The patient with inflammatory spine disease

  • Gunnar B. J. Andersson
  • Thomas W. McNeill


The syndrome described in Table 1 is caused by a group of inflammatory diseases which are thought to result from a derangement of the immune mechanism of the body. These so-called sero-negative spondylarthropathies share a variety of clinical, radiographic and genetic features (Kohler and Vaughan, 1982; Moll, 1974; Brewerton et al. 1973; Jayson, 1986). Although, both inflammatory arthritis and spondylitis are major components of each of these diseases, they are not to be thought of as variations of rheumatoid arthritis. This clinical distinction is important since complications, response to therapy and progress are quite different. Inflammatory spinal disease, extra-articular foci, particularly eye disease, and a tendency for onset in young, mainly male, adults are uniting features linking this group of diseases together. Additionally, three of the five subgroups in this category have a very high incidence of the histocompatibility antigen HLA-B27 among those afflicted with the spinal component of the disease, and an even greater proportion are HLA-B27 positive if they manifest both the eye and spinal components (Table 2). The five sub-groups to be considered are: (1) ankylosing spondylitis; (2) “reactive arthritis”; (3) Reiter’s syndrome; (4) inflammatory bowel disease; and (5) psoriasis (Table 3). In the inflammatory bowel disease and psoriasis the HLA-B27 antigen is not a factor unless there is spinal involvement and then not nearly in as great a proportion as in the other three groups (Mills et al., 1975).


Inflammatory Bowel Disease Lower Back Pain Ankylose Spondylitis Inflammatory Arthritis Sacroiliac Joint 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Kohler PF, Vaughan J (1982) The autoimmune diseases. JAMA 248: 2646–2657Google Scholar
  2. Moll JMH (1974) Association between ankylosing spondylitis, psoriatic, arthritis, Reiter’s disease, the intestinal arthropathies, and Behcet’s syndrome. Medicine 53: 343–364PubMedCrossRefGoogle Scholar
  3. Mills DM, Arai Y, Gupta RC (1975) HL-A antigens and sacroilitis. JAMA 231: 268–270Google Scholar
  4. Cruickshank B (1975) Pathology of ankylosing spondylitis. Bull Rheum Disc 34: 87–91CrossRefGoogle Scholar
  5. Bluestone R (1985) Ankylosing spondylitis. In: McCarty DJ (ed) Arthritis and allied conditions, 10th edn. Lea and Febiger, Philadelphia, pp 819–840Google Scholar
  6. Jayson MIV (1986) Spinal diseases and back pain. In: Dieppe PA et al (eds) Atlas of clinical rheumatology. Lea and Febiger, Philadelphia, pp 17.13–17. 15Google Scholar
  7. Brewerton DA et al (1973) Reiter’s disease and HLA-B27. Lancet 2: 996–998CrossRefGoogle Scholar
  8. Schmorl G, Junghans H (1971) The human spine in health and disease, 2nd edn, translated by EF Besemann. Grune and Stratton, New YorkGoogle Scholar
  9. Sharp JT (1985) Reiter’s syndrome (reactive arthritis). In: McCarty DJ (ed) Arthritis and allied conditions, 10th edn. Lea and Febiger, Philadelphia, pp 841–848Google Scholar
  10. Fassbender HG (1986) Joint destruction in various arthritic diseases. In: Kuettner K et al (ed) Articular cartilage biochemistry. Raven Press, New YorkGoogle Scholar
  11. Habif TP (1985) Clinical dermatology. CV Mosby Co, St. Louis MOGoogle Scholar
  12. Bennett RM (1985) Psoriatic arthritis. In: McCarty DJ (ed) Arthritis and allied conditions, 10th edn. Lea and Febiger, Philadelphia, pp 850–866Google Scholar

Copyright information

© Springer-Verlag/Wien 1989

Authors and Affiliations

  • Gunnar B. J. Andersson
    • 1
  • Thomas W. McNeill
    • 1
  1. 1.Department of Orthopedic SurgeryRush-Presbyterian-St. Luke’s Medical HospitalChicagoUSA

Personalised recommendations