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Background/purpose: Rituximab is effective in treating pemphigus both as the first-line treatment and as an add-on treatment for refractory disease. A high rate of relapse among patients receiving rituximab means that maintenance therapy is frequently required. Therefore, we aimed to evaluate the use of azathioprine as maintenance therapy for patients receiving rituximab and to investigate the efficacy and safety of one or multiple cycles of rituximab treatment. Methods: We retrospectively collected data regarding pemphigus patients treated with rituximab from 2008 to 2015 with at least one year of follow-up at a referral center in Northern Taiwan. The medical records and clinical data were reviewed to determine the efficacy and complication rate of the treatment. Results: A total of 78 pemphigus patients were identified. Ninety-one percent of the patients achieved complete remission after the first cycle of rituximab with a relapse rate of 67.9%. Repeated cycles of rituximab showed a trend to shorten the time to next complete remission and to reduce the rate of subsequent relapses. The adverse events were usually not severe and were manageable. Use of azathioprine significantly prolonged the duration of remission (21.98 ± 16.24 vs. 9.98 ± 7.93 months, P = 0.0232). This effect of azathioprine usage remained after univariate and multivariate logistic regressions. Conclusion: This study provides an insight that azathioprine could serve as a good choice of maintenance therapy for patients receiving rituximab. The efficacy and safety of rituximab remain favorable even with repeated administration. Keywords: Azathioprine, Maintenance, Pemphigus, Rituximab

A 40-year-old female presented with rapid-onset generalized erythematous eruption with pustules agminated over the flexural areas and the flanks for 2 days. In skin histopathology, extensive subcorneal pustules, spongiosis and neutrophilic exocytosis, papillary dermal edema, and perivascular and interstitial mixed-cell infiltrates were observed. No psoriasis history but irregular intake of numerous kinds of Chinese herbal medications and the last-modified regimen including Radix Aucklandiae 14 days before the onset of pustular eruption were unveiled. Patch test showed positive result with only Radix Aucklandiae. Thus, acute generalized exanthematous pustulosis induced by Radix Aucklandiae was diagnosed.

Atopic dermatitis (AD) is generally considered a T-helper type 2-dominated disease. Adult AD is often more severe and less manageable by topical therapies and may require systemic immunosuppressants that bear notable side effects and organ toxicities. There is an unmet need for safe and effective long-term therapy in this population. Dupilumab, a fully human monoclonal antibody, dually inhibits interleukin (IL) IL-4 and IL-13 signaling and has demonstrated promising efficacy and acceptable safety profile in several Phase III trials, followed by recent Food and Drug Administration approval for the treatment of moderate-to-severe AD in adults whose disease is inadequately controlled with topical therapies. Dupilumab may also serve as a new treatment option when other systemic medications have failed or are inadvisable. Nevertheless, long-term safety data beyond 1 year and comparison with the existing therapies remain to be investigated. Other emerging agents targeting pruritogenic proteins, chronic inflammation, and epidermal hyperplasia are under vigorous clinical development. In particular, nemolizumab, blocking IL-31-mediated pruritus, has been reported in Phase II trials to provide symptom relief by interrupting the itch-scratch cycle. Accompanied by thorough characterization of different phenotype and endotype subsets, the era of precision medicine could bring new prospects in the optimal treatment of AD.

Background/Purpose Atopic dermatitis (AD) is a chronic inflammatory disease commonly seen in children and increasingly recognized in adults. With recent advances in the therapeutic development for AD, the Taiwanese Dermatological Association (TDA) established a committee to update the consensus for AD management in Taiwan. This report describes the 2020 updated consensus for the management of AD. Methods A panel of 11 core members was convened to review and discuss aspects of AD management and draft recommendation during the first two meetings. The 2015 TDA consensus and the 2017 European guideline, along with recent peer-reviewed articles, serve as the foundation for the update. In the third meeting, AD expert dermatologists selected on a national scale were invited to vote on the final statements. A total of 27 dermatologists attended the final meeting. The consensus was achieved when ratings of 7–9 (out of a total score of 9) accounted for ≥ 75% of the total votes. Results Consensus was achieved on the therapeutic options for AD by lines of treatment. A treatment algorithm was presented to illustrate the place of each modality in terms of basic care, acute disease control, and maintenance therapy. Special considerations for the pediatric population, as well as for women during pregnancy and lactation, are discussed. Conclusion Topical corticosteroids with long-term emollient-based therapies remain the cornerstone of AD treatment. Systemic treatments are indicated when topical therapies and phototherapy fail to control the disease. The recent approval of dupilumab and emerging targeted therapies are expected to bring significant clinical benefit for patients whose disease is inadequately managed by existing options.

Specific ethnic genetic backgrounds are associated with the risk of Stevens-Johnson syndrome / toxic epidermal necrolysis (SJS/TEN) especially in Asians. However, there have been no large cohort, multiple-country epidemiological studies of medication risk related to SJS/TEN in Asian populations. Thus, we analyzed the registration databases from multiple Asian countries who were treated during 1998-2017. A total 1,028 SJS/TEN cases were identified with the algorithm of drug causality for epidermal necrolysis. Furthermore, those medications labeled by the US Food and Drug Administration (FDA) as carrying a risk of SJS/TEN were also compared with the common causes of SJS/TEN in Asian countries. Oxcarbazepine, sulfasalazine, COX-II inhibitors, and strontium ranelate were identified as new potential causes. In addition to sulfa drugs and beta-lactam antibiotics, quinolones were also a common cause. Only one acetaminophen-induced SJS was identified, while several medications (e.g., oseltamivir, terbinafine, isotretinoin, and sorafenib) labeled as carrying a risk of SJS/TEN by the FDA were not found to have caused any of the cases in the Asian countries investigated in this study.

Background Oncologic treatments may lead to the development of paronychia, which may cause severe pain and disability. However, a detailed objective scoring system is lacking. Objective To develop an objective scoring system to quantify the severity of paronychia and also examine the correlation of this score with a pain index and patients' quality of life. Methods A novel scoring system for paronychia related to oncologic treatments (SPOT), consisting of four parameters, namely redness, oedema, discharge and granulation tissue, was designed to assess the severity of paronychia. The visual analogue scale (VAS) and Dermatology Quality of Life Index (DLQI) were recorded, and their association with the SPOT scores was analysed. Results Ninety patients were enrolled from three medical centres in Taiwan. Severity of paronychia was determined by the scores of SPOT. Patients in the severe group had higher DLQI scores (severe vs. mild: P = 0.0018; severe vs. moderate: P = 0.0015). Both the DLQI and pain index scores were significantly higher in patients with higher dominant hand SPOT scores. Conclusions The SPOT scores demonstrated the association of the paronychia severity with DLQI and pain. It may thus be useful in clinical practice and future studies.

Background/Objective Since 2005, there has been a significant increase in contact allergy to methylisothiazolinon (MI)/methylchloroisothiazolinone (MCI) incidences in European countries, but there has been no documented large-scale studies of such incidences in Taiwan. Methods From 1987 to 2015, a total of 2590 patients received patch testing in our Contact Dermatitis Clinic. Analyzed were patients with positive reactions to MI/MCI (Kathon CG) in patch testing and with suspected allergy to MI/MCI. Results Among the total 2590 patients, 2388 received patch testing during 1987–2005, while 202 received patch testing during 2006–2015. Because Kathon CG was not routinely patch tested for all patients from 1987 to 2005, the incidence of contact allergy to MI/MCI was thus corrected to 3/145 (2.1%) for this time period. After 2005, there were 11 patients (11/202, 5.4%) who showed positive reactions to MI/MCI. Amongst the 14 patients who showed positive reactions to MI/MCI, 12 of them were females (85.7%). The majority of the lesions was located on the hands (10 patients, 71.4%), along with the face (3 patients, 21.4%). Interestingly, 6 patients (42.9%) who showed positive reactions to MI/MCI were associated with contact allergy to essential oils, and five of them were aromatherapists. Conclusion According to our study, the incidence of MI/MCI contact allergy in a referral center in Taiwan was 5.4%. A trend of increasing incidence of contact allergy to MI/MCI was noted after 2005, which is consistent with the findings in Europe. Allergic contact dermatitis to MI/MCI should be suspected in patients who have eczema on the hands and face, especially those who are aromatherapists.

Background/Purpose This report describes the 2016 consensus of the Taiwanese Dermatological Association (TDA) regarding the definition, classification, diagnosis, prevention, and management of skin toxicities resulting from treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). This consensus is distributed to practices throughout Taiwan to provide recommendations for the diagnosis and treatment of such skin toxicities in order to improve the quality of life of patients undergoing EGFR-TKI treatment. The consensus thus serves as an important reference for dermatologists and other interested clinicians, such as oncologists, throughout Taiwan. Methods All the consensus contents were voted on by the participating experts, with approval by no less than 75% required for inclusion. Results The consensus provides a comprehensive overview of EGFR-TKI skin toxicities, including recent advances in identifying their causes and the processes by which they develop. Conclusion All the consensus meeting attendees agreed that there are several major EGFR-TKI-related skin toxicities, including acneiform rash (i.e., papulopustular rash), xeroderma, pruritus, paronychia, stomatitis, mucositis, and hair changes (such as hair loss, slowed hair growth, and trichomegaly). The experts were also generally unanimous in their voting on the specific definitions, onset times, and care suggestions for each of those skin toxicities. Furthermore, the recommended treatment algorithms for the various skin toxicities were ultimately approved by 100% (15/15) of the consensus attendees.

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are used as a treatment for non-small-cell lung cancer. There have been some reports of EGFR-TKIs being associated with vascular adverse events. We found that EGFR-TKIs decreased the proliferation of HMEC-1s (immortalized human dermal microvascular endothelial cells) and HMVECs (human dermal microvascular endothelial cells), and also inhibited the phosphorylation of EGFR and ERK. We examined the mRNA expression profile of erlotinib-treated HMEC-1s and identified IQ motif containing GTPase activating protein 1 (IQGAP1) as the most consistently up-regulated transcript and protein. IQGAP1 was also overexpressed and co-localized with endothelial cells in the lesional skin. Notably, increased IQGAP1 expression was associated with decreased transendothelial electrical resistance and increased vascular permeability in vitro. Erlotinib treatment enriched the staining of IQGAP1 and reduced the intensities of α-catenin at the sites of cell-cell contact. In conclusion, erlotinib induces adherens junction dysfunction by modulating the expression of IQGAP1 in dermal endothelial cells. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Atopic dermatitis is a chronic, inflammatory skin disease characterized by intense pruritus and eczematous lesions. It is considered one of the most common chronic conditions, with an estimated global prevalence of nearly 230 million. As in the rest of the world, prevalence of atopic dermatitis has been increasing in Asian countries over the last few decades. This increased prevalence in Asian countries has been attributed to factors such as rapid urbanization, increasingly Westernized lifestyles, and improved standards of living and education. As a result, it is important to understand the increasing burden of disease in Asian countries and the differences between the countries in terms of epidemiology, diagnostic criteria, management, quality of life and economic burden.

Severe cutaneous adverse reaction (SCAR) is life-threatening. It consists of Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), drug reaction with eosinophilia and systemic symptoms (DRESS), acute generalized exanthematous pustulosis (AGEP), and generalized bullous fixed drug eruptions (GBFDE). In the past years, emerging studies have provided better understandings regarding the pathogenesis of these diseases. These diseases have unique presentations and distinct pathomechanisms. Therefore, theoretically, the options of treatments might be different among various SCARs. However, due to the rarity of these diseases, sufficient evidence is still lacking to support the best choice of treatment for patients with SCAR. Herein, we will provide a concise review with an emphasis on the characteristics and treatments of each SCAR. It may serve as a guidance based on the current best of knowledge and may shed light on the directions for further investigations.

Background /Purpose BRAF and NRAS mutations have been described in melanomas among Caucasians and some Asian populations. However, few large-scale studies have investigated the status and clinical significance of BRAF and NRAS mutations in a Taiwanese population. Methods Melanoma samples ( n = 119) were analyzed for mutations in exons 11 and 15 of the BRAF gene, and in exons 1 and 2 of the NRAS gene. The samples were studied in genomic DNA, using polymerase chain reaction amplification and Sanger sequencing. Mutations of the BRAF and NRAS genes were then correlated with clinicopathological features and patients' prognosis. Results The incidence of somatic mutations within the BRAF and NRAS genes was 14.3% (17/119 patients) and 10.1% (12/119 patients), respectively. Among the 17 patients with BRAF mutations, 15 (88.2%) had V600E mutations. BRAF mutation was frequently detected in younger patients ( p = 0.0035), in thin melanomas ( p = 0.0181), and in melanomas with less ulceration ( p = 0.0089). NRAS mutation was more often seen in patients with lymph node metastasis ( p = 0.0332). Both BRAF and NRAS mutations were not significantly correlated with overall survival and disease-free survival. Conclusion As BRAF and NRAS mutations are rare in Taiwan, BRAF- or NRAS- targeted therapies may be effective only for selected Taiwanese melanoma patients.

Background/aims Ultraviolet light-signature mutations in the telomerase reverse transcriptase ( TERT ) gene promoter have been identified in cutaneous melanomas, basal cell carcinomas (BCCs), and squamous cell carcinomas (SCCs). Whether these mutations also occur in periocular tumours, including periocular sebaceous carcinomas (PSCs) and in situ tumours, has not been studied. Methods DNA extraction, PCR and Sanger sequencing were used to determine the frequency of TERT promoter mutations in periocular tumours. The presence of mutations was correlated with histological evidence of solar elastosis. Results Sixty-three tumours were analysed. TERT promoter mutations were identified in 18 of 22 BCCs (82%), 6 of 10 SCCs (60%), 1 of 2 in situ SCCs (50%), 4 of 9 grade III conjunctival intraepithelial neoplasia (CIN III) (44%) and 0 of 20 PSCs (0%). For BCCs, TERT promoter mutations were not associated with the histological risk categories of the tumours. For CIN III cases, all of the three lesions with solar elastosis had TERT promoter mutations, whereas the mutation was found in only one of the six CIN III cases without solar elastosis. Conclusions We demonstrate that ultraviolet light-signature TERT promoter mutations are very common in periocular BCCs, SCCs and CIN III lesions, indicating important roles of ultraviolet light in the pathogenesis of these tumours. In addition, the mutations are present in in situ stage. By contrast, no TERT promoter mutation is found in PSCs.

Dermatologic adverse events (dAEs) are common with the use of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy. First- and second-generation agents (erlotinib, gefitinib, and afatinib) are frequently associated with acneiform rash, pruritus, xerosis, and paronychia; the incidence and characterization of these dAEs have been well described. However, there is evidence that the dAE profile is different with third-generation EGFR-TKIs. Herein, we describe the dAEs associated with third-generation EGFR-TKIs and our clinical experience with osimertinib, a third-generation EGFR-TKI approved by the U.S. Food and Drug Administration for the treatment of metastatic, EGFR T790M mutation-positive non-small cell lung cancer in patients whose disease has progressed on or after EGFR-TKI therapy. Case summaries of patients from two of our institutions who received osimertinib and were referred to a dermatologist for dAEs are also presented. Overall, the evidence suggests that osimertinib is associated with less severe and less frequent dAEs than first- and second-generation EGFR-TKIs and that therefore a different approach is warranted. Finally, we outline dAE management approaches for osimertinib in the context of those typically employed with first- and second-generation EGFR-TKIs. Implications for Practice Appropriate prevention and management of dermatologic adverse events (dAEs) associated with the use of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) may help patients to continue therapy and lessen any negative impact on their quality of life. EGFR-TKIs are frequently associated with acneiform rash, pruritus, xerosis, and paronychia; however, dAEs associated with third-generation EGFR-TKIs are lower in frequency and severity. Before therapy, health care providers should discuss the potential osimertinib-associated dAEs and encourage patients to report their dAEs. Patients should also be educated on prophylactic measures to minimize the severity of dAEs and the importance of adherence to the treatment regimen.

The pathogenesis of melanomas emerging in plantar surfaces remains unclear; however, mechanical stress has been reported to increase the formation of melanomas. In this study, we conducted a multicenter retrospective analysis of 153 acral melanomas diagnosed between 2000 and 2015 in Taiwan. The male-to-female ratio of the patients in question was 1:1.28, and the mean age at diagnosis was 68 years. We examined whether melanomas which developed in different areas of the patients’ soles differed in their associations with various clinicopathological characteristics and survival. Testing by goodness of fit indicated that stress-bearing areas were significantly more conducive to the generation of melanomas than non-stress-bearing areas (P P P

The editors were made aware of concerns by a reader regarding potential manipulation of data in [this article][1] ([1][2]). An internal review by the editors determined that the same RT-PCR bands appear to be duplicated in the A549/HIF-1α and MDA-MB-231/GAPDH panels in Fig. 1B. In addition, it

Summary Hidradenoma papilliferum (HP) is a benign epithelial tumor most commonly seen in the vulva. It is proposed to be derived from the anogenital mammary–like glands and is histologically very similar to the mammary intraductal papilloma (IP). Approximately 60% of mammary IPs have activating mutations in either PIK3CA or AKT1 , with each gene accounting for 30% of cases. In this study, we screened the mutation statuses of PIK3CA , AKT1 , RAS , and BRAF in 30 HPs. The results showed that activating mutations in either PIK3CA or AKT1 were identified in 20 tumors (67%); 19 tumors had PIK3CA mutations (63%; 13 in exon 20 and 6 in exon 9), and 1 had an AKT1 E17K mutation (3%). BRAF V600E mutation was found in an HP that also had a PIK3CA H1047R mutation. No RAS mutation was found. The mutation status was not correlated with the degree of epithelial cell hyperplasia. We conclude that although there might be site-related variations in the mutation frequencies of PIK3CA and AKT1 genes, HP is histologically and also genetically very similar to the mammary IP, suggesting that HP can be viewed as the extramammary counterpart of mammary IP.

Aims Nipple adenoma (NA) is a rare benign epithelial tumour occurring in the nipple. Histologically, it exhibits variable and often mixed adenosis-like and usual ductal hyperplasia-like growth patterns. Morphologically, it is similar to other benign proliferative breast lesions occurring in the breast parenchyma, which have been shown to harbour activating mutations in PIK3CA, AKT1 or, less frequently, in RAS in more than 50% of cases. In this study, we aimed to analyse the mutation status of PIK3CA, AKT1, RAS and BRAF in NAs and correlated the mutation status with the histological features. Methods and results Mutation analysis of PIK3CA, AKT1, RAS and BRAF was performed in 24 NAs by Sanger sequencing. Our results showed that activating PIK3CA mutations were identified in eight of the 15 NAs (53%) with a predominantly adenosis-like pattern and four of the nine NAs (44%) with a predominantly usual ductal hyperplasia-like pattern. One tumour with a PIK3CA H1047R mutation also had a KRAS Q61H mutation. Two tumours with an adenosis-like pattern had BRAF V600E mutations. Overall, half of the NAs (12 of 24, 50%) in our series had PIK3CA mutations and 58% (14 of 24) had PIK3CA, RAS or BRAF mutations. Conclusions Our data indicate that, similar to other benign proliferative lesions occurring in the breast parenchyma, activating PIK3CA mutations are very common in NAs, and KRAS mutation may occur concurrently with PIK3CA mutation. In addition, as BRAF mutation has not been identified in benign proliferative lesions in previous studies, BRAF-mutated NAs appear to have distinct pathogenesis.

Insulin-like growth factor-II mRNA-binding protein 3 (IMP-3) is an RNA-binding protein expressed in multiple cancers, including melanomas. However, the expression of IMP-3 has not been investigated in acral lentiginous melanoma (ALM). This study sought to elucidate its prognostic value in ALMs. IMP-3 expression was studied in 93 patients diagnosed with ALM via immunohistochemistry. Univariate and multivariate analyses for survival were performed, according to clinical and histologic parameters, using the Cox proportional hazard model. Survival curves were graphed using the Kaplan-Meier method. IMP-3 was over-expressed in 70 out of 93 tumors (75.3%). IMP-3 expression correlated with thick and high-stage tumor and predicted poorer overall, melanoma-specific, recurrence-free and distant metastasis-free survivals (P = 0.002, 0.006, 0.008 and 0.012, respectively). Further analysis showed that patients with tumor thickness ≤ 4.0 mm and positive IMP-3 expression had a significantly worse melanoma-specific survival than those without IMP-3 expression (P = 0.048). IMP-3 (hazard ratio 3.67, 95% confidence intervals 1.35–9.97, P = 0.011) was confirmed to be an independent prognostic factor for melanoma-specific survival in multivariate survival analysis. Positive IMP-3 expression was an important prognostic factor for ALMs.

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have been widely used to treat non–small cell lung cancer. Four major skin toxic effects with different incidences have been reported from clinical studies, including acneiform eruption (60%-94%), pruritus (16%-60%), xerosis (4%-38%), and paronychia (6%-12%). 1,2 However, a direct comparison of the incidences and severities of the 4 types of skin toxic effects for 3 different EGFR-TKIs in the same patient cohort has been lacking to date. Methods | This retrospective study was approved by the research ethics committee of National Taiwan University Hospital. We recruited patients within a named patient program for compassionate use before registration who had ever received afatinib treatment for non–small cell lung cancer between November 1, 2007, and April 30, 2013. Most of the pa

Background Only few studies had investigated the histopathological presentations of drug reaction with eosinophilia with systemic symptoms (DRESS). The results of these studies were diverse and not conclusive. A characteristic histopathological feature is still lacking. Objective We tempted to identify characteristic histopathological features in DRESS and to correlate them with clinical presentations. Methods We retrospectively collected data from patients treated from 1998 through 2015. Available skin specimens from probable or definite cases according to the RegiSCAR criteria were analysed for histopathological patterns, which were then compared with the patients' clinical presentations. Chi-squared test was used for comparisons, while Bonferroni correction was applied if multiple comparison tests were encountered. Results Fifty-six patients with an average age of 52 years were identified, including 22 definite cases. The single most common histopathological pattern was interface dermatitis (75%). The co-existence of two or more patterns in a skin specimen was common (62.5%). In such cases, the co-existence of three patterns (the eczematous pattern, the interface dermatitis pattern and the vascular damage pattern) was most frequently encountered. It exhibited a significantly higher likelihood of being definite cases (P = 0.004) and was significantly associated with high grades of cutaneous abnormalities (P < 0.001). It showed a trend towards having higher grades of haematological abnormalities in patients with co-existence of three patterns (P = 0.04). In addition, patients with the co-existence of three patterns tended to have a higher rate of reactivation of human herpesvirus-6 than those with other patterns but not statistically significant (P = 0.052). Conclusion The co-existence of three histopathological patterns in a skin specimen is characteristic in DRESS and shows a significant association with clinical severity.

Importance Purpuric skin lesions have only rarely been reported in patients receiving epidermal growth factor receptor inhibitors. However, their clinical and histopathologic presentations have varied considerably. Objective To characterize purpuric skin eruptions caused by epidermal growth factor receptor inhibitors. Design, Setting, and Participants This prospective study enrolled 32 patients who presented to an integrated dermato-oncologic clinic in a tertiary referral medical center with purpuric skin lesions after using epidermal growth factor receptor inhibitors from January 1, 2013, through December 31, 2015. Exposures Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib, erlotinib, and afatinib. Main Outcomes and Measures Clinical presentations, histopathologic features, laboratory examinations, and treatment outcomes of patients with purpuric drug eruptions. Results Thirty-two patients, 14 with purpuric drug eruptions without pustules (mean [SD] age, 60 [11] years; 12 female and 2 male) and 18 with purpuric drug eruptions with pustules (mean [SD] age, 64 [11] years; 12 female and 6 male), were identified. The median time to development of skin lesions was 3.5 months. The clinical presentations were characterized by purpuric macules, papules, and confluent plaques predominantly on the lower extremities. Pustules in various sizes could be found in 18 patients (56%). Eleven patients (34%) had skin lesions that covered places other than the lower extremities. Eczema craquele–like features developed in 13 patients (41%). Bacterial pathogens were frequently identified in these skin lesions. Among them,Staphylococcus aureuswas the most predominant and was found in 20 patients (63%), commonly in those with cutaneous pustules. Epidermal dysmaturation, neutrophil exocytosis, perivascular infiltration of lymphocytes and neutrophils, red blood cell extravasation, and plumping endothelium were the main histopathologic features. The expressions of filaggrin and human β-defensin 2 in lesional skin of these patients were markedly reduced. All patients improved after receiving at least 1 week of systemic antibiotic treatment; the doses of epidermal growth factor receptor inhibitors were also changed for 14 patients (44%). Conclusions and Relevance Purpuric drug eruptions caused by epidermal growth factor receptor inhibitors are uncommon and have characteristic clinical and histopathologic presentations. The role of bacterial pathogens in this reaction is important and requires further exploration.

Epidermal growth factor receptor (EGFR) is known to be over-expressed in many different types of cancers, including lung cancer, breast cancer, colorectal cancer, and so on (1). Treatments targeting on EGFR signaling pathway provide better responses in these cancer patients harboring mutations in EGFR gene (2,3). However, adverse effects due to these EGFR inhibitors might lead to a poor drug adherence or discontinued usages of these agents (4). Skin toxicities are commonly encountered adverse effects during the treatment of EGFR inhibitors. Four major skin toxicities have been identified, including papulopustular (acneiform) eruptions, xerosis, pruritus, and paronychia. Therefore, management of these skin toxicities has a critical role in reducing patients’ discomforts, improving patients’ quality of life, maintaining usage of these agents, and further having a better prognosis (5).