Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamic-pituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems - PubMed (original) (raw)

Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamic-pituitary-adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems

P Härle et al. Ann Rheum Dis. 2006 Jan.

Abstract

Objective: To study in parallel the outflow of the sympathetic nervous system (SNS) and the hypothalamic-pituitary adrenal (HPA) axis tone in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Methods: 32 patients with SLE, 62 with RA, and 65 healthy subjects (HS) were included. To measure the tone of the HPA axis, plasma ACTH and serum cortisol were determined. Serum neuropeptide Y (NPY) was used to evaluate the sympathetic outflow.

Results: Patients with SLE had increased NPY levels in comparison with HS, irrespective of prior prednisolone treatment (p<0.001). For patients with RA, only those with prednisolone treatment had increased NPY levels in comparison with HS (p = 0.016). Daily prednisolone dose correlated positively with serum NPY in RA (R(Rank) = 0.356, p = 0.039). In contrast, plasma ACTH levels were generally decreased significantly in comparison with HS in SLE with prednisolone, and in RA with/without prednisolone. Similarly, serum cortisol levels were also decreased in SLE with/without prednisolone, and in RA with prednisolone. The NPY/ACTH ratio was increased in SLE and RA, irrespective of prior prednisolone treatment. The NPY/cortisol ratio was increased in SLE with/without prednisolone, and in RA with prednisolone. Twelve weeks' anti-TNF antibody treatment with adalimumab did not decrease NPY levels in RA, irrespective of prednisolone treatment.

Conclusions: An increased outflow of the SNS was shown and a decreased tone of the HPA axis in patients with SLE and RA. Low levels of cortisol in relation to SNS neurotransmitters may be proinflammatory because cooperative anti-inflammatory coupling of the two endogenous response axes is missing.

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References

    1. Besedovsky H O, del Rey A E, Sorkin E. Immune‐neuroendocrine interactions. J Immunol 1985135750–4s. - PubMed
    1. Saigusa T. Participation of interleukin‐1 and tumor necrosis factor in the responses of the sympathetic nervous system during lipopolysaccharide‐induced fever. Pflugers Arch 1990416225–229. - PubMed
    1. Niijima A, Hori T, Aou S, Oomura Y. The effects of interleukin‐1 beta on the activity of adrenal, splenic and renal sympathetic nerves in the rat. J Auton Nerv Syst 199136183–192. - PubMed
    1. Mastorakos G, Chrousos G P, Weber J S. Recombinant interleukin‐6 activates the hypothalamic‐pituitary‐adrenal axis in humans. J Clin Endocrinol Metab 1993771690–1694. - PubMed
    1. Späth‐Schwalbe E, Born J, Schrezenmeier H, Bornstein S R, Stromeyer P, Drechsler S.et al Interleukin‐6 stimulates the hypothalamus‐pituitary‐adrenocortical axis in man. J Clin Endocrinol Metab 1994791212–1214. - PubMed

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