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Journal of the American Academy of Dermatology
Volume 36, n° 6
pages 935-937 (juin 1997)
Doi : 10.1016/S0190-9622(97)80276-9
accepted : 27 April 1997
Brief communication

Further evidence of the role of HLA-DR4 in the genetic susceptibility to actinic prurigo
 

Teresa Hojyo-Tomoka, MD a, Julio Granados, MD b, Gilberto Vargas-Alarcón, PhD b, Jesús K. Yamamoto-Furusho, MD b, Elisa Vega-Memije, MD a, Roberto Cortós-Franco, MD a, Octavio Flores, MD c, Fernanda Teixeira, MD a, Luciano Domínguez-Soto, MD a,
a Department of Dermatology, Hospital General Dr. Manuel Gea González, Mexico City, Mexico 
b Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico 
c Centro Dermatológico Pascua, Mexico City, Mexico 

*Reprint requests: Luciano Domínguez-Soto, MD, Department of Dermatology, Hospital General Dr. Manuel Gea González, Calz. De Tlalpan 4800, Tlalpan D.F., Mexico 14000.
Abstract
Background:

Actinic prurigo (AP) is triggered by sun exposure. Its prevalence in Mexicans seems to be particularly high, which suggests a genetic susceptibility.

Objective:

Our purpose was to determine the role of major histocompatibility complex (MHC) genes in the genetic susceptibility to AP.

Methods:

Fifty-six Mexican Mestizo patients with AP underwent serologic typing for HLA class I and class II antigens. Class II MHC genes were also studied by DNA analysis. Findings in patients were compared with 100 ethnically matched healthy controls.

Results:

We found that 92.8% of patients with AP were HLA-DR4 positive (corrected p = 0.002; odds ratio [OR] = 10.1). The class I antigens HLA-A28 and ULA-B39 (B 16) were also significantly increased (p <- 0.000001, 0.000001, OR = 20.9 and p = 0.0001, OR = 6.7, respectively) compared with normal controls. Allele-specific oligonucleotide DR4 subtyping showed that 80.7% of HLA-DR4+ patients with AP were also positive for the DRB 1 *0407 allele.

Conclusion:

These results confirm the role of HLA-DR4 (DRB 1 *0407) in the genetic susceptibility to AP and raise the possibility of a role for class I MHC antigens HLA-A28 and B16 in Mexican patients.

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