Complement in inflammatory tissue damage and disease.

Conclusion This conference reflected a growing recognition that a fundamental knowledge and understanding of neuroendocrine interactions with the immunological and nervous systems need to be further acquired and related directly to basic and clinical aspects of rheumatic diseases. Clinically productive research on these complex mechanisms necessitates collaboration between investigators from many diverse specialities and countries. This conference provided an excellent basis for this. References 1 Bijlsma, J.W.J. et al. (1999) The neuroendocrine immune basis of rheumatic diseases. Immunol. Today 20, 298–301 2 Straub, R.H. and Cutolo, M. (2001) Involvement of the hypothalamic–pituitary–adrenal/gonadal axis and the peripheral nervous system in rheumatoid arthritis. Arthritis Rheum. 44, 493–507 3 Masi, A. et al. (2000) Neuroendocrine mechanisms in rheumatic diseases. Rheum. Dis. Clin. North Am. 26, 693–1017 4 Cutolo, M. et al. (2001) Abstracts NEI conference. Clin. Exp. Rheumatol. 19, 598–616 5 Merke, D.P. et al. (2000) Adrenomedullary dysplasia and hypofunction in patients with classic 21-hydroxylase deficiency. New Engl. J. Med. 343, 1362–1368 6 van Everdingen, A.A. et al. Low-dose prednisone therapy for patients with early active rheumatoid arthritis: clinical efficacy, disease-modifying properties and side-effects. A double-blind placebo-controlled clinical trial. Ann. Intern. Med. (in press) Johannes W.J. Bijlsma* Dept of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Box 85500, 3508GA Utrecht, The Netherlands. *e-mail: [email protected]