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Endocrine Abstracts (2015) 37 GP01.01 | DOI: 10.1530/endoabs.37.GP.01.01

ECE2015 Guided Posters Adrenal (8 abstracts)

Low-dose ACTH testing does not predict treatment response to corticosteroids in community-acquired pneumonia

Claudine A Blum 1, , Philipp Schuetz 3 , Nicole Nigro 1 , Bettina Winzeler 1 , Birsen Arici 1 , Julie Refardt 1 , Sandrine A Urwyler 1 , Matthias Briel 1, , Beat Mueller 3 & Mirjam Christ-Crain 1

1Division of Endocrinology, Diabetology and Metabolism, Departments of Internal Medicine and Clinical Research, University Hospital Basel, Basel, Switzerland; 2Service d’Accueil des Urgences, CHU Pitié‐Salpêtrière et AP‐HP, Paris, France; 3Departments of Internal and Emergency Medicine and Department of Endocrinology, Diabetology and Clinical Nutrition, Medical University Clinic, Kantonsspital Aarau, Aarau, Switzerland; 4Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada.

Background: It is controversial whether the attenuated increase of circulating cortisol to ACTH stimulation predicts treatment response to corticosteroids in patients with critical illness. We investigated whether ACTH testing predicts treatment response to corticosteroids in patients with community-acquired pneumonia (CAP).

Methods: We performed a low dose (1 μg) ACTH test on admission in a prospective randomised, double-blind, placebo-controlled multicenter trial comparing prednisone 50 mg for 7 days to placebo in patients hospitalized with CAP. The results of the main study showed a benefit of corticosteroids in community-acquired pneumonia.1 Cortisol was measured at baseline and 30 min after stimulation with 1 μg ACTH. We performed Cox regression models for time to clinical stability (TTCS) to compare baseline and stimulated cortisol levels between both treatment groups.

Results: 348 patients in the prednisone group and 330 patients in the placebo group were evaluated. 176 patients in the prednisone group (50.6%) and 163 patients in the placebo group (49.4%) with a basal cortisol > median (751 nmol/l) had a significantly longer TTCS in both groups (4.4 days vs 2.1 days, P<0.0001 in the prednisone and 5.0 days vs 3.0 days in the placebo group, P=0.0003). Basal plasma cortisol levels did not predict treatment response to prednisone (P for interaction=0.84). Similarly, neither a delta cortisol <250 nmol/l after ACTH stimulation (P for interaction=0.84) nor the combination of basal cortisol and delta cortisol (P for interaction=0.82) predicted treatment response to corticosteroids.

Conclusion: Our data suggest that a low-dose ACTH test does not predict treatment response to corticosteroids in patients with CAP. This suggests a pharmacological effect of corticosteroids in patients with critical illness or CAP and argues against a critical illness-related corticosteroid insufficiency (CIRCI).

Reference: 1. Blum CA et al. Lancet 2015 pii: S0140-6736 (14) 62447–62448 (Jan 16).

Disclosure: This work was supported by the Swiss National Science Foundation (grant numbers PP0P3_123346, P2BSP3_155212, PP00P3_150531/1, 320030-138267, and 320030-150025), the Nora van Meeuwen Häfliger Stiftung and the Gottfried Julia Bangerter-Rhyner Stiftung.

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