Pancreas-related persisting sequelae in ALL survivors with a history of asparaginase-associated pancreatitis: A part of the ALL-STAR study

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  • Mette Tiedemann Skipper
  • Niels Birkebæk
  • Jensen, Rikke Bodin Beck
  • Cecilie Utke Rank
  • Ruta Tuckuviene
  • Peder Skov Wehner
  • Trine-Lise Lambine
  • Arne Hørlyck
  • Schmiegelow, K.
  • Thomas Leth Frandsen
  • Liv Andrés-Jensen
  • Birgitte Klug Albertsen
Objectives
Asparaginase-associated pancreatitis (AAP) occurs in up to 18% of patients treated for acute lymphoblastic leukemia (ALL); however, long-term sequelae are largely unexplored. We aimed to explore pancreatic sequelae among ALL survivors with and without AAP.

Methods
We investigated pancreatic sequelae in a national cohort of ALL survivors, aged 1–45 years at ALL diagnosis treated according to the NOPHO-ALL2008 protocol and included sex- and age-matched community controls.

Results
We included 368 survivors (median follow-up 6.9 years), including 47 survivors with AAP and 369 controls. The p-lipase and p-pancreas-type amylase levels were lower in AAP survivors compared with both non-AAP survivors (Medians: 23 U/L [IQR 14–32] and 18 U/L [IQR 10–25] versus 29 [IQR 24–35] and 22 [17–28], p < .001 and p = .002) and community controls (28 U/L [IQR 22–33] and 21 U/L [IQR 17–26], both p < .006). Fecal-elastase was more frequently reduced in AAP survivors compared with non-AAP survivors (7/31 vs. 4/144, p = .001). Persisting pancreatic sequelae were found in 15/47 of AAP survivors and 20/323 of non-AAP survivors (p < .001), including diabetes mellitus in 2/39 of AAP survivors and 2/273 of non-AAP survivors.

Conclusions
ALL survivors with AAP are at increased risk of persisting pancreatic dysfunction and require special attention during follow-up.
OriginalsprogEngelsk
BogserieEuropean Journal of Haematology
Vol/bind112
Udgave nummer6
Sider (fra-til)944-956
ISSN0902-4441
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
This study has received funding from the Danish Childhood Cancer Foundation (2017‐2082, 2019‐5966, 2019‐5934, 2020‐5769, 2020‐6737, 2022‐8161), The Danish Cancer Society (R192‐A11590, R‐257‐A14720 and R‐302‐A17277), Health Research Foundation of Central Denmark Region (A3697), Aarhus University (grant number not applicable), Grosserer M. Brogaard og Hustrus Mindefond (grant number not applicable), Riisfort Fonden (grant number not applicable), Tømrermester Jørgen Holm og hustru Elisa f. Hansens Mindelegat (20 006‐1975), Aase og Ejnar Danielsens Fond (21‐10‐0133), The Danish Cancer Research Foundation (FID20823), NordForsk (ID 91 172), Ingeniør Otto Christensens Fond (101459), A.P. Møller and Chastine Mc‐Kinney Møller Foundation (18‐L‐0225), Farmer of Oelufgaard Memorial Foundation (grant number not applicable), Helga og Peter Kornings Fond, Torben Iversens travelling scholarship (grant number not applicable) and Skagen Teddy Bear Museum (grant number not applicable). The funding sources had no role in the design of the study, data analysis or interpretation, nor the decision to submit the manuscript for publication.

Publisher Copyright:
© 2024 The Authors. European Journal of Haematology published by John Wiley & Sons Ltd.

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