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Aim: To determine the presence of HLA antigens in people with blinding trachoma., Methods: Fifty Omanis with blinding trachoma were serologically typed for HLA A, B, C, DR, and DQ antigens and DNA typed for class II DR beta and DQ beta alleles and compared with a population of 100 healthy controls., Results: chi 2 analysis of serological reactions did not reveal any significant differences in HLA antigen frequencies after correction of probability, although DR4, DR7, and DR53 were completely absent in the patients and all of the patients were HLA DQ1 positive. In the case of DQ1 the relative risk was 22.6 (95% confidence interval of 20.7-24.7). Class II DNA low resolution DR beta typing showed a significant increase in HLA DR16 (pc = 0.036, relative risk = 3.8) and a significant decrease in HLA DR53 (pc = 0.018, relative risk = 0.05)., Conclusion: The finding that HLA DR16 (a DR2 subtype) is associated with susceptibility to blinding trachoma, a disease that is caused by an intracellular micro-organism, is consistent with reports of an HLA DR2 association with leprosy and tuberculosis, diseases also caused by an intracellular micro-organism. Similarly, resistance to leprosy is associated with HLA DR53 as is the case with blinding trachoma described here. It is postulated that HLA DR2 or subtypes in association with HLA DQ 1 may enable an intracellular micro-organism to enter the cell or are involved in presentation of peptides derived from intracellular micro-organisms to T lymphocytes initiating a delayed hypersensitivity or autoimmune reaction. These findings are the first report that genetic factors are of major importance in the development and protection against blinding trachoma.

We have investigated the frequency of HLA antigens in 50 Omanis with idiopathic dilated cardiomyopathy to establish whether there are ethnic/racial differences in the reported HLA associations with this disease. There were no statistically significant HLA-A, B, C, DR or DQ antigen frequency differences between the patients and 247 healthy Omanis. THe reported association of HLA-DR4 with idiopathic dilated cardiomyopathy in the Caucasian population does not apply to the Omanis. This confirms the heterogeneity of this disease and points to ethnic/racial origins as important factors when examining the HLA association. This is particularly pertinent as HLD-DR4 has been strongly linked to autoantibody formation in idiopathic dilated cardiomyopathy in Caucasians. The lack of any HLA antigen association in Omanis would argue against the proposed HLA-linked autoimmune pathology of idiopathic dilated cardiomyopathy.

Fifty native Omanis with vitiligo were studied to compare the incidence of HLA ABC and DR antigens with a control population. HLA Bw6 was found in 82% of patients compared with 49% controls (Pc = 0.0009 RR = 4.56) and HLA DR7 occurred in 40% of patients and 9% in controls (Pc = 0.00075 RR = 6.17). HLA DR7 was significantly increased in those patients with acrofacial, compared to focal disease (57% vs. 24% P = 0.038). Sixty-six per cent of the patients in this study had parents who were consanguineous and a positive family history was only found in this group with an incidence of 32%. HLA Bw4 segregated 100% with patients with a positive family history compared with 48% in consanguineous patients without a positive family history (Pc = 0.011 RR = 23). Vitiligo appears to be associated with different HLA antigens in different ethnic groups.

Forty-eight Arab patients with steroid-responsive childhood nephrotic syndrome were studied for the frequency of HLA-A, -B, -C and -DR antigens. HLA-DR7 was significantly increased in the patient group (63% vs. 28%, P = 0.0002) confirming reports of a DR7 association in other ethnic groups and indicating a universal association with this antigen. HLA-CW6 was also significantly increased (44% vs. 21%, P corr. = 0.042). HLA-DQW1 was significantly reduced in the patients (29% vs. 57%, P corr. = 0.012) as was HLA-CW4 (6% vs. 24%, P corr. = 0.042).

Eighty-five Arab patients in Kuwait with classical and definite rheumatoid arthritis were typed to examine the frequency of HLA-A, B, C, and DR antigens. The results showed a significant increase in the frequency of HLA-A10, B8, B21, and DR3 antigens when compared to an age- and sex-matched control population. HLA-DR3 was present in 34 per cent of the patients compared with 2 per cent of the controls (p less than 0.001). The association of RA in the Arab population with HLA-DR3 rather than HLA-DR4 or HLA-DR1 as reported in other ethnic groups emphasizes further the complexity of the genetics of RA.

One hundred and fifty-one living donor renal transplants performed in a single centre in Kuwait were analysed for graft survival in relation to HLA matching, mixed lymphocyte reaction (MLR), P and Lewis antigens. There was a significant difference in graft survival (P = .05) but only at 3, 4 and 5 years between HLA identical (97%, 94%, 94%) and haploidentical combinations (83%, 81% and 79%), respectively. The zero haplotype matched combinations were not significantly different in graft survival from the identical or haploidentical groups. Compatibility or incompatibility for P or Lewis antigens did not influence graft survival. The MLR was significant (P = .05) with the MLR negative recipients having 100% graft survival at 4 years compared to 84% in the MLR positive group. In conclusion with an overall actuarial graft survival of 84% at 6 years none of the factors examined 'dramatically' influenced graft survival. The 'Centre Effect' is the main factor influencing graft survival in our Centre.

Increased frequencies of HL-A7 and the HL-A3,7 haplotype have been demonstrated in pernicious anaemia. There was no significant increase in any HL-A specificity in autoimmune atrophic gastritis. In the whole series of patients with either pernicious anaemia or atrophic gastritis there was a significant increase in the frequency of HL-A3. No association has been found between any HL-A specificity and an increased incidence of either serum gastric parietal cell or intrinsic factor antibody compared with the overall incidence in pernicious anaemia, atrophic gastritis or in the whole series.

Twenty patients with idiopathic "warm" autoimmune haemolytic anaemia and 40 controls were types concurrently for human leucocyte antigens (HLA) A, B, C, and DRW. There was a significantly stronger association of HLA-B8 with the disease (chi 2 = 10.39; p = 0.018) than HLA-DRW3 (chi 2 = 3.71; P = 0.35) and the patients also showed a significant increase in BW6 homozygosity (chi 2 = 7.13; P = 0.01) and a corresponding reduction in BW4 (chi 2 = 7.13; P = 0.02). (All p values corrected for number of antigens at each locus.) These findings suggest that susceptibility to idiopathic autoimmune haemolytic anaemia is associated more closely with the HLA-B locus than with DRW3.

HLA typing was carried out in 50 Edinburgh men aged 45 years or under who had experienced a myocardial infarction and in 96 healthy 40-year-old men radomly selected from the same community. No significant differences in antigen frequencies were found, and our results therefore fail to support the hypothesis suggesting an association between HLA-B8 and haplotype A1-B8 with ischemic heart disease.