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  • Osterlund, P.Karolinska Institutet (författare)

Continuation of fluoropyrimidine treatment with S-1 after cardiotoxicity on capecitabine- or 5-fluorouracil-based therapy in patients with solid tumours : a multicentre retrospective observational cohort study

  • Artikel/kapitelEngelska2022

Förlag, utgivningsår, omfång ...

  • Elsevier,2022
  • electronicrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-487238
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-487238URI
  • https://doi.org/10.1016/j.esmoop.2022.100427DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:150847906URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Background: Capecitabine- or 5-fluorouracil (5-FU)-based chemotherapy is widely used in many solid tumours, but is associated with cardiotoxicity. S-1 is a fluoropyrimidine with low rates of cardiotoxicity, but evidence regarding the safety of switching to S-1 after 5-FU- or capecitabine-associated cardiotoxicity is scarce.Patients and methods: This retrospective study (NCT04260269) was conducted at 13 centres in 6 countries. The primary endpoint was recurrence of cardiotoxicity after switch to S-1-based treatment due to 5-FU- or capecitabine-related cardiotoxicity: clinically meaningful if the upper boundary of the 95% confidence interval (CI; by competing risk) is not including 15%. Secondary endpoints included cardiac risk factors, diagnostic work-up, treatments, outcomes, and timelines of cardiotoxicity.Results: Per protocol, 200 patients, treated between 2011 and 2020 [median age 66 years (range 19-86); 118 (59%) males], were included. Treatment intent was curative in 145 (73%). Initial cardiotoxicity was due to capecitabine (n = 170), continuous infusion 5-FU (n = 22), or bolus 5-FU (n = 8), which was administered in combination with other chemotherapy, targeted agents, or radiotherapy in 133 patients. Previous cardiovascular comorbidities were present in 99 (50%) patients. Cardiotoxic events (n = 228/200) included chest pain (n = 125), coronary syndrome/ infarction (n = 69), arrhythmia (n = 22), heart failure/cardiomyopathy (n = 7), cardiac arrest (n = 4), and malignant hypertension (n = 1). Cardiotoxicity was severe or life-threatening in 112 (56%) patients and led to permanent capecitabine/5-FU discontinuation in 192 (96%). After switch to S-1, recurrent cardiotoxicity was observed in eight (4%) patients (95% CI 2.02-7.89, primary endpoint met). Events were limited to grade 1-2 and occurred at a median of 16 days (interquartile range 7-67) from therapy switch. Baseline ischemic heart disease was a risk factor for recurrent cardiotoxicity (odds ratio 6.18, 95% CI 1.36-28.11).Conclusion: Switching to S-1-based therapy is safe and feasible after development of cardiotoxicity on 5-FU- or capecitabine-based therapy and allows patients to continue their pivotal fluoropyrimidine-based treatment.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Kinos, S.Tampere Univ Hosp, Dept Oncol, Tampere, Finland.;Univ Tampere, Tampere, Finland. (författare)
  • Pfeiffer, P.Odense Univ Hosp, Dept Oncol, Odense, Denmark. (författare)
  • Salminen, T.Tampere Univ Hosp, Dept Oncol, Tampere, Finland.;Univ Tampere, Tampere, Finland. (författare)
  • Kwakman, J. J. M.Amsterdam Univ Med Ctr, Dept Oncol, Amsterdam, Netherlands. (författare)
  • Frodin, J-EKarolinska Institutet (författare)
  • Shah, C. H.Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden. (författare)
  • Sorbye, H.Haukeland Hosp, Dept Oncol, Bergen, Norway.;Univ Bergen, Dept Clin Sci, Bergen, Norway. (författare)
  • Ristamaki, R.Turku Univ Hosp, Dept Oncol, Turku, Finland.;Univ Turku, Turku, Finland. (författare)
  • Halonen, P.Helsinki Univ Hosp, Dept Oncol, Helsinki, Finland.;Univ Helsinki, Helsinki, Finland. (författare)
  • Soveri, L. M.Helsinki Univ Hosp, Dept Oncol, Helsinki, Finland.;Univ Helsinki, Helsinki, Finland. (författare)
  • Heerva, E.Turku Univ Hosp, Dept Oncol, Turku, Finland.;Univ Turku, Turku, Finland. (författare)
  • Algars, A.Turku Univ Hosp, Dept Oncol, Turku, Finland.;Univ Turku, Turku, Finland. (författare)
  • Barlund, M.Tampere Univ Hosp, Dept Oncol, Tampere, Finland.;Univ Tampere, Tampere, Finland. (författare)
  • Hagman, H.Skane Univ Hosp, Dept Oncol, Lund, Sweden. (författare)
  • McDermott, R.St Vincents Univ Hosp, Dept Oncol, Dublin, Ireland. (författare)
  • O'Reilly, M.St Vincents Univ Hosp, Dept Oncol, Dublin, Ireland. (författare)
  • Röckert, R.Uppsala Univ Hosp, Dept Oncol, Uppsala, Sweden. (författare)
  • Liposits, G.Odense Univ Hosp, Dept Oncol, Odense, Denmark.;Reg Hosp West Jutland, Dept Oncol, Herning, Denmark. (författare)
  • Kallio, R.Tampere Univ Hosp, Dept Oncol, Tampere, Finland.;Univ Tampere, Tampere, Finland.;Oulu Univ Hosp, Dept Oncol, Oulu, Finland. (författare)
  • Flygare, P.Sundsvall Hosp, Dept Oncol, Sundsvall, Sweden. (författare)
  • Teske, A. J.Univ Med Ctr Utrecht, Dept Cardiol, Utrecht, Netherlands. (författare)
  • van Werkhoven, E.Netherlands Canc Inst, Dept Biometr, Amsterdam, Netherlands. (författare)
  • Punt, C. J. A.Univ Utrecht, Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Dept Epidemiol, Utrecht, Netherlands. (författare)
  • Glimelius, BengtUppsala universitet,Cancerprecisionsmedicin(Swepub:uu)bengglim (författare)
  • Karolinska InstitutetTampere Univ Hosp, Dept Oncol, Tampere, Finland.;Univ Tampere, Tampere, Finland. (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:ESMO Open: Elsevier7:32059-7029

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  • ESMO Open (Sök värdpublikationen i LIBRIS)

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