The 2023 Annual Report of DataDerm: The database of the American Academy of Dermatology.

The American Academy of Dermatology launched DataDerm in 2016 as the clinical data registry platform of American Academy of Dermatology. DataDerm has evolved to be the largest database in the world containing information about dermatology patients, capturing information about their course of disease, associated therapeutic interventions, and health outcomes. As of December 31, 2022, DataDerm contained data from 14.2 million unique patients and 53.5 million unique patient visits, with 415 practices representing 1663 clinicians actively participating in DataDerm in 2022. This article is the fourth in a series of Annual Reports about the status of DataDerm. This year's 2023 Annual Report presents the progress DataDerm has made in conjunction with OM1, the data analytics partner of DataDerm, with a special highlight on the longitudinal care of common dermatologic conditions in the registry and a detailed focus on skin cancer. Furthermore, we review the current status of DataDerm as a robust representation of real world specialty data, reflecting the day-to-day dermatologic care of patients over time.

Atezolizumab (programmed cell death-ligand 1 antibody)-induced inflammation of actinic keratosis: A case report.

Atezolizumab is a programmed cell death-ligand 1 antibody that modulates the immune system response and has shown great promise in treating malignancies. Cutaneous toxicities from immune checkpoint inhibitors are the most commonly reported immune-related adverse events, although toxicities related to immunotherapy are still being characterized. Herein, we present a novel case of inflamed actinic keratoses in a patient after receiving atezolizumab therapy that resolved without requirement of dose adjustment or discontinuation of treatment.

The completeness and accuracy of DataDerm: The database of the American Academy of Dermatology.

The utility of any database or registry depends on the completeness and accuracy of the data it contains. This report documents the validity of data elements within DataDerm, the clinical registry database of the American Academy of Dermatology. An external audit of DataDerm, performed by a third-party vendor, involved the manual review of 1098 individual patient charts from calendar year 2018 from 8 different dermatology practices that used 4 different electronic health records. At each site, 142 discrete data fields were assessed, comparing the data within DataDerm to the source data within the electronic health record. Audited data included 3 domains of data elements (diagnoses, medications, and procedures) and a performance measure ("Biopsy Reporting Time-Clinician to Patient"), which is 1 of several measures used by DataDerm as a Qualified Clinical Data Registry. Overall completeness of data was 95.3%, with a range among practices of 90.6% to 98.5%. Overall accuracy of data was 89.8%, with a range of accuracy among practices of 81.2% to 94.1%. These levels of completeness and accuracy exceed the rates in the literature for registries that are based on data that is extracted from electronic health records; and therefore, this audit validates the excellent quality of data in DataDerm.

Differences in Outpatient Dermatology Encounter Work Relative Value Units and Net Payments by Patient Race, Sex, and Age.

Importance: Clinical productivity measures may be factors in financial incentives for providing care to specific patient populations and thus may perpetuate inequitable health care. Objective: To identify the association of patient race, age, and sex with work relative value units (wRVUs) generated by outpatient dermatology encounters. Design, Setting, and Participants: This cross-sectional study obtained demographic and billing data for outpatient dermatology encounters (ie, an encounter performed within a department of dermatology) from September 1, 2016, to March 31, 2020, at the Emory Clinic, an academic dermatologic practice in Atlanta, Georgia. Participants included adults aged 18 years or older with available age, race, and sex data in the electronic health record system. Main Outcomes and Measures: The primary outcome was wRVUs generated per encounter. Results: A total of 66 463 encounters among 30 036 unique patients were included. Patients had a mean (SD) age of 55.9 (18.5) years and were predominantly White (46 575 [70.1%]) and female (39 598 [59.6%]) individuals. In the general dermatologic practice, the mean (SD) wRVUs per encounter was 1.40 (0.71). In adjusted analysis, Black, Asian, and other races (eg, American Indian or Native American, Native Hawaiian or Other Pacific Islander, and multiple races); female sex; and younger age were associated with fewer wRVUs per outpatient dermatology encounter. Compared with general dermatologic visits with White patients, visits with Black patients generated 0.27 (95% CI, 0.25-0.28) fewer wRVUs per encounter, visits with Asian patients generated 0.22 (95% CI, 0.20-0.25) fewer wRVUs per encounter, and visits with patients of other race generated 0.19 (95% CI, 0.14-0.24) fewer wRVUs per encounter. Female sex was also associated with 0.11 (95% CI, 0.10-0.12) fewer wRVUs per encounter, and wRVUs per encounter increased by 0.006 (95% CI, 0.006-0.006) with each 1-year increase in age. In the general dermatologic practice excluding Mohs surgeons, destruction of premalignant lesions and biopsies were mediators for the observed differences in race (56.2% [95% CI, 53.1%-59.3%] for Black race, 53.2% [95% CI, 45.6%-63.8%] for Asian race, and 53.6% [95% CI, 40.4%-77.4%] for other races), age (65.6%; 95% CI, 60.5%-71.4%), and sex (82.3%; 95% CI, 72.7%-93.1%). In a data set including encounters with Mohs surgeons, the race, age, and sex differences in wRVUs per encounter were greater than in the general dermatologic data set. Mohs surgery for basal cell and squamous cell carcinomas was a mediator for the observed differences in race (46.0% [95% CI, 42.6%-49.4%] for Black race, 41.9% [95% CI, 35.5%-49.2%] for Asian race, and 34.6% [95% CI, 13.8%-51.5%] for other races), age (49.2%; 95% CI, 44.9%-53.7%), and sex (47.9%; 95% CI, 42.0%-54.6%). Conclusions and Relevance: This cross-sectional study found that dermatology encounters with racial minority groups, women, and younger patients generated fewer wRVUs than encounters with older White male patients. This finding suggests that physician compensation based on wRVUs may encourage the provision of services that exacerbate disparities in access to dermatologic care.

Pyoderma gangrenosum underrepresentation in non-dermatological literature.

BACKGROUND: Pyoderma gangrenosum (PG) is a chronic, ulcerative neutrophilic dermatosis. PG presents a diagnostic challenge, largely due to the many mimicking diseases, the lack of confirmatory laboratory or biological markers, and the absence of widely accepted diagnostic criteria. In particular, PG is often mistaken for necrotizing soft tissue infections (NSTI). METHODS: We reviewed four major textbooks each in general surgery, plastic surgery, trauma surgery, vascular surgery, emergency medicine, and dermatology. We also performed a search of review articles addressing NSTI and necrotizing fasciitis (NF). RESULTS: Ten out of the 20 non-dermatology textbooks did not list PG anywhere, and only two listed a differential diagnosis for PG. None of the non-dermatology textbooks indicated PG in the NSTI differential diagnosis, while three of the dermatology textbooks included PG in the NSTI differential diagnosis. PG was listed in all of the dermatology textbooks. Only one of the NSTI and NF articles mentioned PG in the differential diagnosis. CONCLUSIONS: There is an underrepresentation in major textbooks of surgery and emergency medicine and in NSTI and NF review articles when it comes to diagnosing PG. This might be leading to trainees and advanced providers in these fields being uninstructed on PG, and likely contributes to PG misdiagnosis and mismanagement. We recommend PG be included in the differential diagnosis of chronic ulcers and NSTI in non-dermatology textbooks. We also suggest adding identification and diagnosis of inflammatory mimickers of NSTI (e.g. PG) in teaching modules in surgical and emergency specialties to address this knowledge gap.

Validation of the Three-Item Skindex-Mini Among Hidradenitis Suppurativa Patients With Diverse Racial Backgrounds.

BACKGROUND: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that severely impairs patients' quality of life (QoL). Instruments such as the 10-item Dermatology Life Quality Index and 16-item Skindex-16 have been used to assess QoL in HS; however, it is unknown whether the shorter 3-item Skindex-mini can also provide an accurate assessment of skin-related QoL in patients with HS. OBJECTIVES: The aim was to assess how well the Skindex-16 correlates with its shorter adaptation, the Skindex-mini, in capturing QoL among patients with HS. METHODS: This retrospective cross-sectional study included all HS patients seen in the HS Clinic at The Emory Clinic between January 1, 2019, and August 16, 2019. We compared the correlation between the symptom, emotion, and function domains of the Skindex-16 and Skindex-mini using Pearson correlation coefficients (CC). Secondary outcome measures included individual survey item analysis, ItchyQuant scores, and numeric rating scale of pain. RESULTS: We identified 108 encounters among 75 unique hidradenitis suppurativa patients (43 black/African American, 18 white, 5 Asian/Pacific Islander, 3 Latino, 4 Other, 2 unknown). Pearson CC between the Skindex-16 and Skindex-mini domain scores for all encounters were 0.770 (P < .001), 0.787 (P < .001), and 0.801 (P < .001) for the symptom, emotion, and function domains, respectively. The mean pain and ItchyQuant scores were 4.14 (SD 3.31) and 3.55 (SD 3.34), respectively. CONCLUSIONS: The Skindex-mini correlated highly with the Skindex-16 in a racially diverse group of patients with HS. The Skindex-mini is a streamlined QoL instrument that could be practically implemented into routine clinical care among diverse patients presenting to dermatology.

Phosphoinositide 3-Kinase Signaling Can Modulate MHC Class I and II Expression.

Molecular events activating the PI3K pathway are frequently detected in human tumors and the activation of PI3K signaling alters numerous cellular processes including tumor cell proliferation, survival, and motility. More recent studies have highlighted the impact of PI3K signaling on the cellular response to interferons and other immunologic processes relevant to antitumor immunity. Given the ability of IFNγ to regulate antigen processing and presentation and the pivotal role of MHC class I (MHCI) and II (MHCII) expression in T-cell-mediated antitumor immunity, we sought to determine the impact of PI3K signaling on MHCI and MHCII induction by IFNγ. We found that the induction of cell surface MHCI and MHCII molecules by IFNγ is enhanced by the clinical grade PI3K inhibitors dactolisib and pictilisib. We also found that PI3K inhibition increases STAT1 protein levels following IFNγ treatment and increases accessibility at genomic STAT1-binding motifs. Conversely, we found that pharmacologic activation of PI3K signaling can repress the induction of MHCI and MHCII molecules by IFNγ, and likewise, the loss of PTEN attenuates the induction of MHCI, MHCII, and STAT1 by IFNγ. Consistent with these in vitro studies, we found that within human head and neck squamous cell carcinomas, intratumoral regions with high phospho-AKT IHC staining had reduced MHCI IHC staining. IMPLICATIONS: Collectively, these findings demonstrate that MHC expression can be modulated by PI3K signaling and suggest that activation of PI3K signaling may promote immune escape via effects on antigen presentation.

Information technologies in health care delivery and policy: giant steps and missteps.

The influences of information technology have touched almost all aspects of our lives, and health care delivery has been no exception. Law, policy, and regulation have driven the adoption of electronic medical records, particularly over the past decade, driving fundamental changes to the practice of medicine in general and dermatology in particular. This article reviews the history of these changes, the regulations that drove these changes, the intended and unintended consequences of these initiatives, and our insights into the appropriate roles for policy and regulation to drive positive change.

Use and Cost of Actinic Keratosis Destruction in the Medicare Part B Fee-for-Service Population, 2007 to 2015.

Importance: Actinic keratosis is prevalent and has the potential to progress to keratinocyte carcinoma. Changes in the use and costs of actinic keratosis treatment are not well understood in the aging population. Objective: To evaluate trends in the use and costs of actinic keratosis destruction in Medicare patients. Design, Setting, and Participants: A billing claims analysis was performed of the Medicare Part B Physician/Supplier Procedure Summary Master Files and National Summary Data of premalignant skin lesion destructions performed from 2007 to 2015 among Medicare Part B fee-for-service beneficiaries. Main Outcomes and Measures: Mean number of actinic keratosis lesions destroyed and associated treatment payments in 2015 US dollars estimated per 1000 Medicare Part B fee-for-service beneficiaries. Data analysis was performed from November 2017 to July 2018. Results: More than 35.6 million actinic keratosis lesions were treated in 2015, increasing from 29.7 million in 2007. Treated actinic keratosis lesions per 1000 beneficiaries increased from 917 in 2007 to 1051 in 2015, while mean inflation-adjusted payments per 1000 patients decreased from $11 749 to $10 942 owing to reimbursement cuts. The proportion of actinic keratosis lesions treated by independently billing nurse practitioners and physician assistants increased from 4.0% in 2007 to 13.5% in 2015. Conclusions and Relevance: This study's findings suggest that actinic keratosis imposes continuously increasing levels of treatment burden in the Medicare fee-for-service population. Reimbursement decreases have been used to control rising costs of actinic keratosis treatment. Critical research may be warranted to optimize access to actinic keratosis treatment and value for prevention of keratinocyte carcinoma.

Super-Resolution Microscopy Reveals Altered Desmosomal Protein Organization in Tissue from Patients with Pemphigus Vulgaris.

Pemphigus vulgaris (PV) is an autoimmune epidermal blistering disease in which autoantibodies (IgG) are directed against the desmosomal cadherin desmoglein 3. To better understand how PV IgG alters desmosome morphology and function in vivo, biopsies from patients with PV were analyzed by structured illumination microscopy, a form of superresolution fluorescence microscopy. In patient tissue, desmosomal proteins were aberrantly clustered and patient IgG colocalized with markers for lipid rafts and endosomes. Additionally, steady-state levels of desmoglein 3 were decreased and desmosomes were reduced in size in patient tissue. Desmosomes at blister sites were occasionally split, with PV IgG decorating the extracellular faces of split desmosomes. Desmosome splitting was recapitulated in vitro by exposing cultured keratinocytes both to PV IgG and to mechanical stress, demonstrating that splitting at the blister interface in patient tissue is due to compromised desmosomal adhesive function. These findings indicate that desmoglein 3 clustering and endocytosis are associated with reduced desmosome size and adhesion defects in tissue of patients with PV. Further, this study reveals that superresolution optical imaging is a powerful approach for studying epidermal adhesion structures in normal and diseased skin.

Delayed pressure urticaria: response to treatment with sulfasalazine in a case series of seventeen patients.

We retrospectively identified 17 patients with delayed pressure urticaria (DPU), diagnosed by history and confirmed with provocative pressure testing. The average age in the cohort was 42.6 years with 10 women and seven men. The mean duration of disease before diagnosis was 19.7 months (range, 1-60 months). The diagnosis of DPU was not included in the differential diagnosis of referring physicians and was not a diagnostic consideration in any of seven biopsies obtained. None of the patients responded adequately to treatment with antihistamines, but all 17 responded transiently when treated with either oral or intramuscular steroids. Eleven patients experienced complete or near complete resolution of DPU with treatment with sulfasalazine (SZ). Four patients had a partial response while two were unable to continue therapy because of drug intolerance. SZ appears to be a low cost and effective treatment for DPU.

Hypoxia and hypoxia mimetics inhibit TNF-dependent VCAM1 induction in the 5A32 endothelial cell line via a hypoxia inducible factor dependent mechanism.

BACKGROUND: We previously reported that iron chelators inhibit TNFα-mediated induction of VCAM-1 in human dermal microvascular endothelial cells. We hypothesized that iron chelators mediate inhibition of VCAM-1 via inhibition of iron-dependent enzymes such as those involved with oxygen sensing and that similar inhibition may be observed with agents which simulate hypoxia. OBJECTIVE: We proposed to examine whether non-metal binding hypoxia mimetics inhibit TNFα-mediated VCAM-1 induction and define the mechanisms by which they mediate their effects on VCAM-1 expression. METHODS: These studies were undertaken in vitro using immortalized dermal endothelial cells, Western blot analysis, ELISA, immunofluorescence microscopy, quantitative real-time PCR, and chromatin immunoprecipitation. RESULTS: Hypoxia and the non-iron binding hypoxia mimetic dimethyl oxallyl glycine (DMOG) inhibited TNFα-mediated induction of VCAM-1. DMOG inhibition of VCAM-1 was dose-dependent, targeted VCAM-1 gene transcription independent of NF-κB nuclear translocation, and blocked TNFα-mediated chromatin modifications of relevant elements of the VCAM-1 promoter. Combined gene silencing of both HIF-1α and HIF-2α using siRNA led to a partial rescue of VCAM expression in hypoxia mimetic-treated cells. CONCLUSION: Iron chelators, non-metal binding hypoxia mimetics, and hypoxia all inhibit TNFα-mediated VCAM-1 expression. Inhibition is mediated independent of nuclear translocation of NF-κB, appears to target TNFα-mediated chromatin modifications, and is at least partially dependent upon HIF expression. The absence of complete VCAM-1 expression rescue with HIF silencing implies an important regulatory role for an Fe(II)/α-ketoglutarate dioxygenase distinct from the prolyl and asparagyl hydroxylases that control HIF function. Identification of this dioxygenase may provide a valuable target for modulating inflammation in human tissues.

Irritant activation of epithelial cells is mediated via protease-dependent EGFR activation.

Although numerous studies have examined in vivo and in vitro effects of irritants, most focused on events developing hours to days after exposure. Molecular events occurring immediately after skin contact remain incompletely defined. Characterization of early events could lead to the identification of key molecular signals necessary for the production of inflammatory mediators responsible for the signs and symptoms of irritant contact dermatitis (ICD). HaCaT cells treated with sodium lauryl sulfate (SLS), a model irritant, were used to examine early molecular events of ICD. Western analysis showed SLS-mediated induction of early growth response-1 (egr-1), a transcription factor capable of regulating hallmarks of ICD such as angiogenesis, hyperproliferation, and inflammation. Additionally, de novo egr-1 expression was commensurate with transcriptional activation of egr-1 mRNA and heteronuclear RNA. Use of pharmacological inhibitors demonstrated that SLS-induced egr-1 was dependent on MEK1/p44/42 ERK, but not on p38 or JNK signaling. The EGFR inhibitor PD168393 and the metalloprotease inhibitor TAPI-2 both inhibited SLS-induced egr-1. Finally, small interfering RNA silencing of the EGFR diminished SLS-induced egr-1 mRNA. These studies suggest a role of the EGFR in SLS signaling as well as a, to our knowledge, previously unreported association between ICD and EGFR induction of egr-1.