Impaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis

Kebapçılar, Levent; Bilgir, Oktay; Alacacıoğlu, Ahmet; Yıldız, Yaşar; Taylan, Ali; Günaydın, Rezzan; Yüksel, Arif; Karaca, Burçak; Sarı, İ̇smail

doi:10.1007/bf03346548

Cited by 11 publications

(6 citation statements)

References 29 publications

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“…52 A study examining the low-dose adrenocorticotropic hormone (ACTH) test (LDST) showed that after low-dose ACTH, the cortisol increment was significantly lower in AS patients than in controls (20.0 ± 4.4 vs 24 ± 2.2 microg/dl, P < 0.001). 53 The subclinical glucocorticoid deficiency indicated an impaired hypothalamic-pituitary-adrenal (HPA) axis in AS patients, suggesting the involvement of the endocrine system in the etiology of AS.…”

Section: Introductionmentioning

confidence: 99%

Ankylosing spondylitis: etiology, pathogenesis, and treatments

et al. 2019

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Ankylosing spondylitis (AS), a common type of spondyloarthropathy, is a chronic inflammatory autoimmune disease that mainly affects spine joints, causing severe, chronic pain; additionally, in more advanced cases, it can cause spine fusion. Significant progress in its pathophysiology and treatment has been achieved in the last decade. Immune cells and innate cytokines have been suggested to be crucial in the pathogenesis of AS, especially human leukocyte antigen (HLA)‑B27 and the interleukin‑23/17 axis. However, the pathogenesis of AS remains unclear. The current study reviewed the etiology and pathogenesis of AS, including genome-wide association studies and cytokine pathways. This study also summarized the current pharmaceutical and surgical treatment with a discussion of future potential therapies.

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Section: Introductionmentioning

confidence: 99%

Ankylosing spondylitis: etiology, pathogenesis, and treatments

et al. 2019

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“…In the current study, both regimens could not reduce IR and glucose metabolism. Evidence has shown that there was no effect of OCP containing cyproterone acetate on IR and glucose metabolism after 3 months of treatment . With a longer duration of using OCP, there have been contradictory data on the impact of OCP on IR .…”

Section: Discussionmentioning

confidence: 99%

Comparison of desogestrel/ethinyl estradiol plus spironolactone versus cyproterone acetate/ethinyl estradiol in the treatment of polycystic ovary syndrome: A randomized controlled trial

Leelaphiwat

Jongwutiwes

Lertvikool

et al. 2014

J of Obstet and Gynaecol

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“…Low serum levels of sex hormones, especially dehydroepiandrosterone sulfate (DHEAS) (i.e., androgen drain), may also contribute to bone loss in patients with AS, while patients with early or adult reactive arthritis have a high cortisol and DHEA serum levels that might change the course of disease (40,41). After administration of a low-dose of adrenocorticotropic hormone (ACTH), the serum cortisol rise became significantly lower in patients with AS than in controls, suggesting an impaired hypothalamic-pituitary-adrenal (HPA) axis and reinforcing the possibility of involvement of the neuroendocrine system in the etiology of AS ("the disproportion principle") (42). More importantly, low cortisol and testosterone serum levels were found in subjects with active JIA, while the lowest androgen levels were found in those patients in whom disease extended into their adult life (43).…”

Section: Stressors Exposure and Neuroendocrine Immuno-modulationmentioning

confidence: 99%

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Harjaček

2021

Front. Med.

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Juvenile spondyloarthritis (jSpA) is a an umbrella term for heterogeneous group of related seronegative inflammatory disorders sharing common symptoms. Although it mainly affects children and adolescents, it often remains active during adulthood. Genetic and environmental factors are involved in its occurrence, although the exact underlying immunopathophysiology remains incompletely elucidated. Accumulated evidence suggests that, in affected patients, subclinical gut inflammation caused by intestinal dysbiosis, is pivotal to the future development of synovial–entheseal complex inflammation. While the predominant role of IL17/23 axis, TNF-α, and IL-7 in the pathophysiology of SpA, including jSpA, is firmly established, the role of the cytokine macrophage migration inhibitory factor (MIF) is generally overlooked. The purpose of this review is to discuss and emphasize the role of epigenetics, neuroendocrine pathways and the hypothalamic-pituitary (HPA) axis, and to propose a novel hypothesis of the role of decreased NLRP3 gene expression and possibly MIF in the early phases of jSpA development. The decreased NLRP3 gene expression in the latter, due to hypomethylation of promotor site, is (one of) the cause for inflammasome malfunction leading to gut dysbiosis observed in patients with early jSpA. In addition, we highlight the role of MIF in the complex innate, adaptive cellular and main effector cytokine network, Finally, since treatment of advanced bone pathology in SpA remains an unmet clinical need, I suggest possible new drug targets with the aim to ultimately improve treatment efficacy and long-term outcome of jSpA patients.

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Impaired hypothalamo-pituitary-adrenal axis in patients with ankylosing spondylitis

Abstract: Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in AS patients. Anti-TNF treatment seems not to have effect on HPA axis.

Cited by 11 publications

References 29 publications

Ankylosing spondylitis: etiology, pathogenesis, and treatments

Ankylosing spondylitis: etiology, pathogenesis, and treatments

Comparison of desogestrel/ethinyl estradiol plus spironolactone versus cyproterone acetate/ethinyl estradiol in the treatment of polycystic ovary syndrome: A randomized controlled trial

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

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