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J Clin Pathol 2005;58:860-863 doi:10.1136/jcp.2004.022681
  • Original article

Association of chronic fatigue syndrome with human leucocyte antigen class II alleles

  1. J Smith2,
  2. E L Fritz1,
  3. J R Kerr3,
  4. A J Cleare4,
  5. S Wessely4,
  6. D L Mattey5
  1. 1National Heart and Lung Institute, Imperial College London SW3 6NP, UK
  2. 2Tissue Typing Laboratory, Harefield Hospital, Middlesex UB9 6JH, UK
  3. 3Department of Paediatric Infectious Diseases, St Mary’s Campus, Imperial College London UB9 6JH, UK
  4. 4Institute of Psychiatry and Maudsley Hospital, Guy’s, King’s and St Thomas’s School of Medicine, King’s Campus, PO Box 065, 103 Denmark Hill, London SE5 8AZ, UK
  5. 5Staffordshire Rheumatology Centre, University Hospital of North Staffordshire, Stoke on Trent ST6 7AG, UK
  1. Correspondence to:
 Dr J R Kerr
 Department of Paediatric Infectious Diseases, St Mary’s Campus, Imperial College London, Norfolk Place, London W2 1PG, UK; j.kerrimperial.ac.uk
  • Accepted 23 February 2005

Abstract

Background: A genetic component to the development of chronic fatigue syndrome (CFS) has been proposed, and a possible association between human leucocyte antigen (HLA) class II antigens and chronic fatigue immune dysfunction has been shown in some, but not all, studies.

Aims: To investigate the role of HLA class II antigens in CFS.

Methods: Forty nine patients with CFS were genotyped for the HLA-DRB1, HLA-DQA1, and HLA-DQB1 alleles and the frequency of these alleles was compared with a control group comprising 102 normal individuals from the UK. All patients and controls were from the same region of England and, apart from two patients, were white.

Results: Analysis by 2 × 2 contingency tables revealed an increased frequency of HLA-DQA1*01 alleles in patients with CFS (51.0% v 35%; odds ratio (OR), 1.93; p  =  0.008). HLA-DQB1*06 was also increased in the patients with CFS (30.2% v 20.0%; OR, 1.73, p  =  0.052). Only the association between HLA-DQA1*01 and CFS was significant in logistic regression models containing HLA-DQA1*01 and HLA-DRQB1*06, and this was independent of HLA-DRB1 alleles. There was a decreased expression of HLA-DRB1*11 in CFS, although this association disappeared after correction for multiple comparisons.

Conclusions: CFS may be associated with HLA-DQA1*01, although a role for other genes in linkage disequilibrium cannot be ruled out.

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