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The sensitivity, specificity, and positive and negative likelihood ratios were 57.7%, 72.3%, 2.08, and 0.59, respectively. (ROC curves were not plotted for case patients aged 2 years or younger because of the small numbers.)There was significant correlation of serum TARC levels with the SCORAD index (r ¼ 0.538; 95% confidence interval [CI], 0.36-0.68), QOL indices (Infants' Dermatitis QOL: r ¼ 0.823; 95% CI, 0.40-0.96; Children's Dermatology Life Quality Index: r ¼ .380; 95% CI, 0.16-0.57), peripheral eosinophils, and LDH in children older than 2 years but not in the younger age groups (Table II). The correlation with IgE was not significant. In the same age group, for SCORAD index, the correlation was highest with LDH (r ¼ 0.582; 95% CI, 0.40-0.72), followed by serum TARC (r ¼ 0.538; 95% CI, 0.36-0.68), peripheral eosinophils (r ¼ 0.397; 95% CI, 0.19-0.57), and serum IgE (r ¼ 0.331; 95% CI, 0.11-0.52). In concurrence with previous studies, our results suggest that TARC correlates with the severity of AD and QOL indices. 1,5 The sensitivity and specificity were lower than those previously reported (83%-85% and 92%-96%, respectively), possibly due to choosing control individuals with diseases mimicking AD and the use of different enzyme-linked immunosorbent assay systems. 2,4

It has recently been revealed that mutation of the IL36RN gene contributes to the development of generalized pustular psoriasis (GPP). The IL36RN gene encodes interleukin (IL)‐36 receptor antagonist (IL‐36Ra), which has antagonistic roles against IL‐36α, ‐36β, and ‐36γ. Previously, sanger sequencing performed in 62 Chinese GPP patients to identify IL36RN mutations revealed a new variant, c.245C>T (p.Pro82Leu), in a single heterozygous state in a patient with adult‐onset GPP with psoriasis vulgaris. Since this p.Pro82Leu variant was not found in the psoriasis vulgaris or control groups in their study, they speculated that this variant might lead to exacerbated inflammatory responses. Meanwhile, Sorting Intolerant From Tolerant and PolyPhen‐2, pathogenicity prediction tools, predict this variant as tolerated and benign. To date, its pathogenicity is unknown. We experienced a patient with GPP harboring the p.Pro82Leu variant, and investigated mRNA and protein expressions of IL‐36Ra. Polymerase chain reaction conducted on hair follicle samples obtained from the scalp of the patient with GPP harboring the p.Pro82Leu using primers to detect mRNA of exons 2 and 5 in IL36RN demonstrated mRNA expression of IL36RN. Immunohistochemical staining revealed IL‐36Ra expression in the keratinocytes of the patient with GPP harboring the p.Pro82Leu as in those of a GPP patient without the mutation (positive control). Furthermore, quantitative analysis of the immunofluorescent staining by ImageJ revealed that the expression level of IL‐36Ra in the keratinocytes of the patient with GPP harboring p.Pro82Leu was higher than that in the healthy control and not lower than that in the GPP patients without the mutation. Our results indicate no aberrant splicing in this variant. In addition, according to the 1000 Genomes Project, this variant could be a founder mutation. Considering these factors together, this variant is unlikely to be associated with the development of GPP.

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