Profiling of human leukocyte antigens in Eales disease and tuberculosis

Abstract

To analyze the association between Eales disease, histocompatibility leukocyte antigen alleles (HLA-A/B, HLA-DRB/DQB) and tuberculosis infection, and to explore susceptible genes and protective genes associated with Eales disease and tuberculosis infection in a population of Han nationals from Zunyi City in Guizhou Province, China. The subjects were analyzed by a case-control study consisting of three groups--Eales disease group (47 cases), pulmonary tuberculosis group (36 cases) and normal control group (100 cases). The Eales disease group was divided into four parts. Part one consisted of 12 patients who had suffered from pulmonary tuberculosis. Part two consisted of 27 patients who had not suffered from pulmonary tuberculosis. Parts three and four consisted of 27 patients with a positive purified protein derivative test and 12 patients with a negative test, respectively. DNA samples from 47 patients with Eales disease, 36 patients with pulmonary tuberculosis and 100 healthy people were detected by polymerase chain reaction with sequence-specific primers. The 59 HLA-A/B and HLA-DRB/DQB alleles from Eales disease were compared with those from tuberculosis and normal control, and a correlativity test of common susceptible genes was performed to analyze the potential relationship between Eales disease and pulmonary tuberculosis. The frequency distribution of HLA-A*02 alleles (OR 9.719, OR 95 % CI 4.377-21.580, P = 0.000) and HLA-B*07 (OR 11.605, OR 95 % CI 2.397-56.191, P = 0.001) in the Eales disease group was higher than in the normal control group, but the HLA-A*11 alleles (OR 0.495, OR 95 % CI 0.245-1.000, P = 0.048) were lower than in the normal control group, showing a significant difference. Compared with parts two and four, the frequency distribution of HLA-A*02, HLA-A*11 and HLA-B*07 alleles in parts one and three showed no significant difference (P > 0.05). HLA-A*A02, HLA-A*24, HLA-B*07 and HLA-DRB*16 alleles between the Eales disease, pulmonary tuberculosis and normal control group showed statistical significance (P < 0.05). HLA-A*24 alleles in the pulmonary tuberculosis group were lower than the Eales disease group (χ(2) 7.289, P = 0.007), but HLA-A*02 alleles showed no significant difference (P > 0.05) between the two groups. The results show that HLA-A*02 and HLA-B*07 may be genetic predisposing genes, but HLA-A*11 alleles may be protective genes of Eales disease, the HLA-A*02 allele may be a common susceptible gene of Eales disease and pulmonary tuberculosis. HLA-A*11 and HLA-A24 alleles are protective genes of Eales disease and pulmonary tuberculosis, respectively. In summary, the frequency distribution of susceptible genes of Eales disease and pulmonary tuberculosis in a population of Han nationals from Zunyi City in Guizhou Province, China showed no significant difference.

Rare case report: a 26-year-old man with Eales’ disease

“…Furthermore, its association with Mycobacterium tuberculosis, Mycobacterium fortuitum, and Mycobacterium chelonae exposure has been reported, causing a retinal autoimmune response [4,5]. Studies have shown that the tuberculin skin test (TST) was positive in 64% of patients suffering from Eales' disease [6]. In addition, individuals predisposed to HLA (HLA B5, DR1, DR4) are more likely to have an autoimmune response, due to tissue damage caused by mycobacterial antigen [5].…”

“…If presentation of Eales’ disease is unilateral, it is recommended to start treatment with periocular or intravitreal depot corticosteroids (triamcinolone acetonide or dexamethasone) to reduce the side effects of long-term systemic corticosteroids [ 6 ]. Systemics steroids (usually 1 mg/ kg body weight per day) are used in bilateral or severe cases to minimize the site of inflammation in Eales’ disease [ 1 ].…”

“…Unfortunately, in case of Eales’ disease, no documentation of biological drug treatment exists. Biological drugs are currently used for the treatment of vasculitis, such as anti-TNF-alpha agents (infliximab, etanercept, adalimumab, golimumab, and certolizumab), anti-interleukin (IL)-6-receptor antibody (tocilizumab), and anti-CD20 antibody (rituximab) [ 6 , 8 , 9 ]. Even so, we need more research on the use of biological drugs for Eales’ disease, which is aggressive and resistant to medical treatment.…”