ASTHMA in children, ATOPIC dermatitis, ALLERGENS, T cells, GENE expression
Abstract
Background: Childhood allergies of asthma and atopic dermatitis (AD) involve an overactive T‐cell immune response triggered by allergens. However, the impact of T‐cell receptor (TCR) repertoires on allergen sensitization and their role in mediating different phenotypes of asthma and AD in early childhood remains unclear. Methods: A total of 78 children, comprising 26 with asthma alone, 26 with AD alone, and 26 healthy controls (HC), were enrolled. TCR repertoire profiles were determined using a unique molecular identifier system for next‐generation sequencing. Integrative analyses of their associations with allergen‐specific IgE levels and allergies were performed. Results: The diversity in TCR alpha variable region (TRAV) genes of TCR repertoires and complementarity determining region 3 (CDR3) clonality in TRAV/TRBV (beta) genes were significantly higher in children with AD compared with those with asthma and HC (p <.05). Compared with HC, the expression of TRAV13‐1 and TRAV4 genes was significantly higher in both asthma and AD (p <.05), with a significant positive correlation with mite‐specific IgE levels (p <.01). In contrast, TRBV7‐9 gene expression was significantly lower in both asthma and AD (p <.01), with this gene showing a significant negative correlation with mite‐specific IgE levels (p <.01). Furthermore, significantly higher TRAV8‐3 gene expression, positively correlated with food‐specific IgE levels, was found in children with AD compared with those with asthma (p <.05). Conclusion: Integrated TCR repertoires analysis provides clinical insights into the diverse TCR genes linked to antigen specificity, offering potential for precision immunotherapy in childhood allergies. [ABSTRACT FROM AUTHOR]
Lin, Han‐Wen, Chung, Wen‐Hung, and Chen, Chun‐Bing
Subjects
*MEDICAL sciences, *ATOPIC dermatitis, *CYCLIC adenylic acid, *IMMUNOGLOBULIN E, *MEDICAL research
Abstract
This article discusses a case series study that examined the efficacy of topical crisaborole in treating facial dermatitis in patients with atopic dermatitis who were also receiving dupilumab treatment. The study included eight patients who experienced facial dermatitis after starting dupilumab treatment. After four weeks of topical crisaborole treatment, all patients showed clinical improvement in facial and neck erythema. The study suggests that topical crisaborole may be a potential treatment option for dupilumab facial dermatitis, although further research is needed to validate its effectiveness. [Extracted from the article]
Background: Filler injection is among the most popular nonsurgical aesthetic procedures worldwide. Though relatively noninvasive, filler injection can lead to severe vascular adverse events. Even though the incidence is rare, it may cause devastating and irreversible outcomes. A Swiss cheese model has been widely applied for risk analysis and management approach in medical field. Aims: In this review article, we adopt the Swiss cheese model and create a structured approach to prevent severe vascular complications caused by filler injections. Methods: We reviewed the current literature regarding the knowledge and techniques of preventing vascular adverse events in the filler injection. Results: We propose four structured strategies in this model to reduce the risk of severe vascular adverse events of filler injections, including clinical facial anatomy, safe filler injection principles, real time imaging and auxiliary instruments, and implication of checklist. Conclusion: This review provides clinicians a structured approach before and during the filler injection procedure to reduce the risk of vascular adverse events and improve its safety and outcome. [ABSTRACT FROM AUTHOR]
Li, Philip H., Pawankar, Ruby, Thong, Bernard Y. H., Mak, Hugo W. F., Chan, Grace, Chung, Wen‐Hung, Juan, Meng, Kang, Hye‐Ryun, Kim, Byung‐Keun, Lobo, Rommel Crisenio M., Lucas, Michaela, Pham, Duy Le, Ranasinghe, Thushali, Rengganis, Iris, Rerkpattanapipat, Ticha, Sonomjamts, Munkhbayarlakh, Tsai, Yi‐Giien, Wang, Jiu‐Yao, Yamaguchi, Masao, and Yun, James
Subjects
PENICILLIN, ALLERGIES, MEDICAL personnel
Abstract
On average, how many individual consultations/visits on average are patients required to attend for entire penicillin allergy delabelling process (including history taking, allergy testing, provocation testing etc.)
a. If your centre performs penicillin skin prick/intradermal testing, which reagents do you routinely include in your penicillin allergy workup? The overwhelming burden of penicillin "allergy" labels remains a global public health concern associated with a myriad of adverse clinical outcomes.[1] The epidemiology and sensitization patterns of penicillin allergy varies greatly and remain largely unknown in the Asia-Pacific (AP) region.[[2], [4]] This international survey was performed to investigate the epidemiology, healthcare infrastructures and clinical practices pertaining to penicillin allergy in AP. In addition to penicillin allergy labels, what proportion (%) of patients have other drug allergy labels?. [Extracted from the article]
This article discusses a rare skin disease called Papuloerythroderma of Ofuji (PEO) that developed in an 88-year-old male patient following COVID-19 vaccination. PEO is characterized by intensely itchy red papules that can progress to erythroderma, with a distinct sparing of the skin folds. The patient had no other systemic symptoms and was diagnosed with secondary PEO based on clinical and histopathological grounds. Treatment with systemic methylprednisolone and topical betamethasone resulted in significant improvement, and there was no development of malignancy during the follow-up period. This case suggests a potential cutaneous reaction with PEO following COVID-19 vaccination. [Extracted from the article]
COVID-19 vaccines, STEVENS-Johnson Syndrome, TOXIC epidermal necrolysis, DRUG eruptions
Abstract
Since the outbreak of COVID-19, various vaccines have been developed to prevent viral transmission. We included studies reporting at least one patient who developed SJS, TEN, AGEP, and DRESS after at least one dose of a COVID-19 vaccine. Meanwhile, COVID-19 vaccines have been reported potentially to induce severe cutaneous adverse reactions (SCARs).[[1], [3]] SCARs, encompass several disease entities including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), acute generalized exanthematous pustulosis (AGEP), and drug reaction with eosinophilia and systemic symptoms (DRESS). [Extracted from the article]
Chiu, Chih‐Yung, Chang, Ko‐Chun, Chang, Lun‐Ching, Wang, Chia‐Jung, Chung, Wen‐Hung, Hsieh, Wen‐Ping, and Su, Shih‐Chi
Subjects
GUT microbiome, ALLERGIES, JUVENILE diseases, ALLERGIC rhinitis, AIRWAY (Anatomy)
Abstract
Background: Perturbation of gut symbiosis has been linked to childhood allergic diseases. However, the underlying host–microbe interaction connected with specific phenotypes is poorly understood. Methods: To address this, integrative analyses of stool metagenomic and metabolomic profiles associated with IgE reactions in 56 children with mite‐sensitized airway allergies (25 with rhinitis and 31 with asthma) and 28 nonallergic healthy controls were conducted. Results: We noted a decrease in the number and abundance of gut microbiome‐encoded carbohydrate‐active enzyme (CAZyme) genes, accompanied with a reduction in species richness, in the asthmatic gut microflora but not in that from allergic rhinitis. Such loss of CAZymes was consistent with the observation that a CAZyme‐linked decrease in fecal butyrate was found in asthmatics and negatively correlated with mite‐specific IgE responses. Different from the CAZymes, we demonstrated an increase in α diversity at the virulome levels in asthmatic gut microbiota and identified phenotype‐specific variations of gut virulome. Moreover, use of fecal metagenomic and metabolomic signatures resulted in distinct effects on differentiating rhinitis and asthma from nonallergic healthy controls. Conclusion: Overall, our integrative analyses reveal several signatures of systems‐level gut microbiome in robust associations with fecal metabolites and disease phenotypes, which may be of etiological and diagnostic implications in childhood airway allergies. [ABSTRACT FROM AUTHOR]
Su, Hsing‐Jou, Chung, Wen‐Hung, and Lin, Chien‐Yio
Subjects
*DERMATOMYOSITIS, *MYOSITIS, *AUTOANTIBODIES, *SYMPTOMS, *INTERSTITIAL lung diseases, *CUTANEOUS manifestations of general diseases
Abstract
Background: The myositis autoantibodies have been widely used clinically in recent years for the identification of an autoantibody‐associated clinical phenotype in dermatomyositis (DM) patients. However, correlations between myositis autoantibodies and clinical presentations in different populations are lacking, especially in Taiwan. Objectives: To investigate the correlations among cutaneous manifestations, myositis autoantibodies, and systemic diseases, including interstitial lung disease (ILD) and internal malignancy. Methods: A retrospective study of patients with histopathologically confirmed cutaneous manifestations of DM was conducted during 2005 to 2020 in Taiwan. A commercial line blot immunoassay technique was used to detect myositis autoantibodies. Results: A total of 88 DM patients were enrolled, with a mean age of onset of 49.4 years old. The most common systemic features were myositis (56.8%, 50/88), internal malignancy (22.7%, 20/88), dysphagia (19.3%, 17/88), and ILD (17%, 15/88). Among the enrolled patients, 32 patients received serum myositis autoantibodies examination. The most common autoantibodies were ANA (50.7%, 37/73), followed by anti‐TIF1‐γ (34.4%, 11/32) and anti‐MDA5 (31.3%, 10/32) antibodies. Patients with Gottron sign (OR 5.6), arthritis (OR 23.35), or the presence of anti‐MDA5 antibody (OR 11.14) were more susceptible to progressing to ILD, whereas patients with pruritus (OR 1.04), dysphagia (OR 6.73), and the presence of ANA (OR 6.29) had significantly higher risks of developing internal malignancies. Conclusions: Physicians should pay special attention to certain clinical features, which can help with the early detection of systemic diseases. Cancer screening and myositis autoantibodies examination should be conducted in all DM patients if applicable. [ABSTRACT FROM AUTHOR]
AZATHIOPRINE, AUTOIMMUNE diseases, CHINESE people, LEUCOPENIA, GENETIC testing, ASIANS
Abstract
Azathioprine (AZA) is commonly used for many autoimmune disorders; however, the limitation of its clinical use is due to potential toxicities, including severe leukopenia. Recent studies have identified genetic NUDT15 variants strongly associated with AZA‐induced leukopenia in Asian patients. This study aimed to investigate the strength of above genetic association and evaluate the usefulness of prospective screening of the NUDT15 variants to prevent AZA‐induced leukopenia in Chinese patients. AZA‐induced leukopenia in patients with autoimmune disorders were enrolled from multiple medical centers in Taiwan/China between 2012 and 2017 to determine the strength of genetic association of NUDT15 or TPMT variants by whole exome sequencing (WES). Furthermore, a prospective study was conducted between 2018 and 2021 to investigate the incidence of AZA‐induced leukopenia with and without genetic screening. The WES result showed the genetic variants of NUDT15 R139C (rs116855232) (P = 3.7 × 10−25, odds ratio (OR) = 21.7, 95% confidence interval (95% CI) = 12.1–38.8) and NUDT15 rs746071566 (P = 4.2 × 10−9, OR = 7.1, 95% CI = 3.7–13.7), but not TPMT, were associated with AZA‐induced leukopenia and NUDT15 R139C variant shows the highest sensitivity with 92.5%. Furthermore, the targeted screening of 1,013 participants for NUDT15 R139C enabled those identified as carriers to use alternative immunosuppressants. This strategy resulted in a significant decrease in the incidence of AZA‐induced leukopenia compared with historical incidence (incidence rate = from 7.6% decreased to 0.4%; P = 9.3 × 10−20). In conclusion, the NUDT15 R139C variant was strongly associated with AZA‐induced leukopenia in Chinese patients. The genetic screening of NUDT15 R139C followed by use of alternative immunosuppressants in identified carriers effectively decreased the incidence of AZA leukopenia for patients with autoimmune disorders. [ABSTRACT FROM AUTHOR]
Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life‐threatening cutaneous conditions. However, studies of pediatric SJS/TEN are limited. To investigate the causes, clinical course, outcomes and complications of SJS and TEN in children. This retrospective study included 47 pediatric patients (aged < 18 years) with SJS, SJS/TEN, or TEN treated at Chang Gung Memorial Hospital, Taiwan, between January 2009 and December 2019. ALDEN scores and serological tests were used to assess causes and SCORTEN scores were applied to evaluate disease severity. Forty‐seven patients, including 30 with SJS, 6 with SJS/TEN, and 11 with TEN were included. Median age was 8 years (range 1–17 years); 51.1% were male. Thirty‐three cases (70.2%) were caused by drugs and infectious pathogens were suspected in 14 cases (29.8%). Oxcarbazepine (5/47, 10.6%) and amoxicillin (5/47, 10.6%) were the most often‐implicated drugs, and Mycoplasma infection (9/47, 19.1%) was the predominant infectious cause. Only one TENS patient died (mortality rate 1/47, 2.1%) due to septic shock with ARDS, acute renal failure and cardiopulmonary shock. Median hospital stay was 15.5 (3–42) days. Pulmonary involvement (2/39, 5.1%), including pneumonia and ARDS, was noted in acute stage. Long‐term sequelae were ocular involvement (6/39, 15.4%), nail dystrophy (4/39, 10.3%) and post‐inflammatory hypo‐/hyperpigmentation (3/39, 7.7%). In the present study, pediatric patients with SJS, SJS/TEN, or TEN have good outcomes with few long‐term complications and low mortality. Mycoplasma is the most common infectious cause in pediatric SJS/TEN. Ocular discomfort, nail dystrophy and skin dyschromia are common long‐term sequelae requiring regular follow‐up. [ABSTRACT FROM AUTHOR]
VITILIGO, TREATMENT effectiveness, SYSTEM safety, THERAPEUTICS, QUALITY of life, SKIN grafting
Abstract
Vitiligo is a common, psychologically devastating pigmentary disorder. Surgical graftings are used to treat stable vitiligo when medical treatment fails. An automated epidermal micrograft harvesting (AEMH) system was first designated to treat wounds, and very few studies investigated the application of AEMH in vitiligo. In this study, we investigated the efficacy and safety of the AEMH system in patients with stable segmental and nonsegmental vitiligo. The rate of repigmentation and adverse events was recorded bimonthly for at least 12 months. We analyzed the efficacy based on patient characteristics, vitiligo subtypes, and different anatomical locations. A total of 56 depigmented lesions from 34 patients were included. 95.50% of the automated epidermal micrografts were successfully grafted at the recipient sites. There was a significant improvement in Vitiligo Area Scoring Index (VASI) and Dermatologic Life Quality Index (DLQI) in patients treated with AEMH (p < 0.001). The rate of repigmentation by VASI score improves from 96.25 ± 8.59 to 48.30 ± 28.16 after the treatment (p < 0.001). Treatment outcomes were comparable between the patients of segmental and stable nonsegmental vitiligo. The face and neck region achieved a better outcome, followed by the trunk (chest, abdomen, back, and axilla), limbs, and the worse outcome was found in the acral region (p < 0.014). Conclusively, AEMH is an effective treatment procedure with limited adverse events in patients with stable vitiligo. This harvesting method may be a feasible option for vitiligo surgical treatment. [ABSTRACT FROM AUTHOR]
Chiu, Chih‐Yung, Lin, Gigin, Wang, Chia‐Jung, Hung, Shuen‐Iu, Chung, Wen‐Hung, and Genuneit, Jon
Subjects
IMMUNOGLOBULIN E, ATOPIC dermatitis, AMINO acid metabolism, METABOLITES, METABOLOMICS
Abstract
Background: Filaggrin (FLG) gene mutation and immunoglobulin E (IgE)–mediated sensitization are the most important predictors of atopic dermatitis (AD). However, a metabolomics‐based approach to address the metabolic impact of FLG mutations on allergic IgE responses for AD is still lacking. We, though, determine the relationships of metabolic profiles in AD with FLG mutations and allergic responses. Methods: Eighty‐one children with adolescent AD (n = 58) and healthy controls (n = 23) were prospectively enrolled. Mutations in the filaggrin gene were identified using whole‐exome sequencing, and plasma metabolic profiles were determined using 1H‐nuclear magnetic resonance (NMR) spectroscopy. Integrative analyses of their associations related to total serum IgE levels were performed, and further metabolic functional pathways for AD were also assessed. Results: Metabolites contributed to the separation between AD and controls were identified using the supervised partial least squares discriminant analysis (Q2/R2 = 0.90, Ppermutation <0.001). Nitrogen and amino acid metabolisms for energy production, and microbe‐related methane and propanoate metabolisms were significantly associated with AD compared with healthy controls (FDR‐adjusted p <.05). Five of fifteen metabolites related to FLG mutations were positively correlated with total serum IgE levels. Among them, dimethylamine and isopropanol were strongly associated with methane metabolism and propanoate metabolism, respectively, in AD with FLG mutations (FDR‐adjusted p <.01). Conclusion: A strong correlation of microbial‐derived metabolites, dimethylamine and isopropanol, with FLG mutations and IgE allergic reactions provides the influence of host genetics on the microbiome to regulate susceptibility to allergic responses in the pathogenesis of AD. [ABSTRACT FROM AUTHOR]
As COVID-19 vaccination to children ramps up around the world, dermatologists should be vigilant regarding potential cutaneous skin reactions associated with COVID-19 vaccines. Keratosis pilaris-like eruptions in a child following COVID-19 vaccination While COVID-19 vaccination has been extensively administered in adults, its use in the pediatric population is still emerging, and COVID-19 vaccine-related adverse skin reactions in children have been underestimated.[1] Keratosis pilaris (KP) is a folliculocentric skin disorder characterized by the presence of keratotic papules predominantly on the extensor surfaces of the proximal extremities in both children and adults.[2] The exact etiology of KP remains unknown and multifactorial despite often being associated with atopy, ichthyosis, and obesity.[3] Here, we present a case of a child who developed KP-like eruptions following the first mRNA-1273 (Moderna) vaccination, with further progression observed after the second vaccination. [Extracted from the article]
Cheng, Chun Yu, Lin, Chiao‐Yun, Lai, Chyong‐Huey, Chen, Chun‐Bing, and Chung, Wen‐Hung
Abstract
Few articles have described the difference between epidermodysplasia verruciformis (EV) and generalized verrucosis (GV). This study aimed to analyze the clinical findings and virology of the two diseases. The study enrolled patients diagnosed with EV and GV by clinical and histopathological findings. The demographic information, clinical manifestation, treatment, and therapeutic outcome were analyzed. All of the biopsy specimens of enrolled patients were sent for β‐human papillomavirus (HPV) DNA detection. A total of 13 cases were included in the present study, including five EV cases and eight GV cases. Legs and feet were significantly affected in GV cases (p = 0.035). All acquired EV cases had immunocompromised conditions, while only three GV cases could be identified as having an immunocompromised history. All EV cases were detected with β‐HPV infection, especially HPV5, but none of the GV cases were found to be infected with β‐HPV. The therapeutic response was refractory and often relapsed after discontinuation of treatment in both groups. [ABSTRACT FROM AUTHOR]
Background: High rates of posttreatment discomfort, infection, recurrence, and increased time to return to work have been noted after nail plate avulsion resulting from epidermal growth factor receptor tyrosine kinase inhibitor(EGFR‐TKI)‐induced paronychia, which may even interrupt the course of treatment for EGFR‐TKI therapy. Thus, we conducted this study to determine how effectively a topical β‐blocker, betaxolol, prevents EGFR‐TKI‐induced paronychia. Methods: This case–control cohort study included a total of 131 non‐small‐cell lung cancer patients. The prevention group comprised 40 patients treated with topical betaxolol 0.25% solution to prevent paronychia while they received EGFR‐TKI therapy. The control group comprised 91 patients who did not preventively use topical betaxolol 0.25% solution while receiving EGFR‐TKI therapy. The patients' age, gender, antineoplastic regimen, duration of antineoplastic treatment before the appearance of lesions, number of involved digits (fingernails or toenails) with lesions, grading of paronychia, and pain score were recorded. Results: In terms of the cumulative incidence of paronychia, significant differences (P < 0.01) were noted at both the 2nd and 3rd months after starting EGFR‐TKIs. Furthermore, the average visual analogue scale scores were 3.125 and 6.29 in the prevention group and control group, respectively (P < 0.01). The average grades of paronychia were 1.5 and 2.12 in the prevention group and control group, respectively (P < 0.01). The average numbers of involved digits were 2.25 (range: 1–5 digits) in the prevention group and 3.03 (range: 1–7) in the control group (P = 0.07). Conclusions: Preventively using topical betaxolol can significantly decrease the incidence, VAS score, and grading of EGFR‐TKI‐induced paronychia. [ABSTRACT FROM AUTHOR]
Adverse drug reaction, characteristic sign, drug rash with eosinophilia and systemic symptoms, diagnostic clue, erythroderma, facial edema, periorbital sparing Keywords: adverse drug reaction; characteristic sign; diagnostic clue; drug rash with eosinophilia and systemic symptoms; erythroderma; facial edema; periorbital sparing EN adverse drug reaction characteristic sign diagnostic clue drug rash with eosinophilia and systemic symptoms erythroderma facial edema periorbital sparing 1626 1627 2 08/03/23 20230801 NES 230801 An otherwise healthy woman aged 55 years presented with high fever, facial swelling, mild dysphagia, and generalized skin rashes for 20 days. [Extracted from the article]
Drug‐induced hypersensitivity syndrome (DIHS) is a type of severe drug adverse reaction with high morbidity and mortality. DIHS patients have been reported to subsequently develop autoimmune disease, which may be followed by end‐organ decompensation. We report a 47‐year‐old woman who presented with fever, generalized maculopapular eruption, facial edema and eosinophilia with liver function impairment after taking celecoxib and sulfasalazine for 1 month. The patient was diagnosed with definite DIHS. The patient was treated with immunosuppressants including systemic corticosteroid for approximately 1.5 years due to recurrent episodes. Reactivation of human herpesvirus 6 and possible reactivation of cytomegalovirus were detected. Generalized hypopigmentation of the skin and leukotrichia were noted 4 months after the onset of DIHS. Histopathological examination confirmed the diagnosis of vitiligo. Some spontaneous repigmentation was noted 4 years after DIHS without specific treatment. Further immunoserology study showed elevated plasma C‐X‐C motif chemokine 10 level, which is related to vitiligo activity, in our patient. The occurrence of widespread vitiligo after DIHS is an extremely rare condition. This case provides an important reminder for physicians to monitor such severe complications after DIHS. [ABSTRACT FROM AUTHOR]
Background: Childhood asthma is a multifactorial inflammatory condition of the airways, associated with specific changes in respiratory microbiome and circulating metabolome. Methods: To explore the functional capacity of asthmatic microbiome and its intricate connection with the host, we performed shotgun sequencing of airway microbiome and untargeted metabolomics profiling of serum samples in a cohort of children with mite‐sensitized asthma and non‐asthmatic controls. Results: We observed higher gene counts and sample‐to‐sample dissimilarities in asthmatic microbiomes, indicating a more heterogeneous community structure and functionality among the cases than in controls. Moreover, we identified airway microbial species linked to changes in circulating metabolites and IgE responses of the host, including a positive correlation between Prevotella sp oral taxon 306 and dimethylglycine that were both decreased in patients. Several control‐enriched species (Eubacterium sulci, Prevotella pallens, and Prevotella sp oral taxon 306) were inversely correlated with total and allergen‐specific IgE levels. Genes related to microbial carbohydrate, amino acid, and lipid metabolism were differentially enriched, suggesting that changes in microbial metabolism may contribute to respiratory health in asthmatics. Pathway modules relevant to allergic responses were differentially abundant in asthmatic microbiome, such as enrichments for biofilm formation by Pseudomonas aeruginosa, membrane trafficking, histidine metabolism, and glycosaminoglycan degradation, and depletions for polycyclic aromatic hydrocarbon degradation. Further, we identified metagenomic and metabolomic markers (eg, Eubacterium sulci) to discriminate cases from the non‐asthmatic controls. Conclusions: Our dual‐omics data reveal the connections between respiratory microbes and circulating metabolites perturbed in mite‐sensitized pediatric asthma, which may be of etiological and diagnostic implications. [ABSTRACT FROM AUTHOR]
Tsai, Ya‐Wen, Chung, Wen‐Hung, Wang, Chuang‐Wei, and Cheng, Chun‐Yu
Subjects
*EXANTHEMA, *TOXIC epidermal necrolysis, *DRUG side effects, *DRUG eruptions, *COVID-19, *CYTOTOXIC T cells
Abstract
Porebski et al have demonstrated that in vitro cytotoxic-based assays, including granulysin and granzyme B, may be useful for the diagnosis of delayed drug hypersensitivity reactions.9 Moreover, a previous report also supported the diagnostic value of such assay in the diagnosis of SDRIFE.10 In conclusion, we reported the first case of levofloxacin-induced SDRIFE in which the causality was confirmed by a lymphocyte activation assay. Delayed type hypersensitivity, fluoroquinolones, levofloxacin, lymphocyte activation assay, SDRIFE, symmetric drug-related intertriginous and flexural exanthema Keywords: delayed type hypersensitivity; fluoroquinolones; levofloxacin; lymphocyte activation assay; SDRIFE; symmetric drug-related intertriginous and flexural exanthema EN delayed type hypersensitivity fluoroquinolones levofloxacin lymphocyte activation assay SDRIFE symmetric drug-related intertriginous and flexural exanthema 64 66 3 12/17/21 20220101 NES 220101 CASE REPORT A 50-year-old woman presented with multiple erythematous patches over her bilateral axillae and groins (Figure 1) lasting 3 days. [Extracted from the article]
Background: Paronychia is a common adverse event caused by epidermal growth factor receptor (EGFR) inhibitors. However, high rates of post‐treatment discomfort, infection, recurrence, and increased time to return to work have been noted after nail plate avulsion for EGFR inhibitor‐induced paronychia. Furthermore, poor wound healing and malnutrition were common conditions found in cancer patients. The aim of this study is to find an effective, pain‐relieving, and noninvasive treatment for patients with severe paronychia induced by EGFR inhibitors. Methods: Data from a series of 35 non‐small cell lung cancer cases suffering from EGFR inhibitor‐induced paronychia with pyogenic granuloma‐like lesions of digits treated with betaxolol 0.25% ophthalmic solution once daily were collected and analyzed. Results: Of the 35 patients suffering from grade 2 or 3 paronychia with pyogenic granuloma‐like lesions induced by EGFR inhibitors, 34 (97.1%) demonstrated complete resolution and only one (2.9%) had partial resolution after 12 weeks of topical betaxolol treatment. The grading of paronychia according to the Common Terminology Criteria for Adverse Events decreased from an average of 2.29 to 0.63 after 4 weeks of treatment (P = 5.55 × 10−16). All the patients had significant improvement (50% pain reduction), as their pain visual analogue scale scores decreased from an average of 7.06 to 2.26 after one week of treatment (P = 6.11 × 10−25). Conclusion: Betaxolol 0.25% ophthalmic solution is an effective, safe, and pain‐relieving treatment for patients suffering from EGFR inhibitor‐induced paronychia with pyogenic granuloma‐like lesions and deep fissures. [ABSTRACT FROM AUTHOR]
HLA-B*57:01 confers genetic susceptibility to carbamazepine-induced SJS/TEN in Europeans Carbamazepine (CBZ) is a widely used antiepileptic drug for the treatment of epilepsy, as well as bipolar disorder, trigeminal neuralgia, etc Although effective for treating neurological diseases, CBZ may cause cutaneous adverse reactions ranging from mild maculopapular exanthema (MPE) to life-threatening severe cutaneous adverse reactions (SCAR), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS). Furthermore, I HLA-B*57:01 i was absent in any European patient with CBZ-DRESS I HLA-B*57:01 i or I HLA-A*31:01 i was present in 55.26% (21/38) of CBZ-SCAR patients, and only in 10.96% (971/8862) of European general population controls (OR = 10.0, 95% CI = 5.3-19.1; I P i = 3.58 × 10 SP -11 sp ) (Table). Furthermore, CBZ shows affinity to HLA-B*57:01 and HLA-B*15:02 proteins only, but not HLA-B*15:01 or HLA-B*51:01 proteins (Figure B). [Extracted from the article]
DRUG side effects, ALLOPURINOL, XANTHINE oxidase, ALLERGIES, META-analysis
Abstract
The safety of newer xanthine oxidase inhibitor febuxostat compared to allopurinol remains unclear. To compare the risks of allopurinol hypersensitivity and febuxostat hypersensitivity and cardiovascular diseases (CVDs) in Asians, we conducted a population‐based cohort study enrolling patients receiving allopurinol or febuxostat from Chang Gung Memorial Hospital Health System across Taiwan during 2012–2016 and further performed a meta‐analysis incorporating two recent studies. Among the 61,539 users, a corresponding 12,007 and 5,680 patients were identified as new users. The overall incidence of febuxostat hypersensitivity was significantly lower than allopurinol hypersensitivity (0.2 vs. 2.7 per 1,000 new users; P < 0.001). There were 33 allopurinol‐hypersensitivity reactions (including 18 severe cutaneous adverse drug reactions), and only one patient developed febuxostat‐maculopapular exanthema. Moreover, febuxostat did not statistically increase the risk of CVD (hazard ratio (HR), 1.16; P = 0.152) and related death (HR, 1.49; P = 0.496) compared to allopurinol. The result of the meta‐analysis also showed a consistent result. In conclusion, the incidence and severity of febuxostat‐hypersensitivity are lower than with allopurinol. Febuxostat did not show an increased risk of CVD and related death. [ABSTRACT FROM AUTHOR]
Shen, Meng‐Han, Liu, Ming‐Tsan, Chung, Wen‐Hung, and Lu, Chun‐Wei
Abstract
Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) is a life‐threatening hypersensitivity reaction. Long‐term sequelae include dry eyes, visual impairment and psychological complications. TEN is mostly induced by medication; however, viral infections, such as coxsackievirus A6, are known triggers of this disease. However, how to define the role of infection in SJS/TEN is still a problem. Most patients develop SJS/TEN over the course of symptoms of the infection first, and then take medication. Therefore, virus culture and nucleic acid detection at the acute stage cannot predict that the virus itself will indeed produce such a serious reaction. Furthermore, many SJS/TEN patients who are diagnosed with an infection are afraid of receiving the drug rechallenge test. Thus, we report the first case worldwide of a patient who suffered from TEN caused by herpesvirus 7 infection, which was confirmed by both real‐time polymerase chain reaction and lymphocyte transformation test. [ABSTRACT FROM AUTHOR]
Manolio, Teri A., Hutter, Carolyn M., Avigan, Mark, Cibotti, Ricardo, Davis, Robert L., Denny, Joshua C., Grenade, Lois La, Wheatley, Lisa M., Carrington, Mary N., Chantratita, Wasun, Chung, Wen‐hung, Dalton, Andrea D., Hung, Shuen‐iu, Lee, Ming Ta Michael, Leeder, J. Steven, Lertora, Juan J. L., Mahasirimongkol, Surakameth, Mcleod, Howard L., Mockenhaupt, Maja, and Pacanowski, Michael
Subjects
STEVENS-Johnson Syndrome, GENOMICS, TOXIC epidermal necrolysis, DRUG-induced abnormalities, DRUG side effects, GENETICS, PREVENTION, THERAPEUTICS
Abstract
Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is one of the most devastating of adverse drug reactions (ADRs) and was, until recently, essentially unpredictable. With the discovery of several risk alleles for drug‐induced SJS/TEN and the demonstration of effectiveness of screening in reducing incidence, the stage is set for implementation of preventive strategies in populations at risk. Yet much remains to be learned about this potentially fatal complication of commonly used drugs. [ABSTRACT FROM AUTHOR]
Liu, Ren ‐ Feng, Chen, Chun ‐ Bing, Kuo, Tseng ‐ tong, and Chung, Wen ‐ Hung
Subjects
MUCOSITIS, LIP diseases, LYMPHOCYTES, PLASMA cells, HISTOPATHOLOGY, ETIOLOGY of diseases, EPIGLOTTIS, HEALTH outcome assessment
Abstract
Idiopathic lymphoplasmacellular mucositis ( ILPM) is a group of disorders histologically characterized by dense infiltrates of lymphocytes and plasma cells in submucosa. These lesions were initially observed on the glans penis and vulva, and later on buccal mucosa, lips, gingiva, tongue, epiglottis, larynx and other mucosal surfaces have also been reported. We have reviewed the previously reported cases of ILPM with lip involvement, outlining the clinical presentation, treatment and outcome of the entity to date. The etiology of ILPM is unknown, and the diagnosis is largely one of exclusion. To date, no consensus or consistently effective treatment for ILPM is available. Herein, we report an 18-year-old woman presented with markedly swollen lips with severe erosions, bleeding and yellow to black crusts who was diagnosed to have ILPM by histopathological study. The case occurred on rare lip site with an unusual appearance. Various treatment modalities were tried, but the responses were unsatisfactory and the lesion only responded to long-term administration of oral steroids. [ABSTRACT FROM AUTHOR]
Melatonin is a naturally occurring molecule secreted by the pineal gland and known as a gatekeeper of circadian clocks. Mounting evidence indicates that melatonin, employing multiple and interrelated mechanisms, exhibits a variety of oncostatic properties in a myriad of tumors during different stages of their progression. Tumor metastasis, which commonly occurs at the late stage, is responsible for the majority of cancer deaths; metastases lead to the development of secondary tumors distant from a primary site. In reference to melatonin, the vast majority of investigations have focused on tumor development and progression at the primary site. Recently, however, interest has shifted toward the role of melatonin on tumor metastases. In this review, we highlight current advances in understanding the molecular mechanisms by which melatonin counteracts tumor metastases, including experimental and clinical observations; emphasis is placed on the impact of both cancer and non-neoplastic cells within the tumor microenvironment. Due to the broad range of melatonin's actions, the mechanisms underlying its ability to interfere with metastases are numerous. These include modulation of cell-cell and cell-matrix interaction, extracellular matrix remodeling by matrix metalloproteinases, cytoskeleton reorganization, epithelial-mesenchymal transition, and angiogenesis. The evidence discussed herein will serve as a solid foundation for urging basic and clinical studies on the use of melatonin to understand and control metastatic diseases. [ABSTRACT FROM AUTHOR]
Yie-Tone Chen, Zong-Xing Lu, Ruey-Hsun Liang, and Chung-Wen Hung
Subjects
DC transformers, ELECTRIC potential, CAPACITOR switching, HIGH voltages, VOLTAGE multipliers
Abstract
A new high step-up dc-dc converter is proposed in this study. This new high step-up converter utilises the input voltage, clamped-capacitor, and the secondary side of the coupled-inductor to charge the switched-capacitor and the secondary side of the coupled inductor also charges two multiplier capacitors in parallel during the turn-on interval of the switch. The input voltage, coupled-inductor, and multiplier capacitors are in series connection to the output to accomplish the purpose of high voltage gain during the turn-off interval of the switch. By adjusting the turns ratio of the coupled inductors, the proposed circuit does not need to be operated at high duty cycle to achieve the high voltage gain. The voltage stress of the switch and diodes can be decreased to cut down the cost. Moreover, the energy of the leakage inductance can be recovered to reduce the voltage spike of the switch. Therefore, the switch with lower conduction resistance can be applied to reduce the conduction loss and increase the efficiency. Finally, simulation and experiments are conducted. A prototype circuit with input voltage of 24 V, output voltage of 400 V, and output power of 200W is implemented to validate the property of the proposed converter. [ABSTRACT FROM AUTHOR]
Table of contents: Oral Abstracts O1 Functionally distinct HMGB1 isoforms correlate with physiological processes in drug‐induced SJS/TEN Daniel F. Carr, Wen‐Hung Chung, Rosalind E. Jenkiins, Mas Chaponda, Gospel Nwikue, Elena M. Cornejo Castro, Daniel J. Antoine, Munir Pirmohamed O2 Hypersensitivity reactions to beta‐lactams, does the t cell recognition pattern influence the clinical picture? Natascha Wuillemin, Dolores Dina, Klara K. Eriksson, Daniel Yerly O3 Specific binding characteristics of HLA alleles associated with nevirapine hypersensitivity Rebecca Pavlos, Elizabeth Mckinnin, David Ostrov, Bjoern Peters, Soren Buus, David Koelle, Abha Chopra, Craig Rive, Alec Redwood, Susana Restrepo, Austin Bracey, Jing Yuan, Silvana Gaudieri, Mary Carrington, David Haas, Simon Mallal, Elizabeth Phillips O4 Do we need to measure total ige for the interpretation of analytical results of ImmunoCAP dnd 3gAllergy specific IgE? Douwe De Boer, Paul Menheere, Chris Nieuwhof, Judith Bons O5 Neutrophil activation in systemic anaphylaxis: results from the multicentric NASA study Friederike Jonsson, Luc De Chaisemartin, Vanessa Granger, Caitlin Gillis, Aurelie Gouel, Catherine Neukirch, Fadia Dib, Pascale Roland Nicaise, Dan Longrois, Florence Tubach, Sylvie Martin, Pierre Bruhns, NASA Study Group O6 Purpuric drug eruptions due to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR‐TKIs) for non‐small‐cell lung cancer (NSCLC): a clinic‐pathological study of 32 cases Kai‐Lung Chen, Shu‐Ling Liao, Yi‐Shuan Sheen, Yung‐Tsu Cho, Che‐Wen Yang, Jau‐Yu Liau, Chia‐Yu Chu Poster presentations: Poster Walk 1—Anaphylaxis (P01–P09) P1 Anaphylactic reactions during anaesthesia and the perioperative period Rita Aguiar, Anabela Lopes, Natália Fernandes, Leonor Viegas, M. A. Pereira‐Barbosa P2 Anaphylaxis to chlorhexidine: is there a cross‐reactivity to alexidine? Antonia Bünter, Nisha Gupta, Tatjana Pecaric Petkovic, Nicole Wirth, Werner J. Pichler, Oliver Hausmann P3 Cefotaxime‐induced severe anaphylaxis in a neonate Mehtap Yazicioglu, Pinar G. Ozdemir, Gokce Ciplak, Ozkan Kaya P4 Clinical features and diagnosis of anaphylaxis resulting from exposure to chlorhexidine Peter John Cooke P5 Drug‐induced anaphylaxis: five‐year single‐center survey Inês Mota, Ângela Gaspar, Filipe Benito‐Garcia, Marta Chambel, Mário Morais‐Almeida P6 Intraoperative severe anaphylactic reaction due to patent blue v dye Luis Marques, Eva Alcoceba, Silvia Lara P7 Kounis syndrome in the setting of anaphylaxis to diclofenac Leonor Carneiro‐Leão, Carmen Botelho, Eunice Dias‐Castro, Josefina Cernadas P8 Perioperative anaphylaxis audit: Royal Melbourne Hospital Katherine Nicholls, William Lay, Olivia Smith, Christine Collins, Gary Unglik, Kymble Spriggs, Priscilla Auyeung, Jeremy McComish, Jo A. Douglass P9 Recurrent peri‐operative anaphylaxis: a perfect storm Jonny G. Peter, Paul Potter Poster Walk 2: DH regions and patient groups (P10–P19) P10 A rare presentation of amoxicillin allergy in a young child Fabrícia Carolino, Eunice Dias De Castro, Josefina R. Cernadas P11 Adverse drug reactions in children: antibiotics or virus? Ana Sofia Moreira, Carmo Abreu, Eva Gomes P12 Allergic reactions in invasive medical procedures Bárbara Kong Cardoso, Elza Tomaz, Sara Correia, Filipe Inácio P13 Antibiotic allergy in children: room for improvement Annabelle Arnold, Natasha Bear, Kristina Rueter, Grace Gong, Michael O'Sullivan, Saravanan Muthusamy, Valerie Noble, Michaela Lucas P14 Drug hypersensitivity reactions in children and results of diagnostic evaluation Neringa Buterleviciute, Odilija Rudzeviciene P15 Nonimmediate cutaneous drug reactions in children: are skin tests required? Ana Sofia Moreira, Carmo Abreu, Eva Gomes P16 Pediatric patients with a history of penicillin allergy and a positive penicillin skin test may not be at an increased risk for multiple drug allergies Sara May, Thanai Pongdee, Miguel Park P17 Proved hypersensitivity to drugs according data of Vilnius University Hospital Santariskiu Klinikos Linas Griguola, Arturas Vinikovas, Simona Kašinskaite, Violeta Kvedariene P18 Self‐reported prevalence of drug hypersensitivity reactions among students in Celal Bayar University, Turkey Ayse Aktas, Suheyla Rahman, Huseyin Elbi, Beyhan Cengiz Ozyurt P19 Severe drug hypersensitivity reactions in pediatric age Ozlem Cavkaytar, Betul Karaatmaca, Pinar Gur Cetinkaya, Saliha Esenboga, Umit M. Sahiner, Bulent E. Sekerel, Ozge Soyer Poster Walk 3: Desensitisation (P20–P28) P20 A protocol for desensitisation to valaciclovir Celia Zubrinich, Bianca Tong, Mittal Patel, Michelle Giles, Robyn O'Hehir, Robert Puy P21 A rare case of desensitization to modafinil Josefina Cernadas, Luís Amaral, Fabrícia Carolino P22 A sixteen‐day desensitization protocol in delayed type hypersensitivity reactions to oral drugs Semra Demir, Asli Gelincik, Muge Olgac, Raif Caskun, Derya Unal, Bahauddin Colakoglu, Suna Buyukozturk P23 Desensitization to intravenous etoposide using a 12 and a 13‐step protocol. Two cases report Olga Vega Matute, Amalia Bernad, Gabriel Gastaminza, Roselle Madamba, Carlos Lacasa, M. J. Goikoetxea, Carmen D'Amelio, Jose Rifón, Nicolas Martínez, Marta Ferrer P24 Drug desensitisation in oncology: the experience of an immunoallergology department for 5 years Carmelita Ribeiro, Emília Faria, Cristina Frutuoso, Anabela Barros, Rosário Lebre, Alice Pego, Ana Todo Bom P25 Filgrastim anaphylaxis: a successful desensitization protocol Luis Amaral, Josefina Cernadas P26 Galsulfase hypersensitivity and desensitization of a mucopolysaccharidosis VI patient Luis Felipe Ensina, Carolina Aranda, Ines Camelo Nunes, Ana Maria Martins, Dirceu Solé P27 Rapid drug desensitization with biologicals: one‐center experience with four biologicals Sevim Bavbek, Resat Kendirlinan, Pamir Çerçi, Seda Tutluer, Sadan Soyyigit, Zeynep Çelebi Sözener, Ömür Aydin, Reyhan Gümüsburun P28 Successful desensitization to a high dose of methotrexate in a delayed type hypersensitivity reaction Josefina Cernadas, Leonor Carneiro‐Leão, Fabrícia Carolino, Marta Almeida Poster Walk 4: SJS (P29–P38) P29 Assessment of impact of infection on drug‐induced severe cutaneous adverse reactions and rhabdomyolysis using the Japanese adverse drug event report database Kimie Sai, Takuya Imatoh, Ryosuke Nakamura, Chisato Fukazawa, Yasushi Hinomura, Yoshiro Saito P30 Characterization of erythema multiforme and severe cutaneous adverse reactions hospitalizations Bernardo Sousa‐Pinto, Cláudia Correia, Lídia Gomes, Sara Gil‐Mata, Luís Araújo, Luís Delgado P31 Effects of infection on incidence/severity of SJS/TEN and myopathy in Japanese cases analyzed by voluntary case reports Ryosuke Nakamura, Kimie Sai, Takuya Imatoh, Yoshimi Okamoto‐Uchida, Koji Kajinami, Kayoko Matsunaga, Michiko Aihara, Yoshiro Saito P32 Efficacy of tumor necrosis factor—a antagonists in Stevens–Johnson syndrome and toxic epidermal necrolysis: a randomized controlled trial and immunosuppressive effects evaluation Chuang‐Wei Wang, Shih‐Chi Su, Shuen‐Iu Hung, Hsin‐Chun Ho, Chih‐Hsun Yang, Wen‐Hung Chung P33 Evolution of drug causality in Stevens–Johnson syndrome and toxic epidermal necrolysis in Europe: analysis of 10 years RegiSCAR‐Study Maren Paulmann, Ariane Dunant, Maja Mockenhaupt, Peggy Sekula, Martin Schumacher, Sylvia Kardaun, Luigi Naldi, Teresa Bellón, Daniel Creamer, Cynthia Haddad, Bruno Sassolas, Bénédicte Lebrun‐Vignes, Laurence Valeyrie‐Allanore, Jean‐Claude Roujeau P34 Long‐term sequelae in patients with Stevens–Johnson syndrome and toxic epidermal necrolysis: a 5‐year analysis Maren Paulmann, Carmen Kremmler, Peggy Sekula, Laurence Valeyrie‐Allanore, Luigi Naldi, Sylvia Kardaun, Maja Mockenhaupt P35 Major emotional complications and decreased health related quality of life among survivors of Stevens–Johnson syndrome and toxic epidermal necrolysis Roni P. Dodiuk‐Gad, Cristina Olteanu, Anthony Feinstein, Rena Hashimoto, Raed Alhusayen, Sonia Whyte‐Croasdaile, Yaron Finkelstein, Marjorie Burnett, Shachar Sade, Robert Cartotto, Marc Jeschke, Neil H. Shear P36 Retrospective analysis of Stevens–Johnson syndrome and toxic epidermal necrolysis in Japanese patients: treatment and outcome Naoko Takamura, Yumiko Yamane, Setsuko Matsukura, Kazuko Nakamura, Yuko Watanabe, Yukie Yamaguchi, Takeshi Kambara, Zenro Ikezawa, Michiko Aihara P37 Severe physical complications among survivors of Stevens–Johnson syndrome and toxic epidermal necrolysis Roni P. Dodiuk‐Gad, Cristina Olteanu, Rena Hashimoto, Hall Chew, Raed Alhusayen, Sonia Whyte‐Croasdaile, Yaron Finkelstein, Marjorie Burnett, Shachar Sade, Robert Cartotto, Marc Jeschke, Neil H. Shear P38 Stevens–Johnson syndrome/toxic epidermal necrolysis combined with haemophagocytic lymphohistiocytosis: a case report Brittany Knezevic, Una Nic Ionmhain, Allison Barraclough, Michaela Lucas, Matthew Anstey Poster Walk 5: Other organs/unexpected immune reactions (P39–P47) P39 A case report of patient with anti‐tuberculosis drug‐related severe liver failure Toru Usui, Xiaoli Meng, John Farrell, Paul Whitaker, John Watson, Neil French, Kevin Park, Dean Naisbitt P40 Acute interstitial nephritis induced by ibuprofen Ana Castro Neves, Susana Cadinha, Ana Moreira, J. P. Moreira Da Silva P41 Cetuximab induced acneiform rash—two case reports Daniela Ledic Drvar, Sandra Jerkovic Gulin, Suzana Ljubojevic Hadzavdic, Romana Ceovic P42 Enteropathy associated with losartan Ana Montoro De Francisco, Talía De Vicente Jiménez, Amelia García Luque, Natalia Rosado David, José Mª Mateos Galván P43 Granuloma annulare after therapy with canakinumab Razvigor Darlenski P44 Hypersensitivity eosinophilic myocarditis or acute coronary syndrome? Case report Dario Gulin, Jozica Sikic, Jasna Cerkez Habek, Sandra Jerkovic Gulin, Edvard Galic P45 Piperacillin‐induced immune haemolytic anaemia: a severe and frequent complication of antibiotic treatment in patients with cystic fibrosis Philip Specht, Doris Staab, Beate Mayer, Jobst Roehmel P46 Progesterone triggered pemphigus foliaceus: case report Sandra Jerkovic Gulin, Caius Solovan, Anca Chiriac P47 Ramipril: triggered generalized pustular psoriasis Paola Djurinec, Kresimir Kostovic, Mirna Bradamante, Sandra Jerkovic Gulin, Romana Ceovic Poster Walk 6: NSAIDs (P48–P56) P48 Aspirin desensitization in cardiovascular disease—Portuguese experience Jose Pedro Almeida, Joana Caiado, Elisa Pedro, Pedro Canas Da Silva, Manuel Pereira Barbosa P49 Asthma and/or rhinitis to NSAIDs with good tolerance to ASA Gador Bogas, Natalia Blanca‐López, Diana Pérez‐Alzate, Inmaculada Doña, José Augusto Agúndez, Elena García‐Martín, José Antonio Cornejo‐García, Cristobalina Mayorga, María José Torres, Gabriela Canto, Miguel Blanca P50 Clinical characteristics of 196 patients with non‐steroidal anti‐inflammatory drug (NSAIDs) hypersensitivity Sengül Aksakal, Aytül Zerrin Sin, Zeynep Peker Koç, Fatma Düsünür Günsen, Ömür Ardeniz, Emine Nihal Mete Gökmen, Okan Gülbahar, Ali Kokuludag P51 Development of immediate hypersensitivity to several NSAIDs maintaining good tolerance to ASA Natalia Pérez‐Sánchez, Natalia Blanca‐López, Diana Pérez‐Alzate, Gador Bogas, Inmaculada Doña, María Salas, María José Torres, Miguel Blanca, Gabriela Canto P52 Diagnosis of hypersensitivity reactions to paracetamol in a large series of cases Inmaculada Doña, Maria Salas, Francisca Gomez, Natalia Blanca‐Lopez, Diana Perez‐Alzate, Gador Bogas, Esther Barrionuevo, Maria Jose Torres, Inmaculada Andreu, Miguel Ángel Miranda, Gabriela Canto, Miguel Blanca P53 Hypersensitivity to paracetamol according to the new classification of hypersensitivity to NSAIDs Gabija Didžiokaite, Olesia Gaidej, Simona Kašinskaite, Violeta Kvedariene P54 Ibuprofen and other aryl propionic derivates can induce immediate selective hypersensitivity responses Diana Perez‐Alzate, Natalia Blanca‐López, Maria Isabel Garcimartin, Inmaculada Doña, Maria Luisa Somoza, Cristobalina Mayorga, Maria Jose Torres, Gador Bojas, Jose Antonio Cornejo‐Garcia, Maria Gabriela Canto, Miguel Blanca P55 Subjects developing immediate responses to several NSAIDs can be selective with good tolerance to ASA Natalia Blanca‐Lopez, Diana Pérez‐Alzate, Francisco Javier Ruano Perez, Inmaculada Doña, Maria Luisa Somoza, Inmaculada Andreu, Miguel Angel Miranda, Cristobalina Mayorga, Maria Jose Torres, Jose Antonio Cornejo‐Garcia, Miguel Blanca, Maria Gabriela Canto P56 Utility of low‐dose oral aspirin challenges for diagnosis of aspirin exacerbated respiratory disease Elina Jerschow, Teresa Pelletier, Zhen Ren, Golda Hudes, Marek Sanak, Esperanza Morales, Victor Schuster, Simon D. Spivack, David Rosenstreich Poster Walk 7: NSAID 2 (P57–P65) P57 Alternate regulation of cyclooxygenase‐2 (COX‐2) MRNA expression may predispose patients to aspirin‐induced exacerbations Renato Erzen, Mira Silar, Nissera Bajrovic, Matija Rijavec, Mihaela Zidarn, Peter Korosec P58 Anaphylaxis to diclofenac: what about the underlying mechanism? Leonor Carneiro‐Leão, Fabrícia Carolino, Luís Amaral, Carmen Botelho, Eunice Dias‐Castro, Josefina Cernadas P59 COX‐2 inhibitors: are they always a safe alternative in hypersensitivity to nonsteroidal anti‐inflammatory drugs? Luis Amaral, Fabricia Carolino, Eunice Castro, Josefina Cernadas P60 Management of patients with history of NSAIDs reactions prior to coronary angioplasty Mona Al‐Ahmad, Tito Rodriguez P61 Oral drug challenge with non‐steroidal anti‐inflammatory drug under spirometric control: clinical series of 110 patients João Pedro Azevedo, Emília Faria, Beatriz Tavares, Frederico Regateiro, Ana Todo‐Bom P62 Prevalence and incidence of analgesic hypersensitivity reactions in Colombia Pablo Andrés Miranda, Bautista De La Cruz Hoyos P63 Recent endoscopic sinus surgery lessens reactions during aspirin challenge in patients with aspirin exacerbated respiratory disease Teresa Pelletier, Waleed Abuzeid, Nadeem Akbar, Marc Gibber, Marvin Fried, Weiguo Han, Taha Keskin, Robert Tamayev, Golda Hudes, Simon D. Spivack, David Rosenstreich, Elina Jerschow P64 Safe use of imidazole salycilate in a case of multiple NSAIDs induced urticaria‐angioedema Elisa Boni, Marina Russello, Marina Mauro P65 Selective hypersensitivity reactions to ibuprofen—seven years experience Marta Ferreira Neto Poster Walk 8: Epidemiological methods (P66–P72) P66 Allopurinol hypersensitivity: a 7‐year review Lise Brosseron, Daniela Malheiro, Susana Cadinha, Patrícia Barreira, J. P. Moreira Da Silva P67 Antibiotic allergy labelling is associated with increased hospital readmission rates in Australia Brittany Knezevic, Dustin Sprigg, Michelle Trevenen, Jason Seet, Jason Trubiano, William Smith, Yogesh Jeelall, Sandra Vale, Richard Loh, Andrew Mclean‐Tooke, Michaela Lucas P68 Experts' opinions on severe cutaneous adverse drug reactions‐report of a survey from the 9th international congress on cutaneous adverse drug reactions 2015 Roni P. Dodiuk‐Gad, Cristina Olteanu, Wen‐Hung Chung, Neil H. Shear P69 HLA‐A*31‐positive AGEP with carbamazepine use and other severe cutaneous adverse drug reactions (SCARs) detected by electronic medical records screening Sabine Müller, Ursula Amstutz, Lukas Jörg, Nikhil Yawalkar, Stephan Krähenbühl P70 Patients with suspected drug allergy: a specific psychological profile? Eunice Dias‐Castro, Ana Leblanc, Laura Ribeiro, Josefina R. Cernadas P71 Use of an electronic device and a computerized mathematic algorithm to detect the allergic drug reactions through the analysis of heart rate variability Arantza Vega, Raquel Gutierrez Rivas, Ana Alonso, Juan Maria Beitia, Belén Mateo, Remedios Cárdenas, Juan Jesus Garcia‐Dominguez P72 Variation in ERAP influences risk for HLA‐B*57:01 positive abacavir hypersensitivity Rebecca Pavlos, Kaija Strautins, Ian James, Simon Mallal, Alec Redwood, Elizabeth Phillips Poster Walk 9: DRESS/AGEP (P73–P81) P73 A clinical case of DRESS syndrome in a child after administration of amoxicillin‐clavulanic acid Rita Aguiar, Anabela Lopes, Ana Neves, Maria Do Céu Machado, M. A. Pereira‐Barbosa P74 Acute generalized exanthematous pustulosis (AGEP) induced by mesalazine, reliable and oftenly used drug to treat inflammatory bowel disease Ceyda Tunakan Dalgiç, Emine Nihal Mete Gökmen, Fatma Düsünür Günsen, Gökten Bulut, Fatma Ömür Ardeniz, Okan Gülbahar, Ali Kokuludag, Aytül Zerrin Sin P75 Changes of blood plasmacytoid dendritic cells, myeloid dendritic cells, and basophils during the acute stage of drug reaction with eosinophilia and systemic symptoms (DRESS) and other drug eruptions Shao‐Hsuan Hsu, Yung‐Tsu Cho, Che‐Wen Yang, Kai‐Lung Chen, Chia‐Yu Chu P76 Characterization of isoniazid/rifampicin‐specific t‐cell responses in patients with DRESS syndrome Young‐Min Ye, Gyu‐Young Hur, Hae‐Sim Park, Seung‐Hyun Kim P77 DRESS syndrome secondary to sulfasalazine with delayed TEN: a case presentation Syed Ali, Michaela Lucas, Peter N. Hollingsworth, Andrew P. C. Mclean‐Tooke P78 Drug rash with eosinophilia and systemic symptoms (DRESS) features according to the culprit drug Zohra Chadly, Nadia Ben Fredj, Karim Aouam, Haifa Ben Romdhane, Naceur A. Boughattas, Amel Chaabane P79 Drug reaction with eosinophilia and systemic symptoms induced by allopurinol: not always easy to diagnose Marina Lluncor Salazar, Beatriz Pola, Ana Fiandor, Teresa Bellón, Elena Ramírez, Javier Domínguez Ortega, Santiago Quirce, Rosario Cabañas P80 Drug reaction with eosinophilia and systemic symptoms syndrome induced by two drugs simultaneously: a case report Krasimira Baynova, Marina Labella, Manuel Prados P81 The drug reaction with eosinophilia and systemic symptoms (DRESS) induced by the second‐line antituberculosis drugs and Epstein–Barr virus infection Agne Ramonaite, Ieva Bajoriuniene, Brigita Sitkauskiene, Raimundas Sakalauskas Poster Walk 10: Miscellaneous drug hypersensitivity (P82–P91) P82 A case of cycloserine‐induced lichenoid drug eruption confirmed with a lymphocatye transformation test Jae‐Woo Kwon, Shinyoung Park P83 Allergic reaction to topical eye drops: 5 years' retrospective study in a drug allergy unit Diana Silva, Leonor Carneiro Leão, Fabricia Carolino, Eunice Castro, Josefina Cernadas P84 Allergy to heparins Diana Perez‐Alzate, Natalia Blanca‐López, Maria Luisa Somoza Alvarez, Maria Garcimartin, Maria Vazquez De La Torre, Francisco Javier Ruano Pérez, Elisa Haroun, Gabriela Canto Diez P85 Allopurinol‐induced adverse drug reactions Katinka Ónodi‐Nagy, Ágnes Kinyó, Lajos Kemény, Zsuzsanna Bata‐Csörgo P86 Analysis of a population with immediate hypersensitivity to corticosteroids: an 11 year review Joana Sofia Pita, Emília Faria, Rosa Anita Fernandes, Ana Moura, Nuno Sousa, Carmelita Ribeiro, Carlos Loureiro, Ana Todo Bom P87 Anaphylaxis against mivacurium in a 12‐months old boy at first‐time exposure Wolfgang Pfützner P88 Antihistamine‐exacerbated chronic spontaneous urticaria: a paradox? Nadine Marrouche, Clive Grattan P89 Anti‐osteoporotic agents‐induced cutaneous adverse drug reactions in Asians Yu‐En Chen, Chun‐Bing Chen, Wen‐Hung Chung, Yu‐Ping Hsiao, Chia‐Yu Chu P90 Diagnosis of allergic reactions to eye drops Maria Vazquez De La Torre, Natalia Blanca‐Lopez, Diana Perez‐Alzate, Maria Isabel Garcimartin, Francisco Javier Ruano, Maria Luisa Somoza, Elisa Haroun, Gabriela Canto P91 Diagnostic approach in suspected hypersensitivity reactions to corticosteroids Fabrícia Carolino, Eunice Dias De Castro, Josefina R. Cernadas [ABSTRACT FROM AUTHOR]
Jhe-Yu Lin, Dan Chen, Chung-Wen Hung, and Zan Huang
Subjects
METAL oxide semiconductor field-effect transistors, ELECTRIC properties of gallium nitride, ELECTROMAGNETISM, ELECTRIC interference, CASCADE converters
Abstract
The gallium-nitride (GaN) cascode switch has received much attention recently for line-operated medium-high frequency (200 to 500 kHz) medium-power (200-1000 W) applications. Owing to its device structure, there are two TO-220 package options available with regard to the tab internal connection, unlike the conventional vertical power MOSFET. It is pointed out in this study that using proper package combination of GaN cascode devices, the electromagnetic interferences can be reduced in power converters/inverters. A 240 W 200 kHz LLC power converter with a front-end power-factor-correction circuit was built for experimental verification of the theory. Significant reduction was observed. Same theory can be applied to other converter/inverter configurations. [ABSTRACT FROM AUTHOR]
Chung, Wen‐Hung, Wang, Chuang‐Wei, and Dao, Ro‐Lan
Abstract
The clinical manifestations of drug eruptions can range from mild maculopapular exanthema to severe cutaneous adverse drug reactions (SCAR), including drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) which are rare but occasionally fatal. Some pathogens may induce skin reactions mimicking SCAR. There are several models to explain the interaction of human leukocyte antigen (HLA), drug and T-cell receptor (TCR): (i) the 'hapten/prohapten' theory; (ii) the 'p-i concept'; (iii) the 'altered peptide repertoire'; and (iv) the 'altered TCR repertoire'. The checkpoints of molecular mechanisms of SCAR include specific drug antigens interacting with the specific HLA loci (e.g. HLA-B*15:02 for carbamazepine-induced SJS/TEN and HLA-B*58:01 for allopurinol-induced SCAR), involvement of specific TCR, induction of T-cell-mediated responses (e.g. granulysin, Fas ligand, perforin/granzyme B and T-helper 1/2-associated cytokines) and cell death mechanism (e.g. miR-18a-5p-induced apoptosis; annexin A1 and formyl peptide receptor 1-induced necroptosis in keratinocytes). In addition to immune mechanism, metabolism has been found to play a role in the pathogenesis of SCAR, such as recent findings of strong association of CYP2C9*3 with phenytoin-induced SCAR and impaired renal function with allopurinol SCAR. With a better understanding of the mechanisms, effective therapeutics and prevention for SCAR can be improved. [ABSTRACT FROM AUTHOR]
Aim Oral antifungal agent-induced liver injury is a common safety concern that may lead to patients' hesitation in treating fungal infections such as onychomycosis. This study evaluated risk of drug-induced liver injury ( DILI) caused by oral antifungal agents in Taiwanese populations. Methods A population-based study was conducted by analyzing who used oral antifungal agents from 2002 to 2008 from the Taiwan National Health Insurance Database. A comparison control group was randomly extracted from the remainder of the original cohort. Results Of the 90 847 oral antifungal agents users, 52 patients had DILI. Twenty-eight DILI cases used ketoconazole, 12 fluconazole, eight griseofulvin, three itraconazole and two terbinafine. The incidence rates ( IR) of DILI per 10 000 persons were 31.6, 4.9, 4.3, 3.6 and 1.6 for fluconazole, ketoconazole, griseofulvin, itraconazole and terbinafine, respectively. Longer exposure duration increased the risk of DILI, with IR for exposure duration ≥ 60 defined daily dose ( DDD) of 170.9, 62.5, and 36.1 per 10 000 persons for ketoconazole, itraconazole and terbinafine, respectively. Patients taking antifungal agents had higher incidences of developing DILI compared with those in the control group after adjusting for age, gender and co-morbidities (relative risk 2.38, P < 0.001). All of the six patients with fatal DILI used fluconazole. Old age and fluconazole increased the risk of oral antifungal-induced fatal DILI. Conclusions Oral antifungal agents are associated with low incidence of acute liver injury, but which may be fatal, especially for the elderly. Longer treatment duration may increase the risk of antifungal agent-induced liver injury, especially ketoconazole. [ABSTRACT FROM AUTHOR]
The article describes the case of an immunocompromised patient who contracted subcutaneous Pyrenochaeta romeroi infection diagnosed by molecular identification, which, is the first case to be reported in Asia. He had no response to oral intraconazole for more than 6 months, but was treated successfully with amphotericin B for only 3 weeks.
Chung, Wen-Hung, Wang, Chun-Min, and Hong, Hong-Shang
Subjects
*CONTACT dermatitis diagnosis, *TEMPORARY tattoos
Abstract
Abstract Background In recent years, temporary tattoos instead of permanent tattoos have become popular worldwide. Although contact allergy to temporary henna tattoos appears to be rare in the past, it is progressively more commonly reported. Patients Four Taiwanese patients of allergic contact dermatitis following application of temporary tattoos were patch tested and they were followed up for 1 year after treatment. Results All four of the tested patients were positive to paraphenylenediamine. At 1-year follow-up, all four patients still showed various degrees of remnant hyperpigmentation on their previous tattooed areas. Conclusion Temporary tattoos may pose similar risks of allergic reactions associated with permanent tattoos. A high risk of prolonged post-inflammatory hyperpigmentation after allergic contact dermatitis from temporary tattoos should also be alerted, especially in Asian skin type. [ABSTRACT FROM AUTHOR]
A letter to the editor about the case of a 91-year-old female patient with a history of hypertension and diabetes mellitus and multiple erythematous patches after receiving levetiracetam is presented.
Lu CW, Pang JS, Ko YS, Chang CJ, Wang CW, Chen WT, Chen CB, Hui RC, Hung SI, Lu LY, Lu KL, Wang CL, Wu CE, Hsu PC, Fang YF, Li SH, Ko HW, Tseng LC, Shih FY, Chen MJ, and Chung WH
Subjects
Animals, Mice, Rats, ErbB Receptors, Erlotinib Hydrochloride adverse effects, Mutation, Protein Kinase Inhibitors adverse effects, Retrospective Studies, Adenocarcinoma of Lung drug therapy, Exanthema chemically induced, Exanthema drug therapy, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Tyrosine Kinase Inhibitors adverse effects, Zinc metabolism
Kano Y, Tohyama M, Aihara M, Matsukura S, Watanabe H, Sueki H, Iijima M, Morita E, Niihara H, Asada H, Kabashima K, Azukizawa H, Hashizume H, Nagao K, Takahashi H, Abe R, Sotozono C, Kurosawa M, Aoyama Y, Chu CY, Chung WH, and Shiohara T
Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Child, Drug Hypersensitivity Syndrome epidemiology, Eosinophilia complications, Eosinophilia epidemiology, Female, Follow-Up Studies, Humans, Japan epidemiology, Male, Middle Aged, Taiwan epidemiology, Young Adult, Diabetes Mellitus, Type 1 epidemiology, Drug Hypersensitivity Syndrome complications, Infections epidemiology, Thyroid Diseases epidemiology