BACKGROUND:Tattoo aftercare instructions describe how to care for a new tattoo. Unfortunately, tattoo artists often base their advice on personal experience rather than best practices in medical wound management. The diversity of recommendations in these instructions is currently unknown.OBJECTIVES:Our review was performed to determine current recommendations in tattoo aftercare instructions in the United States.METHODS:Using a Google search, a total of 700 aftercare instructions from all 50 states and Washington D.C. were collected and their contents analyzed.RESULTS:Most instructions encouraged washing new tattoos with antibiotic soaps, including chlorhexidine, and 14.9% encouraged using topical antibiotics. Few instructed individuals to wash their hands before touching a healing tattoo. A total of 70 moisturizers were recommended. Of these, 22 were niche products made specifically for tattoo aftercare. Only a subset of instructions provided parameters about when to contact the tattooist (49.9%) and/or a physician (19.4%) should there be a complication in the healing process.CONCLUSION:The content and recommendations of the 700 instructions vary tremendously. Many lacked instructions on appropriate hygiene and when to seek medical care. As skin and wound care experts, there may be an opportunity for the dermatology community to partner with tattooists to create more useful evidence-based tattoo aftercare practices.

Tattooing for medical purposes may have been around more than 5,300 years ago, but most of the interest and changes have occurred during the last 100 years as a consequence of scientific advances leading to quicker, cleaner, and less painful insertion of pigment into the skin as well as advances in medical knowledge allowing for more relevant individual information to be transmitted by the embedded pigment. These changes are ongoing. Cosmetic tattooing or tattooing for camouflage of body surface imperfections, likewise, has advanced during the last 50 years concurrently with the rise of social media, internet access, and the popularity of personal electronic visuals.

mucositis 3 months later, but this also resolved quickly with prednisone, 80 mg, for 6 days.Discussion | Formerly known as Mycoplasma-induced rash and mucositis, RIME has arisen as the preferred terminology to include mucocutaneous eruptions that are caused by other infectious agents. 2 This case describes RIME secondary to SARS-CoV-2 infection, details its resolution with systemic steroids, and notes the potential for recurrence with subsequent milder symptoms, as has been previously reported. 3The combination of anosmia and ageusia, multiple positive SARS-CoV-2 PCR tests, and no other identified contemporaneous infections (the elevated Mycoplasma pneumoniae IgG titer with low IgM titer and negative nasopharyngeal PCR likely indicated prior exposure) suggests SARS-CoV-2 as the infectious trigger.The sparse cutaneous involvement and lack of dusky targetoid lesions also distinguish RIME from Stevens-Johnson syndrome and erythema multiforme (which has been described in association with SARS-CoV-2 infection). 4,5Furthermore, RIME can be distinguished from the newly described multisystem inflammatory syndrome in children, which is associated with Kawasaki disease-like features, including mucocutaneous involvement, systemic symptoms, and dramatically elevated systemic inflammatory markers. 6This case highlights what is to our knowledge the first report of SARS-CoV-2-induced RIME and distinguishes this entity from other mucocutaneous eruptions with substantially different prognoses and treatment algorithms.

IMPORTANCE Psoriasis relapse may involve compensatory T-cell activation pathways in the presence of CD28-CD80/CD86 blockade with abatacept. OBJECTIVE To determine whether costimulatory signaling blockade with abatacept prevents psoriasis relapse after ustekinumab withdrawal. DESIGN, SETTING, AND PARTICIPANTS Psoriasis Treatment with Abatacept and Ustekinumab: a Study of Efficacy (PAUSE), a parallel-design, double-blind, placebo-controlled randomized clinical trial, was conducted at 10 sites in the US and Canada. Participant enrollment opened on March 19, 2014, and concluded on April 11, 2016. Participants were adults with moderate to severe plaque psoriasis and received ustekinumab in a lead-in phase. Those who responded to ustekinumab at week 12 were randomized 1:1 to either the continued with ustekinumab group (ustekinumab group) or the switched to abatacept group (abatacept group). Treatment was discontinued at week 39, and participants were followed up for psoriasis relapse until week 88. Statistical analyses were performed in the intention-to-treat (ITT) and safety samples from May 3, 2018, to July 6, 2021. INTERVENTIONS Participants received subcutaneous ustekinumab at weeks 0 and 4 (45mg per dose for those <= 100 kg; 90mg per dose for those >100 kg). Participants randomized to the abatacept group at week 12 received subcutaneous abatacept, 125mg weekly, from weeks 12 to 39 and ustekinumab placebo at weeks 16 and 28. Participants randomized to the ustekinumab group received ustekinumab at weeks 16 and 28 and abatacept placebo weekly from weeks 12 to 39. MAIN OUTCOMES AND MEASURES The primary end pointwas the proportion of participants with psoriasis relapse (loss of >= 50% of the initial Psoriasis Area and Severity Index improvement) between weeks 12 and 88. Secondary end points included time to psoriasis relapse, proportion of participants with psoriasis relapse between weeks 12 and 40, and adverse events. The psoriasis transcriptome and serum cytokines were evaluated. RESULTS A total of 108 participants (mean [SD] age, 46.1 [12.1] years; 73 [67.6%] men) were treated with open-label ustekinumab; 91 were randomized to blinded treatment. Similar proportions of participants in the abatacept group and the ustekinumab group relapsed between weeks 12 and 88 (41 of 45 [91.1%] vs 40 of 46 [87.0%]; P =.41). Median time to relapse from the last dose of ustekinumab was similar between groups as well: 36 weeks (95% CI, 36-48 weeks) in the abatacept group vs 32 weeks (95% CI, 28-40 weeks) in the ustekinumab group. Similar numbers and rates of adverse events occurred. Abatacept did not maintain suppression of the pathogenic IL-23-mediated psoriasis molecular signature in lesions after ustekinumab withdrawal, and serum IL-19 levels increased. CONCLUSIONS AND RELEVANCE This parallel-design, double-blind randomized clinical trial found that abatacept did not prevent psoriasis relapse that occurred after ustekinumab withdrawal because it did not completely block the pathogenic psoriasis molecular pathways that led to relapse.

Background: Autoimmune cutaneous disorders (AICD have been inconsistently reported during treatment with PD-1 (nivolumab, pembrolizumab, cemiplimab) and PD-L1 (atezolizumab, avelumab, durvalumab) checkpoint inhibitors. Case reports exist in the literature for 2 AICDs, vitiligo (VI) and lichen planus (LP), but an association with a PD1/PDL1 agents has not been well substantiated. The aim of this study was to determine if an association exists for these AICDs and PD-1 and PD-L1 inhibitors within a large database, the FDA Adverse Event Reporting System (FAERS).

Background: Although hidradenitis suppurativa (HS) has been reported to be associated with cardiovascular events, the risk for stroke has been inconsistently reported. The aim of this study is to determine the incidence of stroke in HS patients from real world data within a large urban midwestern US dermatology patient population.

Background: An association between HS and IHD has been inconsistently reported. The aim of this study was to determine whether an association exists for IHD in HS patients from real-world data representing a large Midwestern US dermatology patient population.

Cutaneous malignant melanoma (CMM) survivors are at risk of second primary cutaneous melanoma (SPCM). Although this risk is considered to remain high on a prolonged basis, risk patterns by anatomic region have not been well-reported. This study explored the risk of SPCM in CMM survivors by anatomic region, sex and age. Data were extracted from the SEER database (2000-2015) for patients with a primary CMM who survived > 2 months. CMM cases (defined by ICD-O-3 site codes C440-449 and histology codes 8720-8774) were selected and categorized according to anatomic region: head and neck (HN); trunk (T); upper limb and shoulder (UL), lower limb (LL); Site recode B ICD-O-3 detected SPCM. Standardized Incidence Ratios (SIRs) and 95% confidence intervals (CIs), were calculated. Of 218,393 CMM patients, 9,696 developed >1 SPCM within 5 years. There was a significantly increased overall risk for SPCM (SIR 10.52, 95% CI 10.32-10.73-12.25). Sex-stratified risk for SPCM was higher in HN than for other sites in females (SIR 10.34, 95% CI 8.70-12.21). Age-stratified risk of SPCM was significantly increased for all age groups, with a doubled risk for the youngest group: age range 20-39 years (SIR: 19.46, 95%CI 18.11-20.88); 40-59 (SIR: 11.62, 95%CI 11.23-12.03); 60-85+ (SIR: 9.46, 95%CI 9.22-9.70). The risk of SPCM for HN site was highest in the youngest group (SIR: 23.11, 95%CI 18.72-28.22), and LL was highest for the 2 older age groups: 40-59 (SIR: 12.14, 95%CI 11.20-13.14); 60-85+ (SIR: 12.08, 95%CI 11.25-12.96). In this nationwide patient population, CMM survivors had a significantly increased risk for SPCM, especially for young adults diagnosed with head and neck melanoma. Enhanced surveillance, particularly for head and neck SPCM in young adult melanoma survivors is warranted.

Patients with dermatomyositis have multiple risk factors for serious and opportunistic infections, including immune dysregulation, long-term systemic corticosteroid treatment and comorbid health conditions. We sought to determine whether dermatomyositis is associated with increased odds and burden of systemic, opportunistic and antibiotic-resistant infections. We analyzed data from the Nationwide Inpatient Sample from 2002 to 2012, containing a cross-sectional representative 20% sample of all hospitalizations in the US. Overall, dermatomyositis was associated with serious infections in adults (multivariable logistic regression; adjusted odds ratio [95% confidence interval]: 2.19 [2.08–2.30]) and children (1.45 [1.20–1.76]). In particular, dermatomyositis was significantly associated with 32 of 48 and 15 of 48 infections examined in adults and children, respectively, including infections of skin, bone, joints, brain, heart, lungs, and gastrointestinal system, as well sepsis, antibiotic-resistant and opportunistic infections. Predictors of infections included non-white race/ethnicity, insurance status, history of long-term systemic corticosteroid usage, Cushing’s syndrome (likely secondary to corticosteroid usage), diabetes, and cancer. Serious infections were associated with significantly increased inpatient cost and death in dermatomyositis patients. In conclusion, dermatomyositis is associated with higher odds, costs and inpatient mortality from serious and opportunistic infections.

Hydroxychloroquine (HCQ) is used off-label for morphea, and has been associated with rare yet serious cardiovascular (CV) adverse events. For the first time, we characterize HCQ-associated CV risk (including conduction disorders and ischemic events) in morphea patients. Data from a medical record repository (>6 million patients; Jan 2004 to Nov 2018; aged 18-89 years) were extracted using ICD-9 or 10 codes for those with morphea who had no CV event prior to HCQ exposure and had at least 2 months follow-up after initiation of HCQ. Separate CV risk calculations were performed for morphea patients on HCQ combined with a non-HCQ systemic therapy (methotrexate, prednisone or mycophenolate; N=65) and for those on a non-HCQ systemic therapy (N=431) compared to those morphea patients with no systemic therapy as a control (N=1866). Of 2,398 morphea patients, 38 had HCQ monotherapy (no combined systemic therapy) and were excluded from further analysis as the cohort had no incident CV events. However, patients on HCQ combined therapy had a significantly increased risk for incident CV events (RR: 2.07 CI: 1.33-3.22; p = 0.0013) compared to the control group and there was a significantly increased risk for the non-HCQ systemic therapy cohort compared to control (RR: 1.85 CI: 1.49-2.30; P < 0.0001), with a number needed to harm of 9.86 for non-HCQ systemic therapy versus 7.86 for HCQ in combination with other systemic therapy. Although the findings from this study demonstrate a favorable cardiovascular safety profile for HCQ monotherapy in morphea patients, enhanced monitoring for CV events seems warranted when HCQ is not utilized as monotherapy in the management of morphea.

To the Editor: Although natalizumab is approved for treating multiple sclerosis,1Tysabri prescribing information v. 08/2017.Google Scholar reports have raised concern about malignant melanoma (MM) after natalizumab exposure.2Sabol R.A. Noxon V. Sartor O. et al.Melanoma complicating treatment with natalizumab for multiple sclerosis: a report from the Southern Network on Adverse Reactions (SONAR).Cancer Med. 2017; 6: 1541-1551Crossref PubMed Scopus (16) Google Scholar, 3Mullen J.T. Vartanian T.K. Atkins M.B. Melanoma complicating treatment with natalizumab for multiple sclerosis.N Engl J Med. 2008; 358: 647-648Crossref PubMed Scopus (89) Google Scholar The aim of this study was to determine if an association was detectable for MM after natalizumab exposure in patients with multiple sclerosis. Using RADAR methodology,4McKoy J.M. Fisher M.J. Courtney D.M. et al.Results from the first decade of research conducted by the Research on Adverse Drug events And Reports (RADAR) project.Drug Saf. 2013; 36: 335-347Crossref PubMed Scopus (14) Google Scholar we searched the following databases: FDA Adverse Event Reporting System (FAERS), EudraVigilance (European Medicines Agency), and the Northwestern Medicine Enterprise Data Warehouse (NMEDW). The FAERS search (January 2004-June 2014) comprised terms related to MM combined with natalizumab. The proportional reporting ratio (PRR) was then calculated to determine if a safety signal (defined as >3 events, chi-squared result >4, and PRR >2) was detectable.5Sakaeda T. Tamon A. Kadoyama K. Okuno Y. Data mining of the public version of the FDA Adverse Event Reporting System.Int J Med Sci. 2013; 10: 796-803Crossref PubMed Scopus (274) Google Scholar We extracted data (January 2004-December 2015) from the NMEDW, a large, urban, Midwestern US population (>4 million patients, including a National Cancer Institute–designated comprehensive cancer center) for multiple sclerosis patients exposed to natalizumab who had a diagnosis for MM >3 months after initial exposure (International Classification of Diseases 9th Revision [172.0-172.9]; International Classification of Diseases 10th Revision [C43.0-C43.9]). The EudraVigilance database was searched (December 2001-November 2016) for terms related to MM combined with natalizumab. A signal was detected in the FAERS database (PRR 2.42, 95% confidence interval 2.10-2.8) from 205 reports of MM subsequent to natalizumab exposure. In the NMEDW, of 5097 multiple sclerosis patients, 192 were exposed to natalizumab with 3 (1.6%) subsequently receiving a MM diagnosis (a significant association, Fisher's exact test, P < .0001). The EudraVigilance database comprised 78 reports of MM after natalizumab exposure. These findings substantiate a recent study that linked natalizumab exposure to MM through FAERS analysis.2Sabol R.A. Noxon V. Sartor O. et al.Melanoma complicating treatment with natalizumab for multiple sclerosis: a report from the Southern Network on Adverse Reactions (SONAR).Cancer Med. 2017; 6: 1541-1551Crossref PubMed Scopus (16) Google Scholar Natalizumab-exposed patients had a younger median age at MM diagnosis compared with the general (non–natalizumab-exposed) US population.2Sabol R.A. Noxon V. Sartor O. et al.Melanoma complicating treatment with natalizumab for multiple sclerosis: a report from the Southern Network on Adverse Reactions (SONAR).Cancer Med. 2017; 6: 1541-1551Crossref PubMed Scopus (16) Google Scholar Mechanisms underlying the association for MM with natalizumab are incompletely understood; however, it seems that the drug's inhibitory effects on α4-integrins might relate to MM evolution because melanoma cells expressing α4β1 have increased homotypic intercellular adhesion and decreased ability to invade the extracellular matrix.3Mullen J.T. Vartanian T.K. Atkins M.B. Melanoma complicating treatment with natalizumab for multiple sclerosis.N Engl J Med. 2008; 358: 647-648Crossref PubMed Scopus (89) Google Scholar Inhibition of integrins with natalizumab might increase invasive potential. Of importance, these findings suggest that MM occurrence after natalizumab exposure might be biologically dissimilar to MM de novo. Limitations include possible reporting bias within FAERS and possible redundancy in the EudraVigilance and FAERS databases. Moreover, signals detected from reporting in FAERS constitute reporting ratios and cannot be interpreted as incidence rates or risk ratios.5Sakaeda T. Tamon A. Kadoyama K. Okuno Y. Data mining of the public version of the FDA Adverse Event Reporting System.Int J Med Sci. 2013; 10: 796-803Crossref PubMed Scopus (274) Google Scholar Furthermore, NMEDW database's small sample prevented additional analyses for potential confounding factors. Because determination of PRR requires the total number of adverse events reported for the drug of interest, number of adverse events of interest for the drug of interest, total number of all other adverse events, and the total number of all other drugs,5Sakaeda T. Tamon A. Kadoyama K. Okuno Y. Data mining of the public version of the FDA Adverse Event Reporting System.Int J Med Sci. 2013; 10: 796-803Crossref PubMed Scopus (274) Google Scholar PRR could not be calculated with EudraVigilance data. These findings demonstrate a detectable safety signal within FAERS and a statistically significant association for MM after natalizumab exposure in NMEDW; the EudraVigilance data was not inconsistent with these findings, with 78 reports being found. Of note, the full prescribing information for natalizumab does not refer to melanoma,1Tysabri prescribing information v. 08/2017.Google Scholar but enhanced monitoring of exposed patients seems warranted, especially for those at high risk for melanoma.

Although a lower risk for acute myocardial infarction in patients with alopecia areata (AA) has been reported, the association between AA and ischemic heart disease (IHD) has not been well-examined. The aim of this study was to determine whether an association exists within a large Midwestern US patient population for IHD in patients with AA. Data were extracted from a medical record data repository (>6 million patients; Jan 2001-Nov 2018) for those adults of either sex who had a dermatologist diagnosis for AA (ICD-9-10 codes; 704.01; L63) and had >/= 1 month follow-up visit. Outcome of interest was a subsequent diagnosis for IHD using all base codes relevant to IHD (ICD-9: 410, 413, 414; ICD-10: I20, I21, I22, I23, I24, I25). A control population consisted of all dermatology patients without AA (same time frame). Confounders included IHD risk factors (such as hypertension, hyperlipidemia and diabetes), and race. Stratified analyses by sex and by age group (relevant to IHD-related national guidelines; female (F):18-54 vs 55-89; male (M): 18-44 vs 45-89), crude and adjusted odds ratios (aORs) were calculated using logistic regression. Of data from 114,222 patients (73,934 F, 40,288 M), 1,555 had AA (F=66.4%). When stratified by sex and age group, decreased frequency of IHD was detected for the 45-89 older M cohort (aOR 0.47; 95%CI: 0.28-0.80; p=0.006), but not for the younger M cohort. Notably, an increased frequency (although not significant) was detected for both F age groups (aOR 1.17; 95%CI: 0.64-2.15 and 1.18; 95%CI: 0.78-1.77), respectively. Surprisingly, there was a decreased risk for IHD in the M older age group. These findings from real world data inform practical considerations for risk of IHD in the chronic management of those with AA.

Although literature demonstrates a decreased risk of Alzheimer's disease (AD) in individuals with various cancers, including squamous cell cancers (SCC) and basal cell cancers (BCC) comprising non‐melanoma skin cancers (NMSC), there is a paucity of literature to substantiate an association between malignant melanoma (MM) and AD.

TNF- alpha inhibitors, etanercept (E), adalimumab (A), and infliximab (I), include an indication for the treatment of moderate-to-severe psoriasis and have emerged as an important, and widely used class of drugs. Notably, the incidences of adverse events (AEs) occurring during exposure to these biologic agents are rarely stratified by sex in published trials and are not described in the Full Prescribing Information for each drug. To address this, we conducted a review of literature to determine rates of reported AEs by sex for E, A and I in psoriasis-based randomized clinical trials. PubMed was searched for citations dated from inception-November 2017. Inclusion criteria included English language, (E) OR (A) OR (I), randomized controlled trials, psoriasis and AE data. This generated 556 reports: 259 (E), 164 (A), 133 (I), of which 96 met study criteria: 50 (E), 29 (A), 17 (I) . These 96 reports represented 19,942 patients with psoriasis who were treated with E (11,282 patients), A (5726), or I (2934). Of these 96 reports, only one (E) contained data reporting the incidence of AEs by sex, and only an additional two, one E and one I, contained individual AE data points that explicitly referenced a subject’s sex. Despite the recognized need for sex difference data with drug use, especially in reporting AEs, it remains unclear whether the rates of AEs associated with these biological agents are different for men vs. women. Given the well-known sex differences for cancer and cardiovascular disease, advances and improvements in the collection and reporting of sex differences for AEs with TNF-alpha inhibitors in the management of psoriasis clearly warrant further action to ensure that implementation of mechanisms are put in place to accomplish this unmet need.

To the Editor: New onset or exacerbation of ulcerative colitis (UC) and Crohn's disease (CD), have been reported during premarketing trials for secukinumab1 and ixekizumab2; however, detailed postmarketing reports are limited. The aim of this study was to explore the frequency of UC-related and CD-related reports subsequent to secukinumab or ixekizumab exposure within real world-setting databases.