Psoriasis vulgaris and acute guttate psoriasis in a family

A 33‐year‐old man (Case 1) developed scaling and erythema on the extensor side of his extremities, head, and back, 3 years before his first visit to our hospital. The lesions spread out to form several plaques and became persistent ( Fig. 1a). Serum antistreptolysin O (ASO) was within the normal range and a pharyngeal culture showed normal flora. Histologic findings were compatible with psoriasis vulgaris ( Fig. 1b). Topical steroid therapy was effective; however, scaling and erythema persisted. 1(a) Well‐demarcated scaling and erythema on the leg of Case 1. (b) Skin biopsy specimen from scaling and erythema showing hyperkeratosis, parakeratosis, elongated rete ridges, and inflammatory cell infiltration into the epidermis The 8‐year‐old daughter (Case 2) of Case 1 had suffered severe tonsillitis 2 months prior to the skin eruptions. Numerous rain drop‐like scaly papules appeared on her legs and generalized rapidly ( Fig. 2a). Her tonsils were swollen and reddish. Streptococcus pyogenes was detected by pharyngeal smear. The ASO value was at a high level. Histologic examination showed slightly elongated rete ridges, focal lack of the granular layer, parakeratosis, mild spongiosis, and exostosis of neutrophils ( Fig. 2b). She was diagnosed with acute guttate psoriasis. Administration of oral antimicrobials reduced the ASO value and led to remission of the disease. After 1 month of antimicrobial treatment, the erythematous papules disappeared. 2(a) Numerous rain drop‐like scaly papules on the arm of Case 2. (b) Skin biopsy specimen from scaling and erythema showing elongated rete ridges, focal lack of granular layer, parakeratosis, mild spongiosis, and exostosis of neutrophils The human leukocyte antigen (HLA) typing of the father was HLA‐A24, A31, B7, B39, and Cw7, and that of the daughter was HLA‐A24, A31, B39, and Cw7. Both possessed HLA‐A24, B39, and Cw7. The HLA typing of other family members was also studied. The mother had HLA‐A11, A24, B39, B62, Cw4, and Cw7, and her son had HLA‐A11, A24, B7, B62, Cw4, and Cw7. The result of HLA typing is shown in Table 1. 1 Human leukocyte antigen (HLA) typing in family membersFather (Case 1) A24 A31 B7 B39Mother A11 A24B39 B62 Cw4 Cw7 Daughter (Case 2) A24 A31 B39Cw7 Son A11 A24 B7 B62 Cw4 Cw7Lymphocyte stimulating test was performed using heat‐killed S. pyogenes which were boiled at 70 °C for 10 min and sonicated. The stimulation index was twofold higher in the daughter than in the father ( Fig. 3). 3The result of the lymphocyte stimulating test (LST) using heat‐killed S. pyogenes (S.I., stimulation index)