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Anker, Stefan Dietmar
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Anker, Stefan Dietmar
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Anker, Stefan Dietmar
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Anker, Stefan D.
Anker, S. D.
Anker, Stefan
Anker, S.
Anker, Stephan Dietmar
Anker, Stephan D.
Anker, Stephan
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2015Journal Article [["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Rozentryt, Piotr"],["dc.contributor.author","Niedziela, Jacek T."],["dc.contributor.author","Hudzik, Bartosz"],["dc.contributor.author","Lekston, Andrzej"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","Nowak, Jolanta"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Partyka, Robert"],["dc.contributor.author","Rywik, Tomasz"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Poloński, Lech"],["dc.date.accessioned","2019-07-09T11:42:02Z"],["dc.date.available","2019-07-09T11:42:02Z"],["dc.date.issued","2015"],["dc.description.abstract","Background A higher serum phosphate level is associated with worse outcome. Energy-demanding intracellular transport of phosphate is needed to secure anion bioavailability. In heart failure (HF), energy starvation may modify intracellular and serum levels of phosphate. We analysed determinants of serum phosphates in HF and assessed if catabolic/anabolic balance (CAB) was associated with elevation of serum phosphate. Methods We retrospectively reviewed data from 1029 stable patients with HF and have calculated negative (loss) and positive (gain) components of weight change from the onset of HF till index date. The algebraic sum of these components was taken as CAB. The univariate and multivariable predictors of serum phosphorus were calculated. In quintiles of CAB, we have estimated odds ratios for serum phosphorus above levels previously identified to increase risk of mortality. As a reference, we have selected a CAB quintile with similar loss and gain. Results Apart from sex, age, and kidney function, we identified serum sodium, N-terminal fragment of pro-brain-type natriuretic peptide, and CAB as independent predictors of serum phosphorus. The odds for serum phosphorus above thresholds found in literature to increase risk were highest in more catabolic patients. In most catabolic quintile relative to neutral balance, the odds across selected phosphorus thresholds rose, gradually peaking at 1.30 mmol/L with a value of 3.29 (95% confidence interval: 2.00–5.40, P < 0.0001) in an unadjusted analysis and 2.55 (95% confidence interval: 1.38–2.72, P = 0.002) in a fully adjusted model. Conclusions Metabolic status is an independent determinant of serum phosphorus in HF. Higher catabolism is associated with serum phosphorus above mortality risk-increasing thresholds."],["dc.identifier.doi","10.1002/jcsm.12026"],["dc.identifier.pmid","26672973"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58571"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.euproject","SICA-HF"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Higher serum phosphorus is associated with catabolic/anabolic imbalance in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article [["dc.bibliographiccitation.firstpage","956"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","961"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bauer, Juergen"],["dc.contributor.author","Morley, John E."],["dc.contributor.author","Schols, Annemie M.W.J."],["dc.contributor.author","Ferrucci, Luigi"],["dc.contributor.author","Cruz‐Jentoft, Alfonso J."],["dc.contributor.author","Dent, Elsa"],["dc.contributor.author","Baracos, Vickie E."],["dc.contributor.author","Crawford, Jeffrey A."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Heymsfield, Steven B."],["dc.contributor.author","Jatoi, Aminah"],["dc.contributor.author","Kalantar‐Zadeh, Kamyar"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Landi, Francesco"],["dc.contributor.author","Laviano, Alessandro"],["dc.contributor.author","Mancuso, Michelangelo"],["dc.contributor.author","Muscaritoli, Maurizio"],["dc.contributor.author","Prado, Carla M."],["dc.contributor.author","Strasser, Florian"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Coats, Andrew J.S."],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2020-12-10T14:06:45Z"],["dc.date.available","2020-12-10T14:06:45Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jcsm.12483"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16637"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70011"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Sarcopenia: A Time for Action. An SCWD Position Paper"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article [["dc.bibliographiccitation.firstpage","50"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","CardioRenal Medicine"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Habedank, Dirk"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Bernhardt, Carolin"],["dc.contributor.author","Karhausen, Tim"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Reinke, Petra"],["dc.date.accessioned","2018-11-07T10:29:37Z"],["dc.date.available","2018-11-07T10:29:37Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Previous data have pointed to the fact that vascular function is significantly impaired in patients with end-stage renal disease (ESRD). We aimed to better characterise vasodilation and exercise capacity in both ESRD and chronic heart failure (CHF) patients. Methods: A total of 30 ESRD patients (23 male; mean age 45.7 +/- 9.9 years) were included in a prospective proof-of-concept study at a tertiary care academic centre. The patients underwent forearm venous plethysmography with post-ischaemic peak blood flow (PF) and flow-dependent flow (FDF) testing as well as cardiopulmonary exercise testing during the morning of the day following the last haemodialysis. After matching for age, gender, and body mass index, the data were compared to 30 patients with CHF and 20 age-matched healthy controls. Results: PF in ESRD patients was reduced when compared to that in CHF patients (12.5 +/- 4.2 vs. 15.6 +/- 6.9 ml/100 ml/min; p = 0.048) and healthy controls (26.4 +/- 9.3 ml/100 ml/min; p < 0.001). When compared to controls, FDF was significantly reduced in ESRD patients (7.6 +/- 3.1 vs. 6.0 +/- 2.5 ml/100 ml/min; p = 0.03), but not in CHF patients, whereas resting blood flow did not differ between the ESRD, CHF, and healthy control groups. In contrast to indices of vasodilative capacity, maximum exercise capacity (peakVO(2)) was higher in ESRD when compared to CHF patients (23.8 +/- 7.3 vs. 18.8 +/- 5.2 ml/min/kg), but significantly impaired when compared to controls (32.8 +/- 6.7 ml/min/kg; p < 0.001). Conclusion: In this proof-of-concept study, exercise capacity was relatively preserved, while vasodilative capacity was substantially impaired in ESRD patients. Additional studies are warranted to examine the underlying mechanisms and potential clinical implications of our findings. (C) 2016 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000449174"],["dc.identifier.isi","000389244900006"],["dc.identifier.pmid","27994602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43674"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1664-5502"],["dc.relation.issn","1664-5502"],["dc.relation.issn","1664-3828"],["dc.rights","https://www.karger.com/Services/SiteLicenses"],["dc.title","Vasodilation and Exercise Capacity in Patients with End-Stage Renal Disease: A Prospective Proof-of-Concept Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article [["dc.bibliographiccitation.artnumber","10"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC neurology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Scherbakov, Nadja"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Meisel, Andreas"],["dc.contributor.author","Haeusler, Karl Georg"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D"],["dc.contributor.author","Dirnagl, Ulrich"],["dc.contributor.author","Joebges, Michael"],["dc.contributor.author","Doehner, Wolfram"],["dc.date.accessioned","2019-07-09T11:42:18Z"],["dc.date.available","2019-07-09T11:42:18Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND: Patients with stroke are at a high risk for long-term handicap and disability. In the first weeks after stroke muscle wasting is observed frequently. Early post-stroke rehabilitation programs are directed to improve functional independence and physical performance. Supplementation with essential amino acids (EAAs) might prevent muscle wasting and improve rehabilitation outcome by augmenting muscle mass and muscle strength. We aim to examine this in a double blinded, randomized placebo-controlled clinical trial. METHODS: Patients with ischemic or haemorrhagic stroke will be enrolled at begin of the early post-stroke rehabilitation in a parallel group interventional trial. Oral supplementation of EAAs or placebo will be given for 12 weeks in a double blinded manner. Physical and functional performance will be assessed by exercise testing before supplementation of EAAs as well as at discharge from the in-patient rehabilitation, at 12 weeks and 1 year afterwards. DISCUSSION: This is the first randomized double-blinded placebo-controlled clinical study aiming to assess the effect of the EAAs supplementation on muscle strength, muscle function and physical performance in stroke patients during early post-stroke rehabilitation. Supplementation of EAAs could prevent muscle mass wasting and improve functional independence after stroke. TRIAL REGISTRATION: The study is registered at the German registry for clinical trials as well as at World Health Organization (WHO; number DRKS00005577 )."],["dc.identifier.doi","10.1186/s12883-016-0531-5"],["dc.identifier.pmid","26793971"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58637"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2377"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Influence of essential amino acids on muscle mass and muscle strength in patients with cerebral stroke during early rehabilitation: protocol and rationale of a randomized clinical trial (AMINO-Stroke Study)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article [["dc.bibliographiccitation.firstpage","611"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","620"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Scherbakov, Nadja"],["dc.contributor.author","Pietrock, Charlotte"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Norman, Kristina"],["dc.contributor.author","Haeusler, Karl Georg"],["dc.date.accessioned","2021-06-01T10:50:54Z"],["dc.date.available","2021-06-01T10:50:54Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jcsm.12400"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86821"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Body weight changes and incidence of cachexia after stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2015Journal Article [["dc.bibliographiccitation.firstpage","85"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Turhan, Guelistan"],["dc.contributor.author","Leyva, Francisco"],["dc.contributor.author","Rauchhaus, Mathias"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Jankowska, Ewa A."],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2019-07-09T11:41:23Z"],["dc.date.available","2019-07-09T11:41:23Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Chronic heart failure (CHF) is associated with insulin resistance, indicating impairment in the control of energy metabolism. Insulin resistance in CHF relates to symptomatic status and independently predicts poor prognosis. We sought to determine whether insulin sensitivity is related to skeletal muscle strength in patients with CHF, taking into account muscle size and perfusion. Methods Quadriceps muscle size (square centimetre cross-sectional area at mid-femur level, computed tomography), isometric quadriceps muscle strength [absolute (in N) and strength per unit muscle area (N/cm2)], resting-leg blood flow (plethysmography) and maximal oxygen consumption (treadmill exercise test) were measured in 33 patients with CHF (left ventricular ejection fraction 28 ± 3.2%, mean ± Standard Error of the mean (SEM)) and 20 healthy controls. Insulin sensitivity was assessed by intravenous glucose tolerance tests and minimal modelling analysis. Results Right quadriceps strength (−27.0%, P < 0.0001), strength per muscle area (−18.0%, P < 0.003) and insulin sensitivity (−64.2%, P < 0.001) were lower in patients with CHF. The correlation between insulin sensitivity and absolute muscle strength was significant in the CHF group (r = 0.54, P = 0.001) and borderline in controls (r = 0.47, P = 0.06). This association remained significant between insulin sensitivity and strength per muscle area (CHF: r = 0.52, P < 0.01; controls: r = 0.62, P < 0.05). In stepwise regression analyses in CHF, only insulin sensitivity emerged as a predictor of strength per unit area of muscle [standardized coefficient (SC) = 0.45, P = 0.006; diuretic dose, SC = −0.31, P = 0.051; R2 = 0.37, P = 0.001], while age, left ventricular ejection fraction, maximal oxygen consumption, fasting glucose and insulin and blood flow were excluded. In controls, only insulin sensitivity remained in the final regression model (SC = 0.62, P = 0.004; R2 = 0.39, P = 0.004). Conclusions The myofibril contractile function of the quadriceps, i.e. functional quality of skeletal muscle, is strongly related to insulin sensitivity in patients with CHF and in healthy controls, independently of muscle size. Therapies aimed at improving insulin sensitivity in patients with CHF may clarify whether this relationship is causal."],["dc.identifier.doi","10.1002/ehf2.12035"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58415"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Skeletal muscle weakness is related to insulin resistance in patients with chronic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.firstpage","1242"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","1249"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Garfias Macedo, Tania"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Cleland, John G. F."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2021-04-14T08:24:54Z"],["dc.date.available","2021-04-14T08:24:54Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Skeletal muscle wasting is an extremely common feature in patients with heart failure, affecting approximately 20% of ambulatory patients with even higher values during acute decompensation. Its occurrence is associated with reduced exercise capacity, muscle strength, and quality of life. We sought to investigate if the presence of muscle wasting carries prognostic information. Methods Two hundred sixty‐eight ambulatory patients with heart failure (age 67.1 ± 10.9 years, New York Heart Association class 2.3 ± 0.6, left ventricular ejection fraction 39 ± 13.3%, and 21% female) were prospectively enrolled as part of the Studies Investigating Co‐morbidities Aggravating Heart Failure. Muscle wasting as assessed using dual‐energy X‐ray absorptiometry was present in 47 patients (17.5%). Results During a mean follow‐up of 67.2 ± 28.02 months, 95 patients (35.4%) died from any cause. After adjusting for age, New York Heart Association class, left ventricular ejection fraction, creatinine, N‐terminal pro‐B‐type natriuretic peptide, and iron deficiency, muscle wasting remained an independent predictor of death (hazard ratio 1.80, 95% confidence interval 1.01–3.19, P = 0.04). This effect was more pronounced in patients with heart failure with reduced than in heart failure with preserved ejection fraction. Conclusions Muscle wasting is an independent predictor of death in ambulatory patients with heart failure. Clinical trials are needed to identify treatment approaches to this co‐morbidity."],["dc.identifier.doi","10.1002/jcsm.12603"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81461"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Muscle wasting as an independent predictor of survival in patients with chronic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.firstpage","594"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","605"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Pötsch, Mareike S."],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2021-06-01T10:50:56Z"],["dc.date.available","2021-06-01T10:50:56Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jcsm.12537"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17186"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86832"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","MT‐102 prevents tissue wasting and improves survival in a rat model of severe cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2017-11Journal Article [["dc.bibliographiccitation.firstpage","448"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC heart failure"],["dc.bibliographiccitation.lastpage","457"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Dos Santos, Marcelo R."],["dc.contributor.author","Emami, Amir"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2019-07-09T11:44:42Z"],["dc.date.available","2019-07-09T11:44:42Z"],["dc.date.issued","2017-11"],["dc.description.abstract","AIMS: We aimed to assess determinants of anorexia, that is loss of appetite in patients with heart failure (HF) and aimed to further elucidate the association between anorexia, functional capacity, and outcomes in affected patients. METHODS AND RESULTS: We assessed anorexia status among 166 patients with HF (25 female, 66 ± 12 years) who participated in the Studies Investigating Co-morbidities Aggravating HF. Anorexia was assessed by a 6-point Likert scale (ranging from 0 to 5), wherein values ≥1 indicate anorexia. Functional capacity was assessed as peak oxygen uptake (peak VO2 ), 6 min walk test, and short physical performance battery test. A total of 57 patients (34%) reported any anorexia, and these patients showed lower values of peak VO2 , 6 min walk distance, and short physical performance battery score (all P < 0.05). Using multivariate analysis adjusting for clinically important factors, only high-sensitivity C-reactive protein [odds ratio (OR) 1.24, P = 0.04], use of loop diuretics (OR 5.76, P = 0.03), and the presence of cachexia (OR 2.53, P = 0.04) remained independent predictors of anorexia. A total of 22 patients (13%) died during a mean follow-up of 22.5 ± 5.1 months. Kaplan-Meier curves for cumulative survival showed that those patients with anorexia presented higher mortality (Log-rank test P = 0.03). CONCLUSIONS: Inflammation, use of loop diuretics, and cachexia are associated with an increased likelihood of anorexia in patients with HF, and patients with anorexia showed impaired functional capacity and poor outcomes."],["dc.identifier.doi","10.1002/ehf2.12209"],["dc.identifier.pmid","28960880"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14870"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59070"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.issn","2055-5822"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Anorexia, functional capacity, and clinical outcome in patients with chronic heart failure: results from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2015Journal Article [["dc.bibliographiccitation.firstpage","174"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","180"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Pelgrim, Loes"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Baumgarten, Anna"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T09:56:41Z"],["dc.date.available","2018-11-07T09:56:41Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Activity of xanthine oxidase is induced in cancer cachexia, and its inhibition by allopurinol or oxypurinol improves survival and reduces wasting in the Yoshida hepatoma cancer cachexia model. Here, we tested the effects of the second-generation xanthine oxidase inhibitor febuxostat compared with placebo in the same model as used previously by our group. Methods Wistar rats (similar to 200g) were treated daily with febuxostat at 5mg/kg/day or placebo via gavage for a maximum of 17days. Weight change, quality of life, and body composition were analysed. After sacrifice, proteasome activity in the gastrocnemius muscle was measured. Muscle-specific proteins involved in metabolism were analysed by western blotting. Results Treatment of the tumour-bearing rats with febuxostat led to a significantly improved survival compared with placebo (hazard ratio: 0.45, 95% confidence interval: 0.22-0.93, P=0.03). Loss of body weight was reduced (-26.312.4g) compared with placebo (-50.2 +/- 2.1g, P<0.01). Wasting of lean mass was attenuated (-12.7 +/- 10.8g) vs. placebo (-31.9 +/- 2.1g, P<0.05). While we did not see an effect of febuxostat on proteasome activity at the end of the study, the pAkt/Akt ratio was improved by febuxostat (0.94 +/- 0.09) vs. placebo (0.41 +/- 0.05, P<0.01), suggesting an increase in protein synthesis. Conclusions Febuxostat attenuated cachexia progression and improved survival of tumour-bearing rats."],["dc.description.sponsorship","Sumitomo Life Welfare and Culture Foundation"],["dc.identifier.doi","10.1002/jcsm.12017"],["dc.identifier.isi","000355340500007"],["dc.identifier.pmid","26136193"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37010"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Febuxostat improves outcome in a rat model of cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS