Treatment of calcinosis cutis associated with autoimmune connective tissue diseases.

Calcinosis cutis is a condition that is commonly associated with autoimmune connective tissue diseases. It is characterized by the deposition of insoluble calcium salts in the skin and subcutaneous tissue, which can cause pain, impair function, and have significant impacts on quality of life. Calcinosis cutis is difficult to manage because there is no generally accepted treatment: evidence supporting treatments is mostly comprised of case reports and case series, sometimes yielding mixed findings. Both pharmacologic and procedural interventions have been proposed to improve calcinosis cutis, and each may be suited to different clinical scenarios. This review summarizes current treatment options for calcinosis cutis, with discussion of recommendations based on patient-specific factors and disease severity.

Multi-modal skin atlas identifies a multicellular immune-stromal community associated with altered cornification and specific T cell expansion in atopic dermatitis.

In healthy skin, a cutaneous immune system maintains the balance between tolerance towards innocuous environmental antigens and immune responses against pathological agents. In atopic dermatitis (AD), barrier and immune dysfunction result in chronic tissue inflammation. Our understanding of the skin tissue ecosystem in AD remains incomplete with regard to the hallmarks of pathological barrier formation, and cellular state and clonal composition of disease-promoting cells. Here, we generated a multi-modal cell census of 310,691 cells spanning 86 cell subsets from whole skin tissue of 19 adult individuals, including non-lesional and lesional skin from 11 AD patients, and integrated it with 396,321 cells from four studies into a comprehensive human skin cell atlas in health and disease. Reconstruction of human keratinocyte differentiation from basal to cornified layers revealed a disrupted cornification trajectory in AD. This disrupted epithelial differentiation was associated with signals from a unique immune and stromal multicellular community comprised of MMP12 + dendritic cells (DCs), mature migratory DCs, cycling ILCs, NK cells, inflammatory CCL19 + IL4I1 + fibroblasts, and clonally expanded IL13 + IL22 + IL26 + T cells with overlapping type 2 and type 17 characteristics. Cell subsets within this immune and stromal multicellular community were connected by multiple inter-cellular positive feedback loops predicted to impact community assembly and maintenance. AD GWAS gene expression was enriched both in disrupted cornified keratinocytes and in cell subsets from the lesional immune and stromal multicellular community including IL13 + IL22 + IL26 + T cells and ILCs, suggesting that epithelial or immune dysfunction in the context of the observed cellular communication network can initiate and then converge towards AD. Our work highlights specific, disease-associated cell subsets and interactions as potential targets in progression and resolution of chronic inflammation.

Evaluating the research productivity of academic dermatologists based on the NIH-supported relative citation ratio.

The National Institutes of Health (NIH) recently developed an article-level metric called the relative citation ratio (RCR). It improves upon prior metrics such as the h-index in that it is field-normalized, allowing for more accurate comparisons of author productivity between fields. The RCR is also a more accurate metric for evaluating early-career stage investigators. We sought to provide benchmark RCR data of academic dermatologists and examine how factors such as gender, degrees, and academic rank impact RCR scores. Academic dermatologists were indexed using the NIH iCite database. Gender, additional degrees, academic rank, total number of publications, mean RCR, and weighted RCR were collected for each dermatologist. Mean and weighted RCR scores were compared by gender, degrees, and academic rank, with P values based on multiple linear regression. 1899 dermatology faculty members were included in the analysis. Academic dermatologists had a median mean RCR of 1.12 (interquartile range/IQR 0.65-1.73) and a median weighted RCR of 18.89 (IQR 4.67-62.18). Full professorship as well as Doctor of Philosophy acquisition were associated with an increase in mean and weighted RCR scores. Male gender was associated with an increase in weighted RCR scores. Interestingly, male and female academic dermatologists along with assistant and associate professors had similar mean RCR scores. Limitations of the study include the inability to differentiate dermatologists with the same name. The iCite website also only includes PubMed-listed articles from 1995 to 2021. Overall, academic dermatologists have a median mean RCR value greater than the NIH benchmark value of 1.00, suggesting that their publications are more impactful compared to those published by the general scientific community. The benchmark data from this study may prove useful for self-evaluation and also grant, hiring, and promotional decisions.

Implementing patient safety and quality improvement in dermatology. Part 2: Quality improvement science.

Quality improvement (QI) in medicine is reliant on a team-based approach and an understanding of core QI principles. Part 2 of this continuing medical education series outlines the steps of performing a QI project, from identifying QI opportunities, to carrying out successive Plan-Do-Study-Act cycles, to hard-wiring improvements into the system. QI frameworks will be explored and readers will understand how to interpret basic QI data.