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HLA antigens in Mexican patients with adult rheumatoid arthritis.

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measure reflecting biologically important features of a
crystal surface.
These experiments confirm and extend Mandel’s
work. The results re-emphasize the problems inherent
in all experimental work on crystal-induced inflammation; crystal structure and surfaces are clearly susceptible to widely used laboratory manipulations, and
much previous work on “treated” crystals must be interpreted with caution.
Supported by the Arthritis and Rheumatism
Departments of Medicine and Radiotherapy
Bristol Royal Infirmary
Bristol, BS2 8H W, England
1. Mandel NS: Structural changes in sodium urate crystals on
heating. Arthritis Rheum 23:772-776, 1980
2. Kozin F, McCarty DJ: Protein binding to monosodium
urate, calcium pyrophosphate dihydrate, and silicon dioxide crystals. I. Physical characteristics. J Lab Clin Med
8911314-1325, 1976
3. Denko CW, Whitehouse MW. Experimental inflammation
induced by naturally occurring microcrystalline calcium
salts. J Rheumatol 354-62, 1976
4. Preece AW, Light PA: The macrophage electrophoretic
mobility (MEM) test for malignant disease. Clin Exp J
18:543-552, 1974
5. Preece AW, Sabolovic D: Cell Electrophoresis: Clinical
Application and Methodology. New York, Elsevier, North
Holland, 1978, pp 369
HLA antigens in Mexican patients with adult
rheumatoid arthritis
To the Editor:
The association of rheumatoid arthritis (RA) to
HLA antigens was first suggested through the work of
Stastny (1) and was later confirmed not only for Dw4
but for DR4 as well (2,3). Moreover, the results of the
RA joint report (which was part of the 8th Histocompatibility Workshop) showed that DR4 is the major antigen involved in almost all studied populations (4). The
present paper describes our results in Mexican Mestizo
patients inhabiting the Mexico City area, since in the
mentioned joint report the data were combined with
those coming from a different Latin American group.
Twenty adult patients with RA diagnosed according to
the criteria of the American Rheumatism Association
(5) were classified. Sixteen patients had a classic form of
the disease and 4 had a definite pattern. Fifteen were
women. Their average age was 39.25 years, and the average age at onset was 32 years. Twenty healthy controls with the same ethnic characteristics were studied
for comparison. Typing for ABO, Rh, HLA-A, B, C,
and DR antigens was done in every subject; T (loci A,
B, and C) and B cells (locus DR) were tested with the
standard microlymphocytotoxicity methods (6,7) by using the 300 Workshop antisera, which included 19 specificities for locus A, 37 for locus B, 7 for locus c, and 9
for DR.
No statistical differences were found for red cell
antigens, although group A was higher in the patients
(40% versus 2 1.6%). Concerning HLA antigens, DR4
was significantly increased as shown in Table 1 (P <
0.02). This suggests that in Mexicans as in other racial
groups, DR4, or perhaps a closely linked gene, plays
some role in the etiopathogenesis of RA. A decrease
that did not reach significance was observed in the gene
frequencies of DR5 (20.5% in controls versus 10.5% in
patients) and DR7 (23.90% versus 10.50%). The decrease probably is due to negative compensation to the
increase of DR4.
No correlation was observed when analyzing the
distribution of HLA antigens according to sex, age at
onset, time of evolution, or severity. A deviation in the
frequencies of Aw31 and Bw54 was also found, although not significant. This looks interesting, since
Aw31 is more frequent in American Indian groups (8),
including Mexican Nahuas (9). Conversely, RA has
been associated in the Japanese population with Bw54,
as well as DR4 (10). The former is a mongoloid marker
and possibly exists in the Mestizos due to the genetic
contribution of the Mexican natives. The relative risk
for DR4 was quite high (14.62), and all patients were
Table 1. Gene frequencies of HLA antigens in adult rheumatoid
Aw3 1
(N = 20);
(N = 20).
2 yates
* N = number of subjects.
tNS = not significant.
$ Relative risk for carriers of DR4 = 14.62,
positive for rheumatoid factor. If one looks into the difference in the DR pattern among seropositive and seronegative patients (4), at least two clinical entities
emerge. One involves autoimmune phenomena and the
presence of DR4 in seropositive RA, and the other is
seronegative RA without the participation of HLA
markers, suggesting that if multiple genes are mediating
the seropositive form of RA, DR4 or a closely linked
gene may have some effect on the autologous IgG response and therefore be partly responsible for the development of the disease.
Acknowledgments. We are truly grateful to Dr.
Peter Stastny for providing the typing antisera and to
Dr. Paul Terasaki for computing the data. Our gratitude
goes to Drs. P. Escobar and J. Perez for their technical
assistance and to Mrs. Silvia Diaz for preparing the
Laboratorio de Investigaciones
Immunoldgicas, S. S.A.
Carpi0 492
Mkxico 17, D.F., Mexico
Rheumatology Department
Hospital de Especialidades
Centro Mkdico La Raza, I.M.S.S., Mexico
Laboratorio de Investigaciones
Hospital de Especialidades
Laboratorio de Investigaciones
1. Stastny P: Mixed lymphocyte culture typing cells from patients with rheumatoid arthritis. Tissue Antigens 457 1579, 1979
2. Thomsen M, Morling H, Snorrason E: HLA-Dw4 and
rheumatoid arthritis. Tissue Antigens 13:56-60, 1979
3. Dobloug JH, Ford 0, Thorsby E: HLA-DRw4 and rheumatoid arthritis. Lancet i:548-549, 1979
4. Stastny P: Joint report on rheumatoid arthritis, Histocompatibility Testing 1980. Edited by PI Terasaki. Los
Angeles, UCLA Press, 1980, pp 681-686
5. Ropes MW, Bennett GA, Cobb S, Jacox R, Jessar RA:
1958 revision of diagnostic criteria for rheumatoid arthritis. Bull Rheum Dis 9:175-176, 1958
6. Dausset J: Micro-lymphocytotoxicity technique (Terasaki’s technique modified), Tissue Typing Techniques.
Bethesda, Maryland, National Institutes of Health, 1973,
pp 28-52
7. Van Rood JJ: The leiden B cell, Workshop, May 58, 1976.
Tissue Antigens 8:329-344, 1976
8. Pickbourne P, Piazza A, Bodmer WF: Population analysis, Histocompatibility Testing 1977: Report of the 7th International Workshop and Conference. Edited by WF
Bodmer, JR Betchelor, J G Bodmer, et al. Copenhagen,
Munksgaard, 1978, pp 259-262
9. Gorodezky C, Escobar-Gutierrez A, Assia S, Castro L,
Barroeta 0: Antigens predominant in Nahuas, Histocompatibility Testing 1977: Report of the 7th International Workshop and Conference. Edited by WF Bodmer, JR Barchelor, J G Bodmer, et al. Copenhagen,
Munksgaard, 1978, pp 442-443
10. Sasazuli T, Kaneoka H, Ohta N, Hayase R, Iwamoto I:
Four common HLA haplotypes and their association with
diseases in the Japanese population, Clinical Histocompatibility Testing. Vol. 4. Edited by C Carpenter. New
York, Grune and Stratton, 1980, pp 185-187
HLA in the Negrito
To the Editor:
The people of the Negrito tribe, located in
Northern Luzon in the Philippines, are short and dark
with frizzy hair. Called “Aetas” by the Filipinos, they
inhabit remote, mountainous areas north of Manila and
are distinctly separate from the Filipino people. Their
racial origin is still unknown, although they are not of
the Caucasian or Mongoloid race. Recently, we had an
opportunity to study HLA types in 2 Negrito groups
(one group near Angeles City, Pampanga, and one in
Aubucay, Bataan).
The results of our typing were intriguing, revealing that HLA-B27 was present in 16.1%of the 112 adult
Negritos tested. Such a high frequency of B27 was unexpected. After the HLA typing, radiologic and clinical
examinations were done on the 112 adults.
There have been several reports on the strong association between HLA-B27 and ankylosing spondylitis
or sacroiliitis in Caucasians, American blacks, and
Mongoloids, including Japanese and American Indians.
Gofton et a1 found sacroiliitis in 10% of adult male
Haida Indians, with HLA-B27 in 50% of the population
(1). Calin et a1 found sacroiliitis in 19.7% of 193 Pima
Indians, with B27 in 18% of the population (2). However, in spite of the high frequency of B27 found in the
Negrito population after radiologic and clinical examinations, no evidence of sacroiliitis was present.
This discrepancy, when compared to the Haida/
Pima, might be explained by racial or environmental
differences between the Negrito and other populations.
Another possible explanation for this discrepancy might
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adults, mexican, patients, hla, antigen, arthritis, rheumatoid
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