Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease
Abstract
OBJECTIVES: Dehydroepiandrosterone sulfate (DHEAS) and cortisol are multifunctional adrenal hormones with immunomodulating properties. DHEAS levels were found to be very low in chronic inflammatory diseases. This study aimed to shed more light on the interrelation between DHEAS and cortisol (and humoral markers of inflammation) in chronic inflammatory bowel disease. METHODS: DHEAS and cortisol serum levels were measured by ELISA in the serum of 66 normal subjects, 115 patients with Crohn's disease (CD) and 64 patients with ulcerative colitis (UC). Humoral markers of inflammation and disease activity scores were assessed by standard techniques. RESULTS: DHEAS was lower in patients with CD (p < 0.005) and UC (p < 0.005) than in controls, which was, in part, dependent on previous corticosteroid treatment (p < 0.01). In CD patients, z-normalized DHEAS was inversely correlated with blood sedimentation rate (p = 0.017). Z-normalized DHEAS was negatively correlated with interleukin-6 (IL-6) in the form of a trend (p = 0.068), and z-normalized DHEAS was significantly positively correlated with hemoglobin (p = 0.001) but not with the Crohn's disease activity index. Cortisol, however, was positively correlated with blood sedimentation rate (p = 0.034) and C-reactive protein (p = 0.006). In contrast, in UC patients no such correlation of z-normalized DHEAS or cortisol and parameters of humoral inflammatory activity or Rachmilewitz index exist. CONCLUSIONS: DHEAS as a marker of inflammation was low in CD and UC. In CD patients, low DHEAS and high cortisol serum levels were associated with higher humoral inflammatory activity. With respect to humoral inflammatory activity in CD patients, DHEAS and cortisol seem to be inversely regulated, which may have an impact on several immune functions, such as IL-6 secretion.
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In chronic inflammatory diseases of different etiology, serum androgens are very low.
“In CIDs of different etiology, serum androgens are very low [94-96], but estrogen levels remain relatively normal as a consequence of increased conversion of androgens into estrogens in inflamed tissue [97].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [96]
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Self-citation
- Authors
- Straub, R. H., Vogl, D., Gross, V., Lang, B., Schölmerich, J., & Andus, T.
- Affiliations
- University Hospital Regensburg (DE)
- Venue
- American Journal of Gastroenterology
- Published
- 1998-11
- Volume
- 93
- Issue
- 11
- Pages
- 2197-2202
- ISSN
- 0002-9270 (ISSN-L)
- OpenAlex
- W1992446619
- Cited by
- 114
- References
- 24
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 4 · 2015: 2 · 2014: 3 · 2013: 2 · 2012: 4
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The American Journal of Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
- Keywords
- dehydroepiandrosterone sulfate, cortisol, inflammatory bowel disease, Crohn's disease, ulcerative colitis, interleukin-6, C-reactive protein, erythrocyte sedimentation rate, hemoglobin, corticosteroid therapy, disease activity, adrenal hormones
- MeSH terms
- Adolescent, Adult, Blood Sedimentation, C-Reactive Protein, Colitis, Ulcerative, Crohn Disease, Enzyme-Linked Immunosorbent Assay, Female, Humans, Hydrocortisone, Male, Middle Aged, Tumor Necrosis Factor-alpha, Inflammatory Bowel Diseases, Receptors, Interleukin-2, Cell Adhesion Molecules, Interleukin-6, Receptors, Interleukin-1, Inflammation Mediators, Dehydroepiandrosterone Sulfate
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