HL-A in psoriasis vulgaris and in pustular psoriasis--population and family studies.

Abstract

A collaborative study of HL‐A typing was done on 156 unrelated patients with psoriasis vulgaris and thirty‐one patients with pustular psoriasis. Highly significant increases of HL‐A13 and HL‐A17 were found in psoriasis vulgaris: about half of the patients carried either of these antigens as compared to about 12% of the controls. The effect of HL‐A13 and 17 is confined almost exclusively to psoriasis with onset before the age of 35 years. In contrast, none of these antigens was increased in pustular psoriasis, indicating that pustular and common psoriasis are different aetiological entities. Family studies in psoriasis vulgaris showed that psoriasis can develop in relatives lacking the HL‐A haplotype following psoriasis in the other family members. Hence, it seems most likely that HL‐A represents only part of the genetic basis of psoriasis vulgaris. This disease is probably of a polygenic threshold character, and HL‐A13 and 17 decreases the threshold making the expression of psoriasis more likely in individuals carrying these determinants in addition to other probably non‐HL‐A linked psoriasis determinants. This concept is supported by the observation of a higher incidence of a positive family history in HL‐A13 and/or 17 positive patients than in patients lacking these antigens. Studies of antistreptolysin O and antistreptococcal hyaluronidase titres and of triggering streptococcal infections yielded no clue as to the pathogenetic effect of HL‐A. The frequencies of HL‐A13 and 17 were not significantly increased in twenty‐one patients with psoriatic arthritis, but HL‐A27 may be increased in these patients. This study shows the importance of HL‐A in the subdivision of diseases and stresses the importance of family studies for clarifying the associations between HL‐A and disease.