Eczema Herpeticum Research Articles

A real-world pharmacovigilance analysis of FDA adverse event reporting system database for upadacitinib.

Objective: To mine the adverse drug event (ADE) signals of upadacitinib based on the Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database to provide a reference for the safe clinical use of the drug. Methods: The ADE data for upadacitinib from Q1 2004 to Q1 2023 in the FAERS database were retrieved, and data mining was performed using the reporting odds ratio and proportional reporting ratio. Results: A total of 21,213 ADE reports for the primary suspect drug upadacitinib were obtained, involving 444 ADEs. Patients aged ≥60years (21.48%) and female (70.11%) patients were at a higher risk of ADEs with upadacitinib. After data cleaning, 182 ADE signals from 19 system organ classes (SOCs) were obtained. Six of these SOCs that occurred more frequently and were not mentioned in the drug labeling information included renal and urinary system (1.09%), reproductive and breast diseases (1.14%), ear and labyrinth disorders (0.57%), psychiatric disease (0.57%), blood and lymphatic system disorders (0.57%), and endocrine disorders (0.57%). The top ten most frequent ADE signals reported for upadacitinib were mainly related to: infections and infestations (7), investigations (2), and skin and subcutaneous tissue disorders (1). The top 10 ADEs in signal intensity ranking were lip neoplasm, ureteral neoplasm, eczema herpeticum, vulvar dysplasia, mediastinum neoplasm, eosinopenia, herpes zoster cutaneous disseminated, eye ulcer, acne cystic, and Moraxella infection. The top 10 high-frequency events leading to serious adverse events were urinary tract infection (2.74%), herpes zoster (1.63%), diverticulitis (1.19%), bronchitis (0.68%), nasopharyngitis (0.68%), localised infection (0.66%), nephrolithiasis (0.66%), pulmonary thrombosis (0.66%), blood cholesterol increased (0.55%), and Pneumocystis jirovecii pneumonia (0.53%). Conclusion: Clinicians should be vigilant to upadacitinib-induced events in systems not covered in the drug labeling information and to new and highly signaled ADEs to ensure the safe and effective use of upadacitinib.

Bacterial infections are common among eczema herpeticum inpatients in a cross-sectional analysis of the 2016 Kids' Inpatient Database.

Eczema herpeticum (EH) is a cutaneous infection with herpes simplex virus, typically in the context of atopic dermatitis. Pediatric hospitalizations for EH have increased over the past several decades, yet few studies have investigated comorbidities or epidemiology of pediatric EH inpatients. We searched the 2016 Kids' Inpatient Database and recorded demographics, comorbidities, and associated costs for patients with EH. We found bacterial infections were a common comorbidity which affected nearly half (47.4%) of hospitalized patients, suggesting the importance of regular monitoring of pediatric EH inpatients for bacterial coinfection.

Epstein Barr Virus Positive Hodgkin's Lymphoma in a Patient with NEMO Deficiency

IntroductionHypomorphic mutations in the NF-kappaB essential modulator (NEMO) can manifest in diverse ways, but are best characterized by early susceptibility to viral, pyogenic and mycobacterial infections, ectodermal dysplasia and absent pneumococcal responses. We describe a case of EBV+ Hodgkin's lymphoma in a 9-year-old patient with NEMO on antimicrobial prophylaxis and immunoglobulin replacement therapy (IgRT). Case reportOur patient was diagnosed with NEMO deficiency at 2 years with initial presentation of recurrent pneumonia, recurrent skin abscesses and severe eczema herpeticum. His disease was moderately controlled with IgRT, and prophylaxis with trimethoprim/sulfamethoxazole, azithromycin and acylovir prophylaxis, with primary complications of continued recurrent pneumonia and finger clubbing. At 9 years of age however, he developed acute back pain and weakness, along with night sweats. MRI revealed thoracic spinal cord compression at T5 secondary to a possible neoplastic soft tissue mass. A laminectomy revealed Epstein Barr virus (EBV) positive Hodgkin lymphoma, stage 4 high risk due to PET positivity with uptake at large cervical chain nodal conglomerates bilaterally, mediastinal mass, thoracic paraspinal mass, periportal lymph nodes, splenic, and right medial femoral neck. He also had low level EBV viremia (EBV viral load 7,515 IU/mL). He was treated according to AHOD1331 with ABVE-PC (doxorubicin/bleomycin/vincristine/etoposide/prednisone), and also received rituximab and valganciclovir for treatment of EBV. He is now in remission after 4 months of treatment, and continues on IgRT, pneumocystis jiroveci pneumonia, mycobacterium avium complex, and herpes simplex virus prophylaxis. ConclusionPatients with certain inborn errors of immunity have a higher incidence of malignancy due to impaired immune function. Despite their viral susceptibility, EBV-induced lymphomas are not common in NEMO deficiency. NEMO patients may need further enhanced screening for development of malignancy, including regular surveillance for chronic, cancer-causing infections such as EBV and HPV.

Monkeypox treatment options: current status of antiviral drugs – a correspondence

Dear Editor, At the time of writing this letter, according to Centers for Disease Control and Prevention, a total of 82,474 monkeypox virus-infected cases were reported in 110 countries across the globe. There are no particular therapies for monkeypox. However, since the viruses that cause monkeypox and smallpox are so similar, antiviral medications designed to guard against smallpox may be beneficial in treating monkeypox. Animal studies suggest that certain antivirals, originally developed for the treatment of smallpox, may also be useful against monkeypox. Although human dose–response trials have been performed, the effectiveness of the medications remains unclear1. We take the liberty of enlightening the readers on the currently used antiviral agents in the management of monkeypox. Brincidofovir and cidofovir Brincidofovir has been used to treat smallpox in the United States since June 2021. Brincidofovir (oral) is a drug that is similar to cidofovir (intravenous), but it may have a better safety profile due to less renal toxicity2. These drugs work by inhibiting the viral DNA polymerase3. Animal studies on the efficacy of brincidofovir in the treatment of monkeypox infections are limited, although the drug has been found to be successful against other orthopoxvirus infections4. Although there is currently no human clinical evidence on the effectiveness of cidofovir against monkeypox, it has been shown to be active and effective in vitro against deadly monkeypox virus infections in animals5. Cidofovir must be administered together with intravenous normal saline and probenecid treatment. Due to the potential for brincidofovir to raise serum transaminases and serum bilirubin, liver function tests should be performed before and periodically during therapy. Tecovirimat The first antiviral medication approved for the treatment of smallpox in adults and pediatric patients weighing at least 3 kg, tecovirimat (also known as TPOXX or ST-246) is the drug of choice6. Dual treatment with tecovirimat and brincidofovir may be utilized in individuals with advanced illness. Tecovirimat prevents the propagation of the virus within an infected host by blocking the virion protein VP37, which is responsible for the last stages of viral development and release from the infected cell7. Animal studies have shown that tecovirimat increases survival from deadly monkeypox virus infections relative to placebo-treated animals during various stages of illness; however, the drug’s effectiveness against monkeypox in people has not been studied8. A larger safety trial with 359 human volunteers found that the placebo side-effect profile was rather comparable to that of tecovirimat9. Patients suffering side effects from the smallpox vaccination, such as eczema vaccinatum and developing vaccinia, were given tecovirimat in conjunction with exhibiting vaccinia immune globulin (VIG) in a few trials6. When treating non-variola orthopoxvirus infections like monkeypox, tecovirimat may be used thanks to the Centers for Disease Control and Prevention’s Emergency Access Investigational New Protocol. The protocol also allows for the oral capsule’s contents to be opened and mixed with fluid or a soft diet for patients under 13 kg. Tecovirimat may be taken by mouth as a capsule or injected into the veins10. VIG Hyperimmune globulin (VIG) has been approved by the US Food and Drug Administration for use in treating vaccinia vaccination-related side effects. Vaccinia virus may cause a variety of abnormal illnesses, such as eczema vaccinatum, progressive vaccinia, severe generalized vaccinia, vaccinia infections in people with skin disorders, and vaccinia infections in healthy persons except for ocular infections11. While VIG has shown promise as a cure for both monkeypox and smallpox, there is a dearth of evidence on its efficacy and no human trials of its usage for either disease. Those with extreme immunodeficiency in T-cell function should not get the vaccinia virus vaccine; however, patients with a history of exposure may be administered VIG instead. An Investigational New Drug application is necessary for VIG treatment12. The treatment for monkeypox may rely on a variety of factors, including prior vaccination conditions, initial overall health, and simultaneous illnesses or comorbidities; however, for many people infected with the monkeypox virus, the disease course is mild and self-limiting, even within the lack of specific therapy. Thus, it seems that the most acceptable technique is to design individualized medicines based on each person’s risk of acquiring serious diseases. Ethical approval None. Sources of funding None. Author contribution S.S., D.G., and S.K.R.S. devised the concept, performed the literature search, and drafted the letter. Conflicts of interest disclosure There are no conflicts of interest. Research registration unique identifying number (UIN) None. Guarantor The submission is a correspondence. No new study was performed. All authors accept full responsibility for the submitted letter. Data availability The correspondence is based exclusively on resources that are publicly available on the internet and duly cited in the ‘References’ section. No primary data were generated and reported in this manuscript. Therefore, data has not become available to any academic repository.

Herpeticum

The case of a boy affected by atopic dermatitis with retroauricular and palpebral skin eruption is described. A diagnosis of eczema herpeticum with a superposed staphylococcal infection was eventually made.

Arising Concerns of Atypical Manifestations in Patients with Hand, Foot, and Mouth Disease.

Hand, foot, and mouth disease (HFMD) is a mild exanthematous, febrile disease, but it also remains a threat to global public health. HFMD is characterized by a brief febrile illness in children and with a typical skin rash of the hand and foot, with or without mouth ulcers. However, the morphology and distribution of vesicles, as well as accompanying symptoms, are varied among atypical HFMD. An upsurge in atypical presentations of HFMD caused by Coxsackievirus A6 (CVA6), including Gianotti-Crosti-like eruptions, eczema coxsackium, petechial/purpuric eruption, and vesiculobullous exanthema, can be difficult to diagnose clinically as it may mimic other severe skin diseases, such as eczema herpeticum, varicella, disseminated zoster, and erythema multiforme major. The recognition of the distinguishing features of atypical HFMD is vital for an accurate and timely diagnosis, as is initiating appropriate laboratory evaluation and supportive care. Clinicians must identify the wide range of cutaneous and mucosal alterations caused by atypical HFMD. A systemic, high-quality overview of atypical HFMD is needed for advances in better strategies for clinical diagnosis and treatment. Hence, this review is aimed at summarizing the available data on clinical investigations and differential diagnostics to provide a scientific guide for the timely diagnosis of HFMD for preventing serious complications.

309 Tralokinumab demonstrated a consistent safety profile with up to 42 months of treatment in moderate-to-severe atopic dermatitis: including adverse events of special interest

Abstract As atopic dermatitis (AD) is a chronic and potentially life-long disease, it is important to determine the long-term safety of new treatments. Tralokinumab, which specifically targets interleukin-13, is approved in Europe, Canada and the United States for the treatment of adults with moderate-to-severe AD. During the initial 12–16 week placebo-controlled treatment period of Phase 2 and 3 trials, tralokinumab was well-tolerated with an overall frequency of adverse events (AEs) similar to the placebo. An ongoing open-label extension trial, ECZTEND (NCT03587805), is assessing the safety and efficacy of tralokinumab up to 5 years after parent trials (PT). To report an interim safety analysis of patients treated with tralokinumab for up to 42 months (≤ 1 year in PT and ≤ 2.5 years in the open-label extension ECZTEND), including AEs of special interest (AESI). In ECZTEND, moderate-to-severe AD patients who completed the previous tralokinumab PT received subcutaneous tralokinumab 300 mg every 2 weeks after a 600 mg loading dose; topical corticosteroid use was optional. All AEs were recorded, coded, and classified by severity, causality and outcome. AESIs were predefined in PT based on areas of safety interest for monoclonal antibodies in AD, including eye disorders (e.g. conjunctivitis), skin infections requiring systemic treatment, eczema herpeticum and malignancies diagnosed after dosing. Event rates are presented as the number of events (nE) per 100 patient-years of exposure (PYE). All AEs described were treatment-emergent AEs, defined as AEs reported after the first dosing of the study drug. As of 30 April 2021, the interim safety analysis included 1442 patients from the PT ECZTRA 1, 2, 3, 4, 5 and 7 who had received ≥1 dose of tralokinumab in ECZTEND, with 121.0 weeks mean exposure time on tralokinumab [median 131.5 weeks (IQR 83.4–161.8); min 0.0, max 186.4 weeks]. Total exposure time in ECZTEND was 2446.2 PYE. Overall, 1127 patients experienced an AE (198.7 nE/100 PYE), the majority of which were mild (132.6 nE/100 PYE). The most frequently reported AEs (≥5.0% of patients) were the same as in the PT, including viral upper respiratory tract infection (18.2 nE/100 PYE, mainly reported as the common cold), atopic dermatitis (17.9 nE/100 PYE), upper respiratory tract infection (5.8 nE/100 PYE), headache (4.4 nE/100 PYE) and conjunctivitis (3.8 nE/100 PYE). The rates of AEs were generally lower as compared to short-term rates in the PT. Most of the serious AEs (SAEs; 4.9 nE/100 PYE) were reported as single events without clustering on the type. No events of conjunctivitis AEs were SAEs, and only five patients discontinued due to conjunctivitis AEs. AESI eye disorders, skin infections requiring systemic treatment, eczema herpeticum and malignancies were observed at rates similar to or lower than reported in PT. Consistent safety was demonstrated during up to 42 months of tralokinumab treatment in patients with moderate-to-severe AD. Exposure-adjusted incidence rates of AESIs, including eczema herpeticum and skin infections requiring systemic treatment, were generally lower than rates reported during the short-term, placebo-controlled period up to week 16. Exposure-adjusted incidence rates of conjunctivitis were lower with long-term exposure, and only five patients discontinued due to conjunctivitis. This analysis supports the long-term benefit-risk profile of targeted IL-13 inhibition with tralokinumab for patients with moderate-to-severe AD.

326 Dupilumab: a comparison of infection rates across atopic dermatitis trials in adults, adolescents, children and infants

Abstract Moderate-to-severe atopic dermatitis (AD) is associated with an increased frequency of infections which can lead to hospitalizations. Some treatments used for moderate-to-severe AD can be associated with an increased risk of infection, contributing to a limitation of their long-term use. Dupilumab is a biologic agent that targets the shared signalling pathway for interleukin (IL)-4 and IL-13 and has not been associated with increased risk of overall skin infection rates in clinical trials. To report rates of infection in patients with AD across age groups treated with dupilumab, with a special focus on non-herpetic skin and herpetic infections. We analysed exposure-adjusted infection rates (number of patients per 100 patient-years, nP/100PY) during the study treatment periods for MedDRA terms under the System Organ Class Infections and Infestations (overall infections), including adjudicated skin infections (excluding herpetic infections) and High-Level Term Herpes Virus Infections. Patients with moderate-to-severe AD enrolled in phase 2 (adults) or phase 3 clinical studies received various regimens. Young children (aged 6 months to 5 years, NCT03346434 part B) received dupilumab 200/300 mg (n = 83) every 4 weeks (q4w) or placebo (n = 78) with topical corticosteroids (TCS). Children (aged 6–11 years, NCT03345914) received dupilumab 300 mg q4w (n = 120), or 100/200 mg q2w (n = 122), or placebo (n = 120) with TCS. Adolescents (aged 12–17 years, NCT03054428) received dupilumab 300 q4w (n = 83), or 200/300 mg q2w (n = 82), or placebo (n = 85). Adults (NCT01548404, NCT02210780, NCT01859988, NCT02277743, NCT02277769, NCT02260986 and NCT02755649) received dupilumab 300 mg q2w (n = 746), or 300 mg qw (n = 1095), or placebo (n = 1091). Rates for dupilumab doses are provided in the order specified above. Post-hoc nominal P-values are between dupilumab and placebo. The rate of overall infections (nP/100PY) in the dupilumab treatment groups was numerically lower than in the placebo group in young children (placebo: 246; dupilumab: 185) and in children (placebo: 244; dupilumab: 184, 171) and similar between groups in adolescents (placebo: 204; dupilumab: 210, 181), and in adults (placebo: 129; dupilumab: 134, 126). Adjudicated non-herpetic skin infection rates (nP/100PY) were significantly lower in most dupilumab-treated groups compared with placebo in young children (placebo: 93; dupilumab: 43 [P < 0.05]), children (placebo: 48; dupilumab: 20 [P < 0.05], 28 [n.s.]), and adults (placebo: 27; dupilumab: 16 [P < 0.01], 14 [P < 0.0001]) and numerically lower in adolescents (placebo: 70; dupilumab: 34, 34). Overall herpes infection rates (nP/100PY) in dupilumab treatment groups were similar compared with placebo in young children (placebo: 17; dupilumab: 20), children (placebo: 17; dupilumab: 5, 11), adolescents (placebo: 12; dupilumab: 16, 4) and adults (placebo: 10; dupilumab: 15, 11). Infection rates (nP/100PY) of clinically important herpetic infections, eczema herpeticum and herpes zoster, were numerically lower in dupilumab-treated young children (placebo: 4; dupilumab: 0), adolescents (placebo: 4; dupilumab: 0, 0), and adults (placebo: 4; dupilumab: 2 [n.s.], 1 [P < 0.01]), and numerically higher in children (placebo: 0; dupilumab: 3, 3). Dupilumab treatment in children as young as 6 months of age, and in adolescents and adults with atopic dermatitis is generally associated with lower rates of non-herpetic skin infections compared with placebo and did not increase the risk of overall infections in these data sets.

Systemic herpes simplex virus infection in a child with eczema herpeticum.

Eczema herpeticum (EH) is a disseminated cutaneous infection with herpes simplex virus (HSV) that develops in patients with atopic dermatitis. The kinetics and clinical significance of HSV viremia in EH are poorly understood. Herein, we report HSV DNAemia in a child with EH 12 months after the completion of chemotherapy for Hodgkin lymphoma.

Disseminated life-threatening viral skin rash in a child with atopic dermatitis.

We report the case of a toddler, with a history of mild atopic dermatitis (AD) since early infancy, presented to the Giannina Gaslini, a pediatric polyclinic hospital, 14 days after measles-mumps-rubella (MMR) vaccination, for the occurrence of a disseminated vesico-pustular rash, accompanied by general malaise, fever, restlessness, and anorexia. Eczema herpeticum (EH) was diagnosed clinically and confirmed by laboratory examinations. The exact pathogenesis of EH in AD is still debated and possibly involves an inter-play between altered cell-mediated and humoral immunity, failure to up-regulate antiviral proteins, and exposure of viral binding sites through the dermatitis and an epidermal barrier failure. We hypothesize that in this particular case, MMR vaccination might have played an additional important role in the alteration of innate immune response, facilitating the manifestation of herpes simplex virus type 1 in the form of EH.

Eczema Coxsackium: An Unusual Manifestation of Hand, Foot, and Mouth Disease

Eczema coxsackium is an atypical manifestation of hand, foot, and mouth disease (HFMD). It is a rare manifestation and can be easily mistaken for eczema herpeticum or impetigo. We report two male infants (twins) of 6 months of age who presented with 2 days of fever and diarrhea followed by an erythematous rash over the diaper region with multiple eroded papules. As the presentation coincided with a seasonal clustering of HFMD cases, eczema coxsackium was suspected. Polymerase chain reaction for pan-enteroviral RNA was positive in a throat swab, and a diagnosis of eczema coxsackium over the diaper dermatitis was made.

Eczema herpeticum and impetigo herpetiformis, is there a link?

AbstractImpetigo herpetiformis (IH) is a rare variant of pustular psoriasis with typical onset during the third trimester of pregnancy; it is characterized by erythematous plaques lined with sterile pustules and sometimes there may be systemic involvement. On the other hand, eczema herpeticum (EH) is defined as a disseminated skin infection by herpes simplex virus type 1, which mainly affects patients characterized by an impaired integrity of the skin barrier, mostly atopic dermatitis. We report the case of a 30‐year‐old woman, primigravida at 28 + 3 weeks of gestation, who after asymptomatic severe acute respiratory syndrome coronavirus 2 infection for about 7 days presented to the emergency room with a burning and itching rash on the trunk and limbs. She reported a long‐standing history of atopic dermatitis and recurrent herpetic eruptions. The diagnosis of EH was made and systemic therapy was set with excellent results. A few days later, the patient developed a pustular rash in the areas previously affected by EH, with histologic features of IH. A relation between EH and IH is thus suggested.

046 Influence of dupilumab on HSV-specific immune response in atopic dermatitis

Eczema herpeticum (EH) is a disseminated, potentially life-threatening HSV infection in atopic dermatitis (AD) patients. Recently, we showed a type-2 skewed immune response to viruses in EH patients. Dupilumab is a monoclonal antibody targeting the IL-4Ra chain, and therefore acts directly against type-2 inflammation. Molecular investigations examining the impact of dupilumab on the immune defense against viruses are lacking so far. We aimed to analyze the effect of dupilumab on the antiviral response in AD patients with (ADEH+) and without (ADEH-) a history of EH.

Safety outcomes for topical corticosteroid use in eczema herpeticum: a single-centre retrospective cohort study.

Safety outcomes for topical corticosteroid use in eczema herpeticum: a single-centre retrospective cohort study.

Kaposi`s varicelliform eruption in a case of pustular psoriasis

<p>Kaposi`s varicelliform eruption (KVE) is a disseminated cutaneous infection with herpesvirus type 1 or 2, vaccinia virus, or coxsackievirus A16 in a patient with another underlying dermatosis. When herpesvirus type 1 or 2 is the pathogenic virus, the term ‘‘eczema herpeticum’’ (EH) is used, independent of the underlying dermatologic diagnosis that preceded the eruption. Presenting a case of generalised pustular psoriasis who while on immunosuppressant therapy cyclosporine developed KVE on the 3<sup>rd</sup> week of therapy. Based on the nature of cutaneous eruption and the bed side Tzanck smear test he was diagnosed as Psoriasis herpeticum. He was treated with oral acyclovir for 15 days with complete resolution of the lesions. KVE rarely occurs in psoriasis. It is more often in those patients who are on immunosuppressant therapy like oral methotrexate, cyclosporine etc. A high index of suspicion is needed while managing skin eruptions in a known case of psoriasis.</p>

The Genetics of Eczema Herpeticum.

Eczema herpeticum (EH) is a viral skin infection caused by herpes simplex virus (HSV) superimposed on eczematous skin lesions in atopic dermatitis (AD). Though the pathogenesis of EH has yet to be fully elucidated, the fact that EH is relatively rare despite a majority of adults showing serologic evidence of HSV exposure points to a genetic component predisposing to the disease. A number of genetic variants have been isolated in EH which may help distinguish a subgroup of patients susceptible to developing the condition. These unique genetic characteristics include deficiencies in skin barrier function and hydration, as well as at the level of the immune system. In this review, we summarize the genetic findings associated with EH identified to date. Isolating genetic markers in EH will be instrumental in stratifying patients at risk for EH and will have significant implications in the development and tailoring of targeted therapies.

Allergic conjunctivitis: a risk factor for recurrent herpes simplex virus infections in patients with atopic dermatitis

Patients with atopic dermatitis have an increased risk of herpes simplex virus (HSV) infections. We carried out a retrospective, cross-sectional study to investigate the association of disease severity, concomitant atopic diseases and filaggrin mutations with the risk of cutaneous HSV infections in 463 patients with atopic dermatitis. The correlation between predisposing factors and HSV infections was analysed using chi-square and Mann Whitney U-tests, and the relationship was further studied with binomial logistic regression to ascertain odds ratios. Allergic conjunctivitis (aOR: 1.770; CI: 1.008-3.109; p = 0.047) and patient age (aOR: 1.022; CI: 1.007-1.036; p = 0.004) showed statistically significant associations with recurrent HSV infections and eczema herpeticum. HSV infections were not linked to severity of atopic dermatitis (p = 0.435) or filaggrin mutation status (p = 0.886). The results highlight the importance for attentiveness of HSV infections in atopic dermatitis patients with concomitant allergic conjunctivitis.

Monkeypox: Considerations as a New Pandemic Looms

Monkeypox: Considerations as a New Pandemic Looms

315 Herpes simplex and eczema herpeticum in moderate to severe atopic dermatitis treated with abrocitinib

Patients with atopic dermatitis (AD) have increased risk of herpes simplex (HS) infection. Eczema herpeticum (EH) is a serious complication of HS. In a published safety analysis of abrocitinib, HS was reported in 5.9% (116; IR 11.83) and 6.1% (54; IR 8.73) and EH was reported in 0.4% (8; IR 0.78) and 1.7% (15; IR 2.34) of patients treated with abrocitinib 200 mg (N=1971) and 100 mg (N=885), respectively. Two EH events occurred in patients with IGA score <2 (both 100 mg). This post hoc analysis further characterized HS and EH in the above analysis of pooled data from patients with moderate to severe AD receiving abrocitinib 200 mg or 100 mg in the phase 2b (NCT02780167) and phase 3 JADE MONO-1 (NCT03349060), MONO-2 (NCT03575871), COMPARE (NCT03720470), REGIMEN open-label induction phase (NCT03627767), and EXTEND long-term extension (NCT03422822) trials (data cutoff: April 22, 2020).

528 Vaccinia virus utilizes claudin-1 to bind and infect keratinocytes

Atopic dermatitis (AD) patients suffer from increased susceptibility to cutaneous viral infections and diminished epidermal barrier function, including defects in TJ integrity and reduced claudin-1 (CLDN1) expression. To understand the role of CLDN1 in epidermal viral infections, we generated keratinocytes (KC) lacking CLDN1 using CRISPR/Cas9 technology. CLDN1 knockout (CLDN1KO) KC were evaluated for barrier function, differentiation, and susceptibility to vaccinia virus (VV), the causative agent of the life-threatening, AD-related complication, eczema vaccinatum.