Objectives(1) To estimate weight change from a low-carbohydrate diabetes prevention programme (LC-DPP) and (2) to evaluate the feasibility and acceptability of an LC-DPP.Research designSingle-arm, mixed methods (ie, integration of quantitative and qualitative data) pilot study.SettingPrimary care clinic within a large academic medical centre in the USA.ParticipantsAdults with pre-diabetes and Body Mass Index of ≥25 kg/m2.InterventionWe adapted the Centers for Disease Control and Prevention’s National Diabetes Prevention Program (NDPP)—an evidence-based, low-fat dietary intervention—to teach participants to follow a very low-carbohydrate diet (VLCD). Participants attended 23 group-based classes over 1 year.Outcome measuresPrimary outcome measures were (1) weight change and (2) percentage of participants who achieved ≥5% wt loss. Secondary outcome measures included intervention feasibility and acceptability (eg, attendance and qualitative interview feedback).ResultsOur enrolment target was 22. One person dropped out before a baseline weight was obtained; data from 21 individuals were analysed. Mean weight loss in kilogram was 4.3 (SD 4.8) at 6 months and 4.9 (SD 5.8) at 12 months. Mean per cent body weight changes were 4.5 (SD 5.0) at 6 months and 5.2 (SD 6.0) at 12 months; 8/21 individuals (38%) achieved ≥5% wt loss at 12 months. Mean attendance was 10.3/16 weekly sessions and 3.4/7 biweekly or monthly sessions. Among interviewees (n=14), three factors facilitated VLCD adherence: (1) enjoyment of low-carbohydrate foods, (2) diminished hunger and cravings and (3) health benefits beyond weight loss. Three factors hindered VLCD adherence: (1) enjoyment of high-carbohydrate foods, (2) lack of social support and (3) difficulty preplanning meals.ConclusionsAn LC-DPP is feasible, acceptable and may be an effective option to help individuals with pre-diabetes to lose weight. Data from this pilot will be used to plan a fully powered randomised controlled trial of weight loss among NDPP versus LC-DPP participants.Trial registration numberNCT03258918.

Background Finite clinical data and understanding of COVID-19 immunopathology has led to limited, opinion-based recommendations for management of immune-mediated inflammatory disease (IMID) patients on immunosuppressive (IS) therapeutics. Objective Determine if IS therapeutic type impacts COVID-19 risk among IMID patients. Methods We conducted a retrospective cohort analysis of Henry Ford Health System (HFHS) patients tested for COVID-19 between February 1 st and April 18 th , 2020 treated with IS medication for IMID. Therapeutic class of IS medication, comorbidities, and demographic factors were combined into multivariate models to determine predictors of COVID-19 infection, admission, ventilation, and mortality. Results Of 213 IMID patients, 36.2% tested positive for COVID-19, who had no greater odds of being hospitalized or requiring ventilation relative to the general population. No IS therapeutic worsened the course of disease after multivariate correction, though multi-drug regimens and biologics predicted an increased and decreased rate of hospitalization, respectively, with the latter driven by TNFα inhibitors. Limitations A single-center study somewhat limits generalization to community-based settings. Only patients tested for COVID-19 were analyzed. Conclusion IS therapies for IMIDs are not associated with a significantly greater risk of SARS-CoV-2 or severe sequelae when controlling for other factors, and TNFα inhibitors may decrease odds of severe infection.

Keratoacanthoma (KA) is a common skin tumour that remains controversial regarding classification, epidemiology, diagnosis, prognosis and management. Classically, a KA manifests as a rapidly growing, well-differentiated, squamoid lesion with a predilection for sun-exposed sites in elderly people and a tendency to spontaneously regress. Historically, KAs have been considered a variant of cutaneous squamous cell carcinoma (cSCC) and are often reported as KA-type cSCC. However, the penchant for regression has led many to categorize KAs as biologically benign tumours with distinct pathophysiological mechanisms from malignant cSCC. The clinical and histopathological similarities between KA and cSCC, particularly the well-differentiated variant of cSCC, have made definitive differentiation difficult or impossible in many cases. The ambiguity between entities has led to the general recommendation for surgical excision of KAs to ensure a potentially malignant cSCC is not left untreated. This current standard creates unnecessary surgical morbidity and financial strain for patients, especially the atrisk elderly population. There have been no reports of death from a definitive KA to date, while cSCC has an approximate mortality rate of 1Á5%. Reliably distinguishing cSCC from KA would shift management strategies for KAs towards lessinvasive treatment modalities, prevent unnecessary surgical morbidity, and likely reduce associated healthcare costs. Herein, we review the pathophysiology and clinical characteristics of KA, and conclude on the balance of current evidence that KA is a benign lesion and distinct from cSCC.Defective mismatch repair genes (MLH1, MSH2, MSH6) leading to microsatellite instability 59,60 HPV, human papillomavirus.

Human skin is not only affected by ultraviolet radiation but also by visible light wavelengths emitted by sunlight, electronic devices, and light emitting diodes. Similar to the ultraviolet radiation, visible light has been implicated in photoaging. In this review, the effects of blue light, yellow light, red light, and broad visible light are discussed in relation with photoaging. Different visible light wavelengths likely contribute beneficial and deleterious effects on photoaging by way of interaction with specific photoreceptors, ROS production, and other photon‐mediated reactions. Further in vivo studies are needed to determine the mechanism and action spectrum of photoaging in humans, as well as optimal photoprotection with coverage against visible light wavelengths.

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