What the rheumatologist needs to know about skin biopsy.

The skin biopsy plays an important and powerful role in helping diagnose rheumatic diseases that present with cutaneous findings. As the skin is a very accessible organ, and the skin biopsy can be performed quickly as an in-office procedure, the skin biopsy is utilized frequently in patients with rheumatic diseases. However, the more challenging aspects of performing the biopsy, such as identifying the type of biopsy to perform, the site (s) to biopsy, the type of media to use, and the interpretation of histopathologic data are nuanced and require considerable thought. In this review, we discuss the common skin findings in rheumatic diseases and the general indications for skin biopsies in these diseases. We then summarize how to perform various skin biopsy techniques and how to select the biopsy technique. Finally, we discuss important rheumatic disease-specific considerations for skin biopsy, including where to biopsy and how to interpret the pathologic reports.

Patterns of Tumor-Infiltrating Lymphocytes Used to Distinguish Primary Cutaneous Squamous Cell Carcinomas That Metastasize.

This case-control study examines the type, location, and density of tumor-infiltrating lymphocytes in adult patients with vs without metastatic cutaneous squamous cell carcinoma.

Higher metastasis and death rates in cutaneous squamous cell carcinomas with lymphovascular invasion.

BACKGROUND: Lymphovascular invasion (LVI) is an aggressive histologic finding but is excluded from current staging systems due to its lack of demonstrated independent prognostic significance. OBJECTIVE: To evaluate the impact of LVI on cutaneous squamous cell carcinoma tumor outcomes. METHODS: In total, 10,707 cutaneous squamous cell carcinoma tumors from a 20-year, retrospective, multicenter cohort were stratified by the presence (LVI+) or absence (LVI-) of LVI. Outcomes (local recurrence, in-transit metastasis, nodal metastasis, disease-specific death) were compared based on low (Brigham and Women's Hospital [BWH] stage T1/T2a) and high (BWH T2b/T3) tumor stages. RESULTS: Of the 10,707 tumors, 78 had LVI. The analysis of low-stage BWH tumors showed the LVI+ group had a significantly higher 5-year cumulative incidence of local recurrence (LVI+: 12.3%; LVI-: 1.1%; P < .01), metastasis (LVI+: 4.2%; LVI-: 0.4%; P < .01), and disease-specific death (LVI+: 16.2%; LVI-: 0.4%; P < .01). The analysis of BWH high-stage tumors showed the LVI+ group maintained a higher 5-year cumulative incidence of metastasis (LVI+: 28.5%; LVI-: 16.8%; P = .06) and disease-specific death (LVI+: 25.3%; LVI-: 13.9%; P = .03), however, there was no difference in local recurrence (LVI+: 16.3%; LVI-: 15.8%; P = .11). LIMITATIONS: Retrospective study design. CONCLUSION: LVI+ cutaneous squamous cell carcinomas have higher rates of metastasis and death at 5 years. Future staging systems should consider incorporating LVI.

Genetic and environmental factors underlying keratinocyte carcinoma risk.

Recent large-scale GWAS and large epidemiologic studies have accelerated the discovery of genes and environmental factors that contribute to the risk of keratinocyte carcinoma (KC), which includes basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). This Review summarizes the genomic regions associated with SCC and BCC risk, examines the genetic overlap between SCC and BCC, and discusses biological pathways involved in SCC and BCC development. Next, we review environmental factors that are associated with KC risk, including those that are shared between SCC and BCC as well as others that associated with only one type of KC. We conclude with a critical appraisal of current research and potential directions for future research.

Adverse Events in Hospitalized Pediatric Patients.

: media-1vid110.1542/5789657761001PEDS-VA_2017-3360Video Abstract BACKGROUND: Patient safety concerns over the past 2 decades have prompted widespread efforts to reduce adverse events (AEs). It is unclear whether these efforts have resulted in reductions in hospital-wide AE rates. We used a validated safety surveillance tool, the Global Assessment of Pediatric Patient Safety, to measure temporal trends (2007-2012) in AE rates among hospitalized children. METHODS: We conducted a retrospective surveillance study of randomly selected pediatric inpatient records from 16 teaching and nonteaching hospitals. We constructed Poisson regression models with hospital random intercepts, controlling for patient age, sex, insurance, and chronic conditions, to estimate changes in AE rates over time. RESULTS: Examining 3790 records, reviewers identified 414 AEs (19.1 AEs per 1000 patient days; 95% confidence interval [CI] 17.2-20.9) and 210 preventable AEs (9.5 AEs per 1000 patient days; 95% CI 8.2-10.8). On average, teaching hospitals had higher AE rates than nonteaching hospitals (26.2 [95% CI 23.7-29.0] vs 5.1 [95% CI 3.7-7.1] AEs per 1000 patient days, P < .001). Chronically ill children had higher AE rates than patients without chronic conditions (33.9 [95% CI 24.5-47.0] vs 14.0 [95% CI 11.8-16.5] AEs per 1000 patient days, P < .001). Multivariate analyses revealed no significant changes in AE rates over time. When stratified by hospital type, neither teaching nor nonteaching hospitals experienced significant temporal AE rate variations. CONCLUSIONS: AE rates in pediatric inpatients are high and did not improve from 2007 to 2012. Pediatric AE rates were substantially higher in teaching hospitals as well as in patients with more chronic conditions.

Performance of the Global Assessment of Pediatric Patient Safety (GAPPS) Tool.

BACKGROUND AND OBJECTIVE: Efforts to advance patient safety have been hampered by the lack of high quality measures of adverse events (AEs). This study's objective was to develop and test the Global Assessment of Pediatric Patient Safety (GAPPS) trigger tool, which measures hospital-wide rates of AEs and preventable AEs. METHODS: Through a literature review and expert panel process, we developed a draft trigger tool. Tool performance was tested in 16 academic and community hospitals across the United States. At each site, a primary reviewer (nurse) reviewed ∼240 randomly selected medical records; 10% of records underwent an additional primary review. Suspected AEs were subsequently evaluated by 2 secondary reviewers (physicians). Ten percent of records were also reviewed by external expert reviewers. Each trigger's incidence and positivity rates were assessed to refine GAPPS. RESULTS: In total, 3814 medical records were reviewed. Primary reviewers agreed 92% of the time on presence or absence of a suspected AE (κ = 0.69). Secondary reviewers verifying AE presence or absence agreed 92% of the time (κ = 0.81). Using expert reviews as a standard for comparison, hospital-based primary reviewers had a sensitivity and specificity of 40% and 91%, respectively. As primary reviewers gained experience, their agreement with expert reviewers improved significantly. After removing low-yield triggers, 27 and 30 (of 54) triggers met inclusion criteria to form final manual and automated trigger lists, respectively. CONCLUSIONS: GAPPS reliably identifies AEs and can be used to guide and monitor quality improvement efforts. Ongoing refinement may facilitate future interhospital comparisons.

RhoC GTPase Is a Potent Regulator of Glutamine Metabolism and N-Acetylaspartate Production in Inflammatory Breast Cancer Cells.

Inflammatory breast cancer (IBC) is an extremely lethal cancer that rapidly metastasizes. Although the molecular attributes of IBC have been described, little is known about the underlying metabolic features of the disease. Using a variety of metabolic assays, including (13)C tracer experiments, we found that SUM149 cells, the primary in vitro model of IBC, exhibit metabolic abnormalities that distinguish them from other breast cancer cells, including elevated levels of N-acetylaspartate, a metabolite primarily associated with neuronal disorders and gliomas. Here we provide the first evidence of N-acetylaspartate in breast cancer. We also report that the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role in cytoskeletal rearrangement.