| Article Access Statistics|
| Viewed||1765 |
| Printed||100 |
| Emailed||0 |
| PDF Downloaded||0 |
| Comments ||[Add] |
Click on image for details.
|Year : 1978 | Volume
| Issue : 1 | Page : 1-3
Histocompatibility antigen and arthritis
GH Tilve, KG Nair
Department of Medicine, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012, India
G H Tilve
Department of Medicine, Seth G. S. Medical College and K.E.M. Hospital, Parel, Bombay-400 012
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Tilve G H, Nair K G. Histocompatibility antigen and arthritis. J Postgrad Med 1978;24:1-3
The term "rheumatism" is derived from the Greek word rheumatismos which means mucus as an evil humor which flows from the brain to the joints producing pain.  Arthritis is one of the oldest and yet one of the most neglected disease. Chronic arthritis of the spine was present in the ape man of 2 million years ago.  There are different forms of arthritis, some caused by known agents but many caused by unknown agents. But, there is a group of common rheumatic disorders which have many clinical, pathological and radiographic features in common. This group includes ankylosing spondylitis, arthritis following infection, colonic disorders etc. One of the features common to these disorders is the histocompatibility antigen HLA-B27.
Gibson and Medawar  studied the fate of a skin graft from a man to his burned sister.  The skin graft was rejected. The recipient organism recognises the graft as foreign. Every cell carries on its surface, the antigens which are derived from the parents. Over 40 such antigens have been identified and an individual may have at the most four out of these antigens. There can be thousands of such combinations of antigens which characterise individuals. Their detection is useful in organ transplantation, cross matching before transfusion, and paternity testing. These are known as histocompatibility antigens. As they were first detected on leucocyte and are most conveniently determined on blood leucocytes they are called "human leucocyte antigens".
A short description of the human leucocyte antigen is relevant. The inheritance of these antigens is controlled by a small region of the 6th pair of autosomes.  The serologically defined (S.D.) antigens are controlled by two loci named A and B which in turn are occupied by more than 40 co-dominant alleles. Further, family studies have proved that other genetic determinants responsible for stimulation in the mixed lymphocyte culture test are also situated on the same chromosomes and closely linked with the (S.D.) HL-A determinants. There is a genetic linkage between the HL-A loci and a genetic locus controlling the immune responsiveness.
It was gradually established that people who inherit particular HLA antigens are more likely to develop certain diseases. It is not yet known whether the HL-A antigens are directly involved in the disease process or whether susceptibility to disease results from the inheritance of abnormal immune responses very closely associated with particular HL-A antigen.
The simplest explanation for such correlation is that the inheritance of a particular HL-A antigen makes the individual susceptible to a particular viral or a bacterial infection by providing a cell membrane receptor site, thus leading to tolerance for the viral or bacterial antigen and later leading to the disease. Recent data have shown that patients with rapidly progressing multiple sclerosis may lack cellular immunity and are unable to prevent rapid progress of the disease.  These sufferers have HLA-A7 antigen.
Ankylosing Spondylitis : Bernard  first wrote about ankylosing spondylitis.  Until a few years ago, ankylosing spondylitis was considered a variant of rheumatoid arthritis. Recent evidence, however, suggests that it is an independent disease. In 1973-74, Brewerton et al  and Schlosstein  revolutionised our thinking about the etiology of ankylosing spondylitis by showing the association between HLA-B27 and ankylosing spondylitis. This antigen is found in 4 to 7°% of the general population in the West,  and in 90% to 95% of patients with ankylosing spondylitis. Thus, it is clear that the individual having HLA-B27 is 300 times more likely to develop clinical ankylosing spondylitis. The disease is rare in females, M/F ratio being 7:1. There must be some other factors to account for this sex difference and probably environmental factors modify the genetic factors. Certain groups such as the North American Indians have shown a high incidence of ankylosing spondylitis. The Haida Indian tribe in British Columbia has 10 %; of the population suffering from ankylosing spondylitis.  The African Negro is nearly free from HLA-B27 and only two cases of ankylosing spondylitis has been reported from this community. 
Arthritis following infections: Reiter's disease is regarded as a post-infectious syndrome following venereal or enteric infections. The major manifestations are urethritis, conjunctivitis, mucocutaneous lesions and arthritis. No infective agent has been definitely established in this disease. Arthritis may also follow infections with Shigella flexner, Yersinia More Details enterocolitica or Salmonella More Details. Reiter's disease occurs between 18 and 40 years with a male/female ratio of 50: 1. Seventy to ninety per cent of these sufferers are positive to HLA-B27.  These HLA-B27 people react peculiarly to these infections.
| :: Colotic arthropathies|| |
Many diseases affect both the bowel and the joints. Ulcerative colitis and regional enteritis are the commonest among these diseases. The prevalence of spondylitis in these patients is 30 times more than in the general population. Arthritis is seen in 12 to 20 b of patients with these colonic disorders.  The arthritic manifestations may precede the colonic manifestations by many years. It is well established that HLA-B27 is present in a very high proportion of such cases.
| :: Juvenile Polyarthritis|| |
From among children with polyarthritis about 25% have HLA-B27. Ankylosing spondylitis may begin in the peripheral joints in children.  It is difficult to distinguish this condition from the juvenile rheumatoid arthritis.
| :: Psoriatic arthritis|| |
Psoriatic arthritis is different from rheumatoid arthritis. A joint involvement is seen in 5.4 to 6.8% of patients with psoriasis. The onset of arthritis may precede, coincide with or may follow the onset of psoriasis. The incidence of HLAB27 in psoriatic arthopathy varies from 28% 9 to 38%.  The incidence of HLA-B27 frequency increases from 35% to 90%  if one considers psoriatic spondylitis.
Histocompatibility antigens can now be used as one of the diagnostic tests in arthritic conditions where the diagnosis cannot be arrived by routine methods. At present, no advice can be given on genetic counselling as our knowledge of histocompatibility antigens is meagre. However, it is likely that with the availability of more information about the susceptibility of certain genotypes to certain environmental agents, one might be able to devise ways and means of preventing the development of clinical disease in these individuals.
| :: References|| |
|1.||Bernard, C. (1958): as quoted by Newstadt8 D. H.: Ankylosing spondylitis. Postgrad. Med., 61: 125-135, 1977. |
|2.||Brewerton, D.: Reports on Rheumatic Disease. "The inherited antigen (HLA-27) and Arthritis" No. 55, February 1974. |
|3.||Brewerton, D. A., Caffrey, M., Nicholls, A . , Walters, D. and Jomes, D. G. O.: HLA-27 and Arthropathies associated with ulcerative colitis and psoriasis. Lancet, 1: 956-957, 1974. |
|4.||Gibson and Medavar: as quoted by Brewerton' D.: Reports on Rheumatic Disease. "The inherited antigen (HLA-27) and Arthritis" No. 55, February 1974. |
|5.||Hollander, J. L.: Introduction to arthiritis and the rheumatic diseases. In "Arthritis and Allied Conditions" Editors: Hollander, J. L., McCarty, D. J. 8th Edition, Philadelphia, 1972, pp.: 3-14. |
|6.||Kemple, K.: The histocompatibility complex and rheumatic diseases. Med. Clin. North. Amer., 61: 331-346, 1977. |
|7.||Lockshin M. D., Fontino, M., Cough, W. W. and Litwin, S. D.: Ankylosing spondylitis and I-ILA. A genetic disease plus? Amer. J. Med., 58: 695-703, 1975. |
|8.||Newstadt, D. H.: Ankylosing spcndylitis. Postgrad. Med., 61: 125-135, 1977. |
|9.||O'Duffy, J.: Psoriatic arthritis. Postgrad. Med., 61: 165-171, 1977. |
|10.||Ramer, S. and Bluestone, R.: Colotic artbropathies. Postgrad. Med., 61: 141-147, 1977. |
|11.||Schlosstein, L., Terasaki, P. I., Bluestone, R. and Pearson, C. M.: High association of HLA antigen W-27 with ankylosing spondylitis, New Eng. J. Med., 2£8: 704-706. 1973. |
|12.||Schaller, J.: Juvenile rheumatoid arthritis. Postgrad. Med., 61: 177-184, 1977. |