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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.

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


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


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.


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.


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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