ACTH, cortisol and prolactin in active rheumatoid arthritis

被引:55
作者
Zoli, A
Lizzio, MM
Ferlisi, EM
Massafra, V
Mirone, L
Barini, A
Scuderi, F
Bartolozzi, F
Magaró, M
机构
[1] Univ Cattolica Sacro Cuore, Div Reumatol, Ist Med Interna & Geriatria, Stat Lab, I-00168 Rome, Italy
[2] Univ Cattolica Sacro Cuore, Ist Chim Biol, Stat Lab, I-00168 Rome, Italy
[3] Univ Cattolica Sacro Cuore, Ist Patol Gen, Stat Lab, I-00168 Rome, Italy
[4] Univ Cattolica Sacro Cuore, Ist Igiene, Stat Lab, I-00168 Rome, Italy
关键词
ACTH; cortisol; cytokines; prolactin; rheumatoid arthritis;
D O I
10.1007/s100670200076
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Prolactin (PRL) and glucocorticoids are hormones involved in the regulation of the immune system. Rheumatoid arthritis (RA) is an inflammatory condition that presents a diurnal rhythm of disease activity. ACTH, PRL, cortisol, IL-1beta and TNF-alpha circadian rhythms have been studied in active RA (aRA) to evaluate a possible relationship between the neuroendocrine system and immunological activity in rheumatoid patients. ACTH, PRL, cortisol, PRL/cortisol ratio and IL-1beta and TNF-alpha levels were determined in aRA patients and in control subjects at 6.00, 10.00, 14.00, 18.00, 22.00 and 02.00 h. In aRA patients we observed lower ACTH and cortisol levels at 22.00 h and 2.00 h, respectively and higher PRL and PRL/cortisol ratio at 2.00 h when compared to controls. IL-1beta and TNF-alpha reached their highest serum levels in aRA patients at 2.00 and 6.00 h. This study provides evidence that in aRA there could be a temporary and probably causal relationship between diurnal disease activity, hormonal disequilibrium and cytokine secretion. An imbalance in favour of proinflammatory hormones (PRL and cytokines) as opposed to levels of anti-inflammatory hormones could be responsible for the diurnal rhythm of activity disease observed in aRA patients.
引用
收藏
页码:289 / 293
页数:5
相关论文
共 38 条
[1]  
ALTOMONTE L, 1992, CLIN RHEUMATOL, V11, P1
[2]   THE IMMUNOLOGY OF PROLACTIN [J].
BERCZI, I .
SEMINARS IN REPRODUCTIVE ENDOCRINOLOGY, 1992, 10 (03) :196-219
[3]   REGULATION OF HUMORAL IMMUNITY IN RATS BY PITUITARY-HORMONES [J].
BERCZI, I ;
NAGY, E ;
KOVACS, K ;
HORVATH, E .
ACTA ENDOCRINOLOGICA, 1981, 98 (04) :506-513
[4]   The immune effects of neuropeptides [J].
Berczi, I ;
Chalmers, IM ;
Nagy, E ;
Warrington, RJ .
BAILLIERES CLINICAL RHEUMATOLOGY, 1996, 10 (02) :227-257
[5]   Are both genetic and reproductive associations with rheumatoid arthritis linked to prolactin? [J].
Brennan, P ;
Ollier, B ;
Worthington, J ;
Hajeer, A ;
Silman, A .
LANCET, 1996, 348 (9020) :106-109
[6]  
CASH JM, 1992, J RHEUMATOL, V19, P1692
[7]  
CHIKANZA IC, 1991, BRIT J RHEUMATOL, V30, P203
[8]   Neuroendocrine immune responses to inflammation: The concept of the neuroendocrine immune loop [J].
Chikanza, IC ;
Grossman, AB .
BAILLIERES CLINICAL RHEUMATOLOGY, 1996, 10 (02) :199-225
[9]  
CHIKANZA IC, 1993, BRIT J RHEUMATOL, V32, P445
[10]   DEFECTIVE HYPOTHALAMIC RESPONSE TO IMMUNE AND INFLAMMATORY STIMULI IN PATIENTS WITH RHEUMATOID-ARTHRITIS [J].
CHIKANZA, IC ;
PETROU, P ;
KINGSLEY, G ;
CHROUSOS, G ;
PANAYI, GS .
ARTHRITIS AND RHEUMATISM, 1992, 35 (11) :1281-1288