Prolactin/Cortisol Ratio in Rheumatoid Arthritis

Zoli, Angelo; Ferlisi, E. M.; Lizzio, Marco Maria; Altomonte, L; Mirone, L.; Barini, Angela; Scuderi, Flavia; Bartolozzi, Francesco; Magarò, M.

doi:10.1111/j.1749-6632.2002.tb04255.x

Cited by 9 publications

(6 citation statements)

References 8 publications

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“…The size of abdominal aortic aneurisms has been correlated with the ratio of proinflammatory interleukin-6 to anti-inflammatory interleukin-10 [22]. Similarly, patients with rheumatoid arthritis had a ratio of proinflammatory prolactin to anti-inflammatory cortisol that corresponded with the diurnal onset of disease activity [23].…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory phenotype with imbalance of KLF2 and RelA: Risk of childhood stroke with sickle cell anemia

et al. 2009

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Altered inflammation signaling within the cerebral vasculature may be an important risk factor for stroke in children with sickle cell anemia (SCA). This study examines how differential expression of NFjB/p65 (RelA), KLF2, and other transcription factors may act as switches in inflammation signaling leading to observed differences between non-SCA (NS) African Americans and African Americans with SCA who are either at risk (AR) or not at risk (NAR) of childhood stroke based on occurrence of Circle of Willis disease. Clover/ Transfac analysis was used to identify overrepresented transcription factor binding motifs on genes associated with inflammation. Transcription factor binding motifs for the NFjB family and RFX1 were overrepresented on inflammation signaling gene set analysis. Variations in protein expression were determined by flow cytometry of blood outgrowth endothelial cells (BOECs) from NS, AR, and NAR donors and Western blots of protein extracts from both unstimulated and TNFa/IL1b-stimulated BOECs. BOECs from patients with SCA had more cytoplasmic-derived RelA compared with NS BOECs. Sickle BOECs also had heightened responses to inflammatory stimuli compared with NS BOECs, as shown by increased nuclear RelA, and intracellular adhesion molecule (ICAM) response to TNFa/IL1b stimulation. Multiple control points in RelA signaling were associated with risk of childhood stroke. The ratio of proinflammatory factor RelA to anti-inflammatory factor KLF2 was greater in BOECs from AR donors than NS donors. Group risk of childhood stroke with SCA was greatest among individuals who exhibited increased expression of proinflammatory transcription factors and decreased expression of transcription factors that suppress inflammation. Am. J. Hematol. 85:18-23, 2010. V

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Section: Discussionmentioning

confidence: 99%

Proinflammatory phenotype with imbalance of KLF2 and RelA: Risk of childhood stroke with sickle cell anemia

et al. 2009

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“…A peak of RA activity is clinically characterized early in the morning. Especially higher PRL/cortisol ratio during nocturnal hours together with increased levels of IL-1 and TNF-of the diurnal rhythm coincided with disease activity in patients with RA [102,103]. Decreased PRL response to hypoglycemic stress has been reported in RA patients, suggesting a close relationship between abnormal PRL secretion and HPA dysfunction [104,105].…”

Section: Prl In Immunopathogenesis Of Ramentioning

confidence: 96%

Recent Advances in Neuro-Endocrine-Immune Interactions in the Pathophysiology of Rheumatoid Arthritis

Yoshikawa¹,

Nara²,

Suzuki

2006

CRR

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Rheumatoid arthritis (RA) is an autoimmune disorder resulting from the combination of several predisposing factors, including hormonal influences and immune responses. Stress response system, including hypothalamic-pituitaryadrenal/gonadal axes and sympathetic nervous system plays important roles for its pathophysiology. Proinflammatory cytokines secreted by synovial cells and activation of inflammatory cells provoke systemic as well as local inflammatory stresses in RA. However, the decreased secretion of adrenal androgens and gonadal testosterone, and the decreased number of sympathetic nerve fibers (norepinephrine) in the synovial tissue are observed in RA, and eventually leading to the Th1 dominant immune aberration. These suggest a loss of the stress-induced feedback regulation in endocrineimmune and neuro-immune interactions, leading to acceleration of chronic inflammation in RA. The local nociceptive input and sensitization of corresponding segments of spinal cord, resulted in continuous pain with stabilization of afferent sensory fibers and continuous release of proinflammatory neuropeptides, including substance P. Thus, inappropriate secretion of hormones and neuropeptides contributes to vicious cycle in progression of inflammatory responses. In this review, we discuss the recent advances of immunological aberrations and neuro-endocrine-immune interactions in pathophysiology of RA.

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“…Although the HPA axis in RA appears normal, it has been suggested that there is an inherent defect in its failure to respond to inflammation with increased cortisol secretion (2,(11)(12)(13)(14). Straub and Cutolo (15) asked whether the chronic proinflammatory state depends on a persistent trigger (e.g.…”

Section: Known Effects Of Acute and Chronic Inflammation On The Hypotmentioning

confidence: 99%

Sixty Years after Hench—Corticosteroids and Chronic Inflammatory Disease

Edwards

2012

The Journal of Clinical Endocrinology & Metabolism

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The systemic effects of enhancing 11β-HSD1 activity may amplify the inflammatory response. Thus, increased conversion of cortisone to cortisol can alter the circadian rhythm of cortisol secretion (lower nadir, later rise, impaired stress response) with consequent relative nocturnal cortisol deficiency when inflammatory cytokines are highest. This could contribute to the circadian symptomatology in rheumatoid arthritis, the effectiveness of early morning (0200 h) low-dose corticosteroids, the significant correlation between total body 11β-HSD1 activity and erythrocyte sedimentation rate, and the effectiveness of 11β-HSD inhibition in both the prevention and treatment of adjuvant arthritis in rat models of rheumatoid arthritis. It could also explain why anti-TNF therapy benefit can be predicted on the basis of the pretreatment plasma cortisol and the subsequent cortisol rise. In contrast, this mechanism is likely to be beneficial in the body's response to chronic infections such as tuberculosis and could explain why anti-TNF treatment markedly increases the risk of reactivation of the disease.

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Prolactin/Cortisol Ratio in Rheumatoid Arthritis

Cited by 9 publications

References 8 publications

Proinflammatory phenotype with imbalance of KLF2 and RelA: Risk of childhood stroke with sickle cell anemia

Proinflammatory phenotype with imbalance of KLF2 and RelA: Risk of childhood stroke with sickle cell anemia

Recent Advances in Neuro-Endocrine-Immune Interactions in the Pathophysiology of Rheumatoid Arthritis

Sixty Years after Hench—Corticosteroids and Chronic Inflammatory Disease

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