This is a case of atypical ARPC without an associated disease. The pathogenesis of this disease is not exactly the same as that of classic ARPC, which has led to some people considering atypical ARPC to be pseudoperforation, often triggered by scratching or superficial trauma. However, in our case, the skin lesions were symmetric and crater-like, and the ARPC diagnosis was clinically and pathologically indisputable. Although some drugs were administered before disease onset, there is no evidence that the condition was drug-induced. Some ARPC cases are associated with complications such as diabetes mellitus, chronic renal disease, AIDS, pulmonary fibrosis, tumours, thyroid disease, liver failure, scabies, and insect bites [
3]. Interestingly, two cases did not show laboratory abnormalities. The present case is also rare. Regular medical examinations for 2 consecutive years have confirmed that the patient is healthy. We suspect that the disease is the result of a series of immune responses triggered by tinea pedis.
While several modes of treatment have been investigated, there is no effective standard treatment of ARPC. Allopurinol therapy has been effective in treating ARPC, but only for patients with diabetes mellitus [
4,
5]. Thus, it is worth exploring how the target therapy for treating ARPC should be selected. Collagen constitutes one of the vital components of the basement membrane scaffolds. Non-collagenous domains derived from collagen attaining significance in regulation of angiogenesis promoted diseases. The collagen eliminated in RPC may be derived from the basement membrane zone [
6]. Angiogenesis is a crucial mechanism of vascular growth and regeneration that requires biosynthesis and cross-linking of collagen in vivo and is induced by collagen in vitro [
7]. The anti-angiogenic, anti-Hedgehog pathway, and anti-inflammatory properties of itraconazole have been widely reported [
6]. The effectiveness of treatment of lichen planus, mycosis fungoides, basal cell carcinoma, palmoplantar pustulosis, and infantile haemangioma has been reported [
8]. Furthermore, we found that itraconazole has a significant effect on ARPC whose pathogenesis may involve vascular damage [
1]. Thus, we infer that the possible mechanism was based on the inhibition of fibroblast growth factors and vascular endothelial growth factors to treat ARPC [
9]. In particular, itraconazole inhibits neutrophil chemotaxis, interleukin-8 production, and the formation of pro-inflammatory metabolites, which are beneficial for ulcer healing [
10].