PPP is a chronic disease with a high recurrence rate and a poor response to treatment. It occurs most often in patients aged 50–60 years [
1]. In the present study, a total of 48 patients diagnosed with PPP were recruited, including 8 males and 40 females. The mean age was 49.8 years (range 18–79 years). Plantar involvement was more frequent than palmar involvement, which was consistent with previously reported cases [
1,
5]. This suggests that PPP is frequently found in the palmoplantar region. In Olazagasti et al.’s retrospective review of 215 patients with PPP, systemic agents that elicited a complete response included acitretin (6 of 24 patients; 25%), methotrexate (2 of 20 patients; 10%), and cyclosporine (2 of 4 patients; 50%). Several treatments—dapsone (3 patients), etanercept (3 patients), and prednisone (5 patients)—elicited no response [
5]. In the present study, 48 patients with PPP received monotherapy with cyclosporine. The PPPASI score was 0.6–47.4 before treatment (mean 12.8). After 8 weeks of treatment, the efficacy was evaluated. Results showed complete remission in 8.3% of patients, remission in 41.7%, improvement in 22.9%, and treatment ineffectiveness in 20.8%, with an overall effectiveness rate of 50%. These results are consistent with relevant results in the literature [
5‐
7] and they confirm that cyclosporine is an effective treatment for PPP.
Cyclosporine A is safer than other commonly used systemic treatments. Adverse reactions disappeared after cyclosporine reduction or withdrawal, and increased body hair recovery was relatively slow. These findings indicate that cyclosporine is an effective treatment for PPP with few adverse effects, and that these adverse effects are mild and may resolve after treatment termination. However, routine monitoring is necessary and the dose of cyclosporine should be determined according to the guidelines in order to reduce or avoid the adverse effects of cyclosporine.
The pathogenesis of PPP is still poorly understood. Smoking, emotional stress, focal infection, certain drugs, genetics, immunity, and metal sensitization are reported to be involved in the occurrence or aggravation of pustulosis [
5]. Smoking plays a particularly important role in the pathogenesis of PPP. Tobacco smoke is considered to be a possible trigger of PPP, and it may increase the expression of IL-17 and IL-22 [
8]. Recent studies have shown that IL-17, IL-23, and TNF-α play crucial roles in the pathogenesis of psoriasis [
9], and PPP is closely related to this pathogenesis [
10,
11]. Several reports have reported an overexpression of IL-17 in periodontitis [
12,
13]. IL-17 is expressed not only in Th17 cells but also in inflamed tissues such as gingiva [
12,
13]. Elevated IL-17 expression has been noted in the skin lesions and sera of PPP patients, and TNF-α is significantly increased in the sera of PPP patients, but IL-23 is not [
14]. As a result of this low IL-23 expression in the sera of PPP patients, it was assumed that the expression of IL-17 in inflamed tissues such as gingiva may relate to the pathogenesis of PPP [
14]. Our results showed that the serum concentrations of IL-17, IL-23, and TNF-α decreased after 8 weeks of cyclosporine treatment in PPP patients. Significant reductions were noted in IL-23 and TNF-α, while the serum IL-17 concentration decreased slightly. This implies that the therapeutic effects of cyclosporine may be related to the downregulation of IL-17, IL-23, and TNF-α expression, especially that of IL-23 and TNF-α. Note that the sample size was small in the present study, and the specific mechanisms underlying the therapeutic effects of cyclosporine were not investigated further. Thus, more clinical studies with elegant designs and large sample sizes are needed to confirm the etiology and pathogenesis of PPP as well as the mechanisms underpinning the therapeutic effects of cyclosporine.