PMID- 15922688
OWN - NLM
STAT- MEDLINE
DCOM- 20050623
LR  - 20220316
IS  - 0002-9343 (Print)
IS  - 0002-9343 (Linking)
VI  - 118
IP  - 6
DP  - 2005 Jun
TI  - Spondyloarthritis: update on pathogenesis and management.
PG  - 592-603
AB  - A great deal of progress has occurred in the past few years in elucidating the 
      causes and designing new treatments for ankylosing spondylitis and other types of 
      spondyloarthritis. In addition to the human leukocyte antigen (HLA)-B27 and other 
      major histocompatibility complex (MHC) genes, chromosomal regions and genes 
      elsewhere in the genome are being implicated both in disease susceptibility and 
      severity. The various ways HLA-B27 may function in causing spondyloarthritis now 
      are better understood to encompass not only antigen presentation but also other 
      mechanisms, possibly all being operative in pathogenesis (misfolding of the 
      HLA-B27 molecule, impaired intracellular killing of bacteria, and HLA-B27 itself 
      serving as an autoantigen). Specific enteric and sexually acquired infections can 
      trigger reactive arthritis, though no specific microbe has been identified in 
      other forms of spondyloarthritis. Intestinal inflammation with impairment of the 
      gut:blood barrier may be operative in driving ankylosing spondylitis and 
      enteropathic arthritis. A number of treatments have been tried in 
      spondyloarthritis, including older agents such as methotrexate and sulfasalazine 
      but also newer drugs such as pamindronate. The recent introduction of tumor 
      necrosis factor (TNF) blockers in the treatment of spondyloarthritis has offered 
      the most hope in not only relieving symptoms and signs of both peripheral 
      arthritis and enthesitis but also spinal disease, which often has been refractory 
      to other agents. Their high cost and considerable side effect profile, however, 
      have necessitated the establishment of guidelines for their use in these diseases 
      in order to target the patient in whom they are likely to have the most benefit.
FAU - Reveille, John D
AU  - Reveille JD
AD  - Division of Rheumatology, Department of Internal Medicine, The University of 
      Texas-Houston Health Science Center, USA. john.d.reveille@uth.tmc.edu
FAU - Arnett, Frank C
AU  - Arnett FC
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Am J Med
JT  - The American journal of medicine
JID - 0267200
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (HLA-B27 Antigen)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Anti-Bacterial Agents/therapeutic use
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Antibodies, Monoclonal/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Disease Susceptibility
MH  - HLA-B27 Antigen/genetics
MH  - Humans
MH  - Infliximab
MH  - Major Histocompatibility Complex/genetics
MH  - Spondylitis, Ankylosing/drug therapy/*etiology/genetics
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
RF  - 116
EDAT- 2005/06/01 09:00
MHDA- 2005/06/24 09:00
CRDT- 2005/06/01 09:00
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/06/24 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
AID - S0002-9343(05)00002-1 [pii]
AID - 10.1016/j.amjmed.2005.01.001 [doi]
PST - ppublish
SO  - Am J Med. 2005 Jun;118(6):592-603. doi: 10.1016/j.amjmed.2005.01.001.