Increased cytokine production capacity and persistent inflammation after achieving remission of Cushing's syndrome.

Pepijn van Houten, Annenienke C van de Ven, Antonius E van Herwaarden, Mihai G Netea, Martin Jaeger, Romana T Netea-Maier

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Article in Journal of clinical & translational endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Pepijn van HoutenDepartment of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, the Netherlands.

Annenienke C van de VenDepartment of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, the Netherlands.

Antonius E van HerwaardenDepartment of Laboratory Medicine, Radboud University Medical Center, Nijmegen, the Netherlands.

Mihai G NeteaDepartment of Internal Medicine, Radboud Community for Infectious Diseases, Radboud University Medical Center, Nijmegen, the Netherlands.

Martin JaegerDepartment of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, the Netherlands.

Romana T Netea-MaierDepartment of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, the Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous Cushing's syndrome (CS) is characterized by chronic hypercortisolism. After achieving remission, morbidity remains increased and quality of life remains impaired. Moreover, the incidence of inflammatory disorders increases after remission of CS. Despite these immune-mediated clinical consequences, the course of innate immune cell function after remission of CS is poorly known. In this study we aimed to assess changes in innate immune cell function and systemic inflammatory markers after achieving remission of CS. Blood samples were collected from nine CS patients (six adrenal CS and three Cushing's disease) at diagnosis and after achieving remission and fully tapering off glucocorticoid suppletion. Peripheral blood mononuclear cell (PBMC) cellularity and monocyte-derived cytokine responses upon 24 h of

Indexed as

Cushing’s diseaseCushing’s syndromeInflammationInnate immunityMonocytes

Identifiers

PMID42125601

DOI10.1016/j.jcte.2026.100443

PMCPMC13158595

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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.