neuropeptide-y and Lupus-Erythematosus--Systemic

Cardiovascular autonomic neuropathy (CAN) in patients with rheumatic diseases may result in sudden death, possibly from arrhythmia and myocardial infarction due to its frequent association with microvascular disease. Autonomic dysfunction may contribute to initiation and perpetuation of rheumatic diseases. Thus, we aimed to assess cardiovascular autonomic function in lupus and juvenile idiopathic arthritis (JIA) patients.. Assessment of cardiovascular autonomic function was done in 20 lupus and 20 JIA patients, aged 8-16 years, by five non-invasive autonomic function tests (AFTs) and serum levels of neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP), as indicators of sympathetic and parasympathetic functions, respectively, in comparison with 40 matched healthy control subjects.. Clinical evidence of CAN was found in 65 and 40% of lupus and JIA patients, respectively, and in none of healthy controls. Lupus and JIA patients had significantly lower serum NPY and VIP than controls (P < 0.001). The five AFTs score had significant negative correlations to NPY and VIP (P < 0.001). Patients with CAN had significantly lower serum NPY and VIP than patients without (P < 0.001). Clinical evidence of CAN was found in 41.7 and 14.3% of asymptomatic lupus and JIA patients, respectively. There was significant positive association between CAN and important disease manifestations, including activity, in these patients.. CAN is common in lupus and JIA patients, even in absence of relevant symptoms. Thus, assessments of cardiac autonomic function, by AFTs and serum autonomic neuropeptides (NPY and VIP), and the therapeutic effects of NPY and VIP are recommended in these patients.

Topics: Adolescent; Arthritis, Juvenile; Autonomic Nervous System; Blood Pressure; Cardiovascular System; Case-Control Studies; Child; Cross-Sectional Studies; Egypt; Female; Heart Rate; Humans; Logistic Models; Lupus Erythematosus, Systemic; Male; Neuropeptide Y; Neuropeptides; Posture; Rheumatic Diseases; Vasoactive Intestinal Peptide

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).. 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.. 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.. 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.

Topics: Adalimumab; Adrenocorticotropic Hormone; Adult; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Arthritis, Rheumatoid; Female; Glucocorticoids; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Lupus Erythematosus, Systemic; Male; Middle Aged; Neuropeptide Y; Pituitary-Adrenal System; Prednisolone; Severity of Illness Index; Sympathetic Nervous System; Tumor Necrosis Factor-alpha

It has been reported that more than 50% of lupus patients show various forms of neurological deficits including impaired cognitive functions and psychiatric disorders. Using an animal model of lupus we investigated the production of neuropeptides in the brain of NZB/W F1 female hybrid mice and its parental strain NZB and NZW. Our results indicate that the alteration in learning and memory described in lupus mice are paralleled by a decrease in calcitonin gene-related peptide, substance P and neuropeptide Y (NPY) levels in the hippocampus and a significant decrease of NPY in the cortex. These findings are interesting in the light of previously reported results suggesting that these neuropeptides can play an important role in cognitive functions. We also observed a decrease of NPY and vasoactive intestinal polypeptide levels in the hypothalamus of lupus prone mice and these changes may be related to the disregulation of the hypothalamus-pituitary-adrenal axis observed in lupus prone mice.

Topics: Animals; Brain; Calcitonin Gene-Related Peptide; Cerebral Cortex; Female; Hippocampus; Hypothalamus; Lupus Erythematosus, Systemic; Mice; Neuropeptide Y; Neuropeptides; Substance P; Vasoactive Intestinal Peptide

In the present study we used a well-characterised model of murine lupus, the female NZB/W hybrid, to study the possible involvement of neuropeptides in the pathogenesis of systemic lupus erythematosus (SLE). Analysis of neuropeptides with a possible role in inflammation showed that substance P (SP) calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) are present in increased quantities in the inflamed kidneys of SLE mice, confirming their involvement in local inflammation, while there is a general reduction in the peptide concentrations in the lymphoid organs of lupus mice, except for NPY. Our results suggest that the altered neuropeptide concentrations observed in the SLE lymphoid organs may be partly responsible for the altered immune response and contribute to the development of autoimmune diseases.

Topics: Animals; Calcitonin Gene-Related Peptide; Female; Kidney; Lupus Erythematosus, Systemic; Mice; Neuroimmunomodulation; Neuropeptide Y; Neuropeptides; Spleen; Substance P; Thymus Gland; Vasoactive Intestinal Peptide