ArticleEndocrine2014
Adrenocorticotropin responsiveness to acute octreotide administration is not affected by mifepristone premedication in patients with Cushing's disease.
Article in Endocrine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Glucocorticoid Receptor Antagonism Upregulates Somatostatin Receptor Subtype 2 Expression in ACTH-Producing Neuroendocrine Tumors: New Insight Based on the Selective Glucocorticoid Receptor Modulator Relacorilant.Frontiers in endocrinology · 2021Article
- Role of "old" pharmacological agents in the treatment of Cushing's syndrome.Journal of endocrinological investigation · 2016Review
- Mifepristone Improves Octreotide Efficacy in Resistant Ectopic Cushing's Syndrome.Case reports in endocrinology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Octreotide (OCT) is ineffective in patients with Cushing's disease (CD) due to the cortisol-induced down-regulation of somatostatin receptor subtype 2 which was shown to be reversible in vitro by using anti-glucocorticoid mifepristone. This study aimed to verify, in vivo, if mifepristone can modulate response to acute OCT administration in patients with CD. Three men and two postmenopausal women (age 52.5 ± 2 years) with CD were enrolled in the study. OCT (100 μg, s.c.) was administered alone on the first day (OCT-only), and it was then given after mifepristone administration (2 × 200 mg, p.os, 12 and 1 h before OCT), 3 days later (OCT-mif). ACTH and cortisol levels were measured before OCT administration and every 60 min thereafter for 6 h. Baseline ACTH and cortisol values, nadir values and percentage decrements (Δn) were compared during both tests. Mean ACTH-Δn did not differ significantly during the two tests. Both tests induced a <30 % decrease in plasma ACTH in three patients (#1, 2 and 3) and a >50 % decrease in the other two cases (#4 and 5). Cortisol decreased in patients #4 and 5, during both tests. ACTH-Δn did not correlate with morning cortisol nor with urinary free cortisol values. Patients #4 and 5 with the highest ACTH-Δn had the lowest cortisol values after 1 mg of dexamethasone. Brief mifepristone pre-treatment does not modify ACTH and cortisol response to acute OCT administration in CD. However, OCT seems to be more effective in patients with partially preserved cortisol inhibitory feedback.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.