Wnt/β-catenin in a rat model of renal ischemia-reperfusion injury (IRI) and hypoxia/reoxygenation (H/R) or TGF-β1-induced HK-2 cells. Methods: Western blot and immunohistochemical staining were used to examine protein expression, while qRT-PCR was used to examine mRNA expression. Coimmunoprecipitation, chromatin immunoprecipitation, RNA interference, and luciferase reporter gene analysis were employed to explore the mechanisms of PAA and melatonin’s renoprotective effects. Results: PAA and combined therapy exhibited renoprotective and antifibrotic effects, but the underlying mechanisms were different during AKI-to-CKD continuum. Melatonin suppressed Smad-dependent and Smad-independent pathways, while PAA selectively inhibited Smad3 phosphorylation through distrupting the interactions of Smad3 with TGFβRI and SARA. Further studies demonstrated that the inhibitory effects of melatonin and PAA were partially depended on Smad3, especially PAA. Melatonin and PAA also inhibited the Wnt/β-catenin pathway and its profibrotic downstream targets, and PAA performed better. We further determined that IRI induced a nuclear Smad3/β-catenin complex, while melatonin and PAA disturbed the interaction of Smad3 and β-catenin, and supplementing with PAA could enhance the inhibitory effects of melatonin on the TGF-β/Smad and Wnt/β-catenin pathways. Conclusions: Combined melatonin and PAA provides a promising therapeutic strategy to treat renal fibrosis during the AKI-to-CKD continuum.
{"title":"Combined melatonin and poricoic acid A inhibits renal fibrosis through modulating the interaction of Smad3 and β-catenin pathway in AKI-to-CKD continuum","authors":"Dan-Qian Chen, Gang Cao, Hui Zhao, Lin Chen, Tian Yang, Ming Wang, N. Vaziri, Yan Guo, Ying-yong Zhao","doi":"10.1177/2040622319869116","DOIUrl":"https://doi.org/10.1177/2040622319869116","url":null,"abstract":"Background: Acute kidney injury (AKI) is one of the major risk factors for progression to chronic kidney disease (CKD) and renal fibrosis. However, effective therapies remain poorly understood. Here, we examined the renoprotective effects of melatonin and poricoic acid A (PAA) isolated from the surface layer of Poria cocos, and investigated the effects of combined therapy on the interaction of TGF-β/Smad and Wnt/β-catenin in a rat model of renal ischemia-reperfusion injury (IRI) and hypoxia/reoxygenation (H/R) or TGF-β1-induced HK-2 cells. Methods: Western blot and immunohistochemical staining were used to examine protein expression, while qRT-PCR was used to examine mRNA expression. Coimmunoprecipitation, chromatin immunoprecipitation, RNA interference, and luciferase reporter gene analysis were employed to explore the mechanisms of PAA and melatonin’s renoprotective effects. Results: PAA and combined therapy exhibited renoprotective and antifibrotic effects, but the underlying mechanisms were different during AKI-to-CKD continuum. Melatonin suppressed Smad-dependent and Smad-independent pathways, while PAA selectively inhibited Smad3 phosphorylation through distrupting the interactions of Smad3 with TGFβRI and SARA. Further studies demonstrated that the inhibitory effects of melatonin and PAA were partially depended on Smad3, especially PAA. Melatonin and PAA also inhibited the Wnt/β-catenin pathway and its profibrotic downstream targets, and PAA performed better. We further determined that IRI induced a nuclear Smad3/β-catenin complex, while melatonin and PAA disturbed the interaction of Smad3 and β-catenin, and supplementing with PAA could enhance the inhibitory effects of melatonin on the TGF-β/Smad and Wnt/β-catenin pathways. Conclusions: Combined melatonin and PAA provides a promising therapeutic strategy to treat renal fibrosis during the AKI-to-CKD continuum.","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622319869116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42609562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-10-19eCollection Date: 2019-01-01DOI: 10.1177/2040622318806848
Elliot M Friedman, Daniel K Mroczek, Sharon L Christ
Background: Using longitudinal data from the Survey of Mid-Life Development in the United States, this study examined the role of systemic inflammation in mediating the link between multimorbidity and increases in and onset of functional limitations over a 17-19 year follow-up period.
Methods: Participants completed questionnaire assessments of chronic conditions and functional limitations. Interleukin-6, C-reactive protein, and fibrinogen were assayed in serum. Structural equation models were used to predict increases in and onset of functional limitations associated with baseline multimorbidity status; mediation by inflammation was also determined.
Results: Multimorbidity (versus 0-1 conditions) predicted more functional limitations and greater odds of onset of limitations over time. Significant indirect effects showed that inflammation partially mediated the link between multimorbidity and changes in, but not onset of, limitations.
Discussion: These results show that inflammation, a nonspecific marker of multiple disease conditions, explains in part the degree to which multimorbidity is disabling.
{"title":"Multimorbidity, inflammation, and disability: a longitudinal mediational analysis.","authors":"Elliot M Friedman, Daniel K Mroczek, Sharon L Christ","doi":"10.1177/2040622318806848","DOIUrl":"10.1177/2040622318806848","url":null,"abstract":"<p><strong>Background: </strong>Using longitudinal data from the Survey of Mid-Life Development in the United States, this study examined the role of systemic inflammation in mediating the link between multimorbidity and increases in and onset of functional limitations over a 17-19 year follow-up period.</p><p><strong>Methods: </strong>Participants completed questionnaire assessments of chronic conditions and functional limitations. Interleukin-6, C-reactive protein, and fibrinogen were assayed in serum. Structural equation models were used to predict increases in and onset of functional limitations associated with baseline multimorbidity status; mediation by inflammation was also determined.</p><p><strong>Results: </strong>Multimorbidity (<i>versus</i> 0-1 conditions) predicted more functional limitations and greater odds of onset of limitations over time. Significant indirect effects showed that inflammation partially mediated the link between multimorbidity and changes in, but not onset of, limitations.</p><p><strong>Discussion: </strong>These results show that inflammation, a nonspecific marker of multiple disease conditions, explains in part the degree to which multimorbidity is disabling.</p>","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2018-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6700847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43682209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2016-11-24DOI: 10.1177/2040622316672544
Daniel Hammersley, Mark Signy
The aim of pharmacological lipid modification is to reduce low-density lipoprotein cholesterol (LDL-C) as a means of either secondary or primary prevention of cardiovascular disease. Statins are the first-line therapy for pharmacological lipid modification. Ezetimibe is a drug which reduces LDL-C by selectively inhibiting intestinal cholesterol absorption. This provides an alternative pharmacological approach to that of statin therapy to reduce LDL-C. Ezetimibe has been shown to significantly reduce levels of LDL-C and recently, as demonstrated in the IMPROVE-IT trial, to reduce the rate of cardiovascular events in high-risk patients. Ezetimibe therefore has an important role in pharmacological lipid modification. In this paper, we examine the body of research behind ezetimibe and assess its current clinical applications in different patient subgroups.
{"title":"Ezetimibe: an update on its clinical usefulness in specific patient groups.","authors":"Daniel Hammersley, Mark Signy","doi":"10.1177/2040622316672544","DOIUrl":"10.1177/2040622316672544","url":null,"abstract":"<p><p>The aim of pharmacological lipid modification is to reduce low-density lipoprotein cholesterol (LDL-C) as a means of either secondary or primary prevention of cardiovascular disease. Statins are the first-line therapy for pharmacological lipid modification. Ezetimibe is a drug which reduces LDL-C by selectively inhibiting intestinal cholesterol absorption. This provides an alternative pharmacological approach to that of statin therapy to reduce LDL-C. Ezetimibe has been shown to significantly reduce levels of LDL-C and recently, as demonstrated in the IMPROVE-IT trial, to reduce the rate of cardiovascular events in high-risk patients. Ezetimibe therefore has an important role in pharmacological lipid modification. In this paper, we examine the body of research behind ezetimibe and assess its current clinical applications in different patient subgroups.</p>","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5298356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43928778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.1177/2040622316679933
F. Gelman, J. Atrio
The pathophysiology, diagnosis and treatment of female sexual interest in pre- and post-menopausal women present a complex arena for patients and physicians to navigate. Flibanserin was the first pharmacologic treatment, approved by the United States Food and Drug Administration in August 2015, for hypoactive sexual desire disorder (HSDD) in premenopausal women. Side effects, contraindications and lack of approval in postmenopausal women are all limitations, as are issues surrounding patient and physician knowledge and access. Testosterone, buspirone, sildenafil, bupropion, bremelanotide, as well as herbal medications (Herbal vX or Tribulus terrestris) have demonstrated some clinical benefit in women with sexual dysfunction disorders however, trials have significant design, dosing or generalizability limitations. Nonpharmaceutical cognitive behavioral therapy, mindfulness meditation, pelvic floor therapy, and clitoral stimulators are also interventions women may pursue. This manuscript will explore the clinical data regarding these therapeutic modalities so as to bring attention to this issue of female HSDD, to offer an overview of current research, and to incite providers to initiate discussion among themselves and their patients.
{"title":"Flibanserin for hypoactive sexual desire disorder: place in therapy","authors":"F. Gelman, J. Atrio","doi":"10.1177/2040622316679933","DOIUrl":"https://doi.org/10.1177/2040622316679933","url":null,"abstract":"The pathophysiology, diagnosis and treatment of female sexual interest in pre- and post-menopausal women present a complex arena for patients and physicians to navigate. Flibanserin was the first pharmacologic treatment, approved by the United States Food and Drug Administration in August 2015, for hypoactive sexual desire disorder (HSDD) in premenopausal women. Side effects, contraindications and lack of approval in postmenopausal women are all limitations, as are issues surrounding patient and physician knowledge and access. Testosterone, buspirone, sildenafil, bupropion, bremelanotide, as well as herbal medications (Herbal vX or Tribulus terrestris) have demonstrated some clinical benefit in women with sexual dysfunction disorders however, trials have significant design, dosing or generalizability limitations. Nonpharmaceutical cognitive behavioral therapy, mindfulness meditation, pelvic floor therapy, and clitoral stimulators are also interventions women may pursue. This manuscript will explore the clinical data regarding these therapeutic modalities so as to bring attention to this issue of female HSDD, to offer an overview of current research, and to incite providers to initiate discussion among themselves and their patients.","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622316679933","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43187928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-01Epub Date: 2016-10-19DOI: 10.1177/2040622316665350
Edgardo Kaplinsky
Despite significant therapeutic advances, patients with chronic heart failure (HF) remain at high risk for HF progression and death. Sacubitril/valsartan (previously known as LCZ696) is a first-in-class medicine that contains a neprilysin (NEP) inhibitor (sacubitril) and an angiotensin II (Ang-II) receptor blocker (valsartan). NEP is an endopeptidase that metabolizes different vasoactive peptides including natriuretic peptides, bradykinin and Ang-II. In consequence, its inhibition increases mainly the levels of both, natriuretic peptides (promoting diuresis, natriuresis and vasodilatation) and Ang-II whose effects are blocked by the angiotensin receptor blocker, valsartan (reducing vasoconstriction and aldosterone release). Results from the 8442 patient PARADIGM-HF study showed in patients with New York Heart Association (NYHA) class II-IV and reduced ejection fraction treated with LCZ696 (versus enalapril), the following benefits: reduction of the risk of death from cardiovascular causes by 20%; reduction of HF hospitalizations by 21%; reduction of the risk of all-cause mortality by 16%. Overall there was a 20% risk reduction on the primary endpoint, composite measure of cardiovascular (CV) death or time to first HF hospitalization. PARADIGM-HF was stopped early after a median follow up of 27 months. Post hoc analyses of PARADIGM-HF as well as the place in therapy of sacubitril/valsartan, including future directions, are included in the present review.
{"title":"Sacubitril/valsartan in heart failure: latest evidence and place in therapy.","authors":"Edgardo Kaplinsky","doi":"10.1177/2040622316665350","DOIUrl":"10.1177/2040622316665350","url":null,"abstract":"<p><p>Despite significant therapeutic advances, patients with chronic heart failure (HF) remain at high risk for HF progression and death. Sacubitril/valsartan (previously known as LCZ696) is a first-in-class medicine that contains a neprilysin (NEP) inhibitor (sacubitril) and an angiotensin II (Ang-II) receptor blocker (valsartan). NEP is an endopeptidase that metabolizes different vasoactive peptides including natriuretic peptides, bradykinin and Ang-II. In consequence, its inhibition increases mainly the levels of both, natriuretic peptides (promoting diuresis, natriuresis and vasodilatation) and Ang-II whose effects are blocked by the angiotensin receptor blocker, valsartan (reducing vasoconstriction and aldosterone release). Results from the 8442 patient PARADIGM-HF study showed in patients with New York Heart Association (NYHA) class II-IV and reduced ejection fraction treated with LCZ696 (<i>versus</i> enalapril), the following benefits: reduction of the risk of death from cardiovascular causes by 20%; reduction of HF hospitalizations by 21%; reduction of the risk of all-cause mortality by 16%. Overall there was a 20% risk reduction on the primary endpoint, composite measure of cardiovascular (CV) death or time to first HF hospitalization. PARADIGM-HF was stopped early after a median follow up of 27 months. <i>Post hoc</i> analyses of PARADIGM-HF as well as the place in therapy of sacubitril/valsartan, including future directions, are included in the present review.</p>","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5076745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66121099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-08-11DOI: 10.1177/2040622316659863
F. Menzella, M. Lusuardi, C. Galeone, S. Taddei, N. Facciolongo, L. Zucchi
Severe asthma is characterized by major impairment of quality of life, poor symptom control and frequent exacerbations. Inflammatory, clinical and causative factors identify different phenotypes and endotypes of asthma. In the last few years, new treatment options have allowed for targeted treatments according to the different phenotypes of the disease. To accurately select a specific treatment for each asthmatic variant, the identification of appropriate biomarkers is required. Eosinophilic asthma is a distinct phenotype characterized by thickening of the basement membrane and corticosteroid responsiveness. This review reports the latest evidence on an anti-IL-5 monoclonal antibody, mepolizumab, a new and promising biological agent recently approved by the FDA specifically for the treatment of severe eosinophilic refractory asthma.
{"title":"Mepolizumab for severe refractory eosinophilic asthma: evidence to date and clinical potential","authors":"F. Menzella, M. Lusuardi, C. Galeone, S. Taddei, N. Facciolongo, L. Zucchi","doi":"10.1177/2040622316659863","DOIUrl":"https://doi.org/10.1177/2040622316659863","url":null,"abstract":"Severe asthma is characterized by major impairment of quality of life, poor symptom control and frequent exacerbations. Inflammatory, clinical and causative factors identify different phenotypes and endotypes of asthma. In the last few years, new treatment options have allowed for targeted treatments according to the different phenotypes of the disease. To accurately select a specific treatment for each asthmatic variant, the identification of appropriate biomarkers is required. Eosinophilic asthma is a distinct phenotype characterized by thickening of the basement membrane and corticosteroid responsiveness. This review reports the latest evidence on an anti-IL-5 monoclonal antibody, mepolizumab, a new and promising biological agent recently approved by the FDA specifically for the treatment of severe eosinophilic refractory asthma.","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2016-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/2040622316659863","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66121025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-01Epub Date: 2016-02-01DOI: 10.1177/2040622315624276
Silvia Puglisi, Sebastiano Emanuele Torrisi, Virginia Vindigni, Riccardo Giuliano, Stefano Palmucci, Massimiliano Mulè, Carlo Vancheri
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive parenchymal lung disease characterized by a median survival of 3-5 years following diagnosis. The diagnosis is based on clinical, radiological and histopathological evaluation. Therefore, a multidisciplinary team is needed to reach the correct diagnosis. For a long time, supportive care and lung transplantation in selected cases, have been considered the only possible treatments for IPF. In the last decade many studies have investigated IPF pathogenesis, leading to an improved knowledge of the mechanisms underlying the disease and to the approval of two new drugs for IPF treatment (pirfenidone and nintedanib). The therapeutic approach of IPF cannot be limited to the administration of antifibrotic drugs, but it is necessary for improving the quality of life of patients and for facilitating, as far as possible, the performance of normal daily activities and relationships. IPF patients are also afflicted by disease-related complications such as gastroesophageal reflux, pulmonary hypertension, acute exacerbations and an increased risk of developing lung cancer. The clinician who treats IPF patients, should also treat these possible complications to slow disease progression, thus maintaining the possibility of a pulmonary transplantation.
{"title":"New perspectives on management of idiopathic pulmonary fibrosis.","authors":"Silvia Puglisi, Sebastiano Emanuele Torrisi, Virginia Vindigni, Riccardo Giuliano, Stefano Palmucci, Massimiliano Mulè, Carlo Vancheri","doi":"10.1177/2040622315624276","DOIUrl":"10.1177/2040622315624276","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive parenchymal lung disease characterized by a median survival of 3-5 years following diagnosis. The diagnosis is based on clinical, radiological and histopathological evaluation. Therefore, a multidisciplinary team is needed to reach the correct diagnosis. For a long time, supportive care and lung transplantation in selected cases, have been considered the only possible treatments for IPF. In the last decade many studies have investigated IPF pathogenesis, leading to an improved knowledge of the mechanisms underlying the disease and to the approval of two new drugs for IPF treatment (pirfenidone and nintedanib). The therapeutic approach of IPF cannot be limited to the administration of antifibrotic drugs, but it is necessary for improving the quality of life of patients and for facilitating, as far as possible, the performance of normal daily activities and relationships. IPF patients are also afflicted by disease-related complications such as gastroesophageal reflux, pulmonary hypertension, acute exacerbations and an increased risk of developing lung cancer. The clinician who treats IPF patients, should also treat these possible complications to slow disease progression, thus maintaining the possibility of a pulmonary transplantation. </p>","PeriodicalId":22960,"journal":{"name":"Therapeutic Advances in Chronic Disease","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66121189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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