Multivariable Prediction Model for Biochemical Response to First-Generation Somatostatin Receptor Ligands in Acromegaly.


Journal

The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362

Informations de publication

Date de publication:
01 09 2020
Historique:
received: 12 06 2020
accepted: 22 06 2020
pubmed: 27 6 2020
medline: 25 2 2021
entrez: 27 6 2020
Statut: ppublish

Résumé

First-generation somatostatin receptor ligands (fg-SRLs) represent the mainstay of medical therapy for acromegaly, but they provide biochemical control of disease in only a subset of patients. Various pretreatment biomarkers might affect biochemical response to fg-SRLs. To identify clinical predictors of the biochemical response to fg-SRLs monotherapy defined as biochemical response (insulin-like growth factor (IGF)-1 ≤ 1.3 × ULN (upper limit of normal)), partial response (>20% relative IGF-1 reduction without normalization), and nonresponse (≤20% relative IGF-1 reduction), and IGF-1 reduction. Retrospective multicenter study. Eight participating European centers. We performed a meta-analysis of participant data from 2 cohorts (Rotterdam and Liège acromegaly survey, 622 out of 3520 patients). Multivariable regression models were used to identify predictors of biochemical response to fg-SRL monotherapy. Lower IGF-1 concentration at baseline (odds ratio (OR) = 0.82, 95% confidence interval (CI) 0.72-0.95 IGF-1 ULN, P = .0073) and lower bodyweight (OR = 0.99, 95% CI 0.98-0.99 kg, P = .038) were associated with biochemical response. Higher IGF-1 concentration at baseline (OR = 1.40, (1.19-1.65) IGF-1 ULN, P ≤ .0001), the presence of type 2 diabetes (oral medication OR = 2.48, (1.43-4.29), P = .0013; insulin therapy OR = 2.65, (1.02-6.70), P = .045), and higher bodyweight (OR = 1.02, (1.01-1.04) kg, P = .0023) were associated with achieving partial response. Younger patients at diagnosis are more likely to achieve nonresponse (OR = 0.96, (0.94-0.99) year, P = .0070). Baseline IGF-1 and growth hormone concentration at diagnosis were associated with absolute IGF-1 reduction (β = 0.90, standard error (SE) = 0.02, P ≤ .0001 and β  = 0.002, SE = 0.001, P = .014, respectively). Baseline IGF-1 concentration was the best predictor of biochemical response to fg-SRL, followed by bodyweight, while younger patients were more likely to achieve nonresponse.

Identifiants

pubmed: 32589751
pii: 5863389
doi: 10.1210/clinem/dgaa387
pii:
doi:

Substances chimiques

Biomarkers 0
Biomarkers, Pharmacological 0
Ligands 0
Peptides, Cyclic 0
Receptors, Somatostatin 0
lanreotide 0G3DE8943Y
Human Growth Hormone 12629-01-5
Somatostatin 51110-01-1
Insulin-Like Growth Factor I 67763-96-6
Octreotide RWM8CCW8GP

Types de publication

Journal Article Meta-Analysis Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© Endocrine Society 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Eva C Coopmans (EC)

Department of Medicine, Endocrinology section, Pituitary Center Rotterdam, Erasmus University Medical Center, Rotterdam, the Netherlands.

Tim I M Korevaar (TIM)

Department of Medicine, Endocrinology section, Pituitary Center Rotterdam, Erasmus University Medical Center, Rotterdam, the Netherlands.

Sebastiaan W F van Meyel (SWF)

Department of Medicine, Endocrinology section, Pituitary Center Rotterdam, Erasmus University Medical Center, Rotterdam, the Netherlands.

Adrian F Daly (AF)

Endocrinologie Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart-Tilman, Liège, Belgium.

Philippe Chanson (P)

Assistance Publique-Hôpitaux de Paris, Hôpital de Bicêtre, Service d'Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de l'Hypophyse, Le Kremlin Bicêtre, France.
Université Paris-Saclay, Univ. Paris-Sud, Inserm, Signalisation Hormonale, Physiopathologie Endocrinienne et Métabolique, Le Kremlin-Bicêtre, France.

Thierry Brue (T)

Aix-Marseille Université, CNRS, Marseille, France.
APHM, Hôpital Conception, Service d'Endocrinologie, Diabète et Maladies Métaboliques, Centre de Référence des Maladies Rares d'Origine Hypophysaire, Marseille, France.

Brigitte Delemer (B)

Department of Endocrinology, Diabetes, and Nutrition, University Hospital of Reims, Reims, France.

Václav Hána (V)

3rd Department of Internal Medicine, First Medical Faculty, Charles University, Prague, Czech Republic.

Annamaria Colao (A)

Dipartimento di Medicina Clinica e Chirurgia, Università Federico II di Napoli, Naples, Italy.

Davide Carvalho (D)

Department of Endocrinology, Diabetes and Metabolism Section and Instituto de Investigação e Inovação em Saúde, University of Porto, Centro Hospitalar S. João, Porto, Portugal.

Marie-Lise Jaffrain-Rea (ML)

Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila and Neuromed, IRCCS, Pozzilli, Italy.

Günter K Stalla (GK)

Clinical Neuroendocrinology, Max-Planck-Institute of Psychiatry, Munich, Germany.

Carmen Fajardo-Montañana (C)

Servicio de Endocrinología, Hospital Universitario La Ribera, Valencia, Spain.

Albert Beckers (A)

Endocrinologie Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart-Tilman, Liège, Belgium.

Aart J van der Lely (AJ)

Department of Medicine, Endocrinology section, Pituitary Center Rotterdam, Erasmus University Medical Center, Rotterdam, the Netherlands.

Patrick Petrossians (P)

Endocrinologie Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart-Tilman, Liège, Belgium.

Sebastian J C M M Neggers (SJCMM)

Department of Medicine, Endocrinology section, Pituitary Center Rotterdam, Erasmus University Medical Center, Rotterdam, the Netherlands.

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Classifications MeSH