Shannon C. Trotter, DO, is a dermatologist and podcast host from Springfield, Ohio.

Discussing Granuloma Annulare, Lichenoid Disorders, and Social Media, With Shannon Trotter, DO

2025 Society of Dermatology Physician Associates (SDPA) Fall Conference

 in San Antonio, Texas, featured a variety of interviews with experts in the field of dermatology.

One such interview featured Shannon C. Trotter, DO, a dermatologist and podcast host with DOCS Dermatology, who discussed the topics covered in several sessions she presented at SDPA. First, Trotter was asked about the biggest highlights from her talk regarding social media and its connection to dermatology.

“You've got to get used to it,” Trotter said. “You have got to be aware of it and consume it, just like your patients do. Social media is, in fact, the new Web MD. Actually, one out of five patients will go to check social media, in particular, TikTok, before they even consult their doctor. It's important for us to be aware of what's out there, so that we can combat any misinformation, and that we can be a force as clinicians to really educate the public on everything skin.”

Later in her interview, Trotter was asked to discuss some of the most notable takeaways from her session titled ‘Advanced Breakout - I'm Lichen It! Lichenoid Disorders in Dermatology.’

 Trotter spoke about lichenoid disorders and several tips worth highlighting for clinicians.

“In particular, lichen planus can affect anything from skin that you think of classic skin locations like the hair and the nails,” Trotter explained. “In addition, it can also have different variations for effects inside the ear, or even the esophagus or the bladder. So it's important to be aware that it's more than just your regular LP, or lichen planus. Next is the fact that we have to have good treatments. The problem is, for these lichenoid disorders, we just don't have a lot of treatments to offer, so we have to get creative and often go off-label. And lastly, be aware of lichenoid drug eruptions.”

Trotter also pointed to the cancer management space, noting immunotherapy and targeted therapy with immune checkpoint therapy are leading to lichenoid drug reactions. She urged clinicians to keep this in mind. Later, Trotter touched on the topic of granuloma annulare.

“Granuloma annulare is one of my favorite rashes in all of dermatology,” Trotter said. “But keep in mind, although it's benign and more common than you might think, it does have associations that you want to be aware of, including autoimmune disorders and some lymphoproliferative disorders, in particular, non-Hodgkin's and Hodgkin's lymphoma. It can be very challenging to treat as well, so you might have to get creative to help your patients get successful with treatment, and you might have to do more workup than you might expect.”

The quotes used in this video summary were edited for clarity.

Trotter disclosures include her work for Castle Biosciences as a consultant, researcher, and speaker.

Trotter S. Social Media Trends 2025. Presented at the Society of Dermatology Physician Associates (SDPA) Fall Conference, November 5-9, San Antonio, TX.

Trotter S. Advanced Breakout - I'm Lichen It! Lichenoid Disorders in Dermatology. Presented at the Society of Dermatology Physician Associates (SDPA) Fall Conference, November 5-9, San Antonio, TX.

Trotter S. The Ringmaster: Taming Granuloma Annulare. Presented at the Society of Dermatology Physician Associates (SDPA) Fall Conference, November 5-9, San Antonio, TX.

Videos

This interview at the SDPA Fall Dermatology Conference highlights several topics covered in sessions presented by Trotter.

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Matthew Dapas, PhD, research assistant professor at Northwestern University Feinberg School of Medicine

Polygenic Risk Scores Reveal Genetic Drivers of Lupus Heterogeneity, With Matthew Dapas, PhD

At the American College of Rheumatology (ACR) Convergence 2025 in Chicago, Matthew Dapas, PhD, research assistant professor at Northwestern University Feinberg School of Medicine, discussed how polygenic risk scores are helping to clarify the heterogeneity of systemic lupus erythematosus (SLE) and inform clinical understanding of disease manifestations.

Systemic lupus erythematosus (SLE) presents a wide range of clinical manifestations, complicating diagnosis. Mayo Clinic notes symptoms such as fatigue, fever, joint pain, a butterfly-shaped facial rash, sun-sensitive skin lesions, color changes in fingers and toes, shortness of breath, chest pain, dry eyes, headaches, confusion, and memory loss.

 Clinicians use classification criteria, like those from the Systemic Lupus International Collaborating Clinics (SLICC), to guide diagnosis and management.

“[Lupus is] a very heterogeneous disease,” Dapas told 

during ACR. “[Lupus in] one individual …might look pretty different from another individual that has lupus. So how do we engineer these diagnosis classification criteria to best fit this wide variety of manifestations that can come about from this one disease? With my work, we build these genetic risk models to…see to what extent these different diagnostic criteria or classification criteria [capture] different types of disease…We can use these genetic models and their associations as a tool to basically increase our ability to pinpoint the exact disease in an individual. It's part of this push towards personalized medicine.”

Using data from a genome-wide association study of 6,748 SLE cases and 11,516 controls of European ancestry, Dapas and colleagues developed a polygenic risk score that predicted SLE with an area under the curve of 0.724.

Within the Northwestern cohort (n = 1,061), the polygenic risk score showed strong associations with lupus diagnoses (“Lupus [localized and systemic],” P = 1.6×10⁻⁹; “systemic lupus erythematosus,” P = 3.0×10⁻⁹), and nominal associations with cardiac complications (P = 2.8×10⁻³) and impaired renal function (P = 4.6×10⁻³), suggesting genetic risk may drive distinct phenotypic patterns.

The team then analyzed the correlation between the polygenic risk score and individual SLICC classification criteria in > 32,000 eMERGE participants. The polygenic risk score was significantly associated with 5 of 6 immunologic criteria and 3 of 11 clinical criteria, including acute cutaneous lupus, thrombocytopenia, and leukopenia. The strongest association was with low complement levels (P = 7.4×10⁻³¹), where patients in the highest polygenic risk score decile were nearly twice as likely to have low complement as those in the lowest decile (55% vs. 30%).

These findings suggest that immunologic features more closely reflect underlying genetic risk, while some clinical manifestations may be influenced by environmental factors or represent phenotypes not captured in the original genome-wide association study.

“We want to get to a place where, if a clinician [is] seeing a new patient that they suspect may have an autoimmune disease like lupus, they can order a genetic panel in addition to the other labs that they might order to try and assess this patient. This could go for newly diagnosed lupus patients as well. If you have a genetic risk panel, that genetic risk could be specific to certain complications or classification, or just lupus itself. You can include particular HLA alleles that can essentially inform the physician with greater certainty what the individual risk profile is for that patient.

He said that a patient with a greater genetic risk score for lupus with certain HLA alleles may be at a greater risk for particular outcomes from lupus that may warrant more observation or the order of a specific test.

“Ultimately, we're trying to use genetics as an additional tool in the physician’s toolkit to better tailor their treatment to their individual patients and better understand the disease of the individual patients, because, like I said from the outset, conditions like lupus [are] very heterogeneous, and it's not a one-size-fits-all solution for everyone.”

Dapas has no relevant reported disclosures.

Forrest N, Tuteja S, Pacheco J, Mitrovic V, Ramsey-Goldman R, Walunas T, Dapas M. Polygenic risk of lupus is differentially associated with individual EHR-derived classification criteria [abstract]. Arthritis Rheumatol. 2025; 77 (suppl 9). 

https://acrabstracts.org/abstract/polygenic-risk-of-lupus-is-differentially-associated-with-individual-ehr-derived-classification-criteria/

Mayo clinic. Lupus - Symptoms and Causes. Mayo Clinic. Published October 21, 2022. 

https://www.mayoclinic.org/diseases-conditions/lupus/symptoms-causes/syc-20365789

Polygenic risk scores are enhancing the understanding of systemic lupus erythematosus (SLE) by clarifying its heterogeneity and informing clinical practice. SLE's diverse manifestations complicate diagnosis, but genetic models are helping to refine classification criteria. A study using genome-wide association data developed a polygenic risk score with significant predictive power for SLE and its complications. The score showed strong associations with immunologic criteria, suggesting genetic risk influences certain phenotypes. This approach supports personalized medicine, enabling clinicians to tailor treatments based on individual genetic risk profiles.

At ACR 2025, Dapas discusses how polygenic risk scores link genetic risk to SLICC criteria, advancing precision medicine in systemic lupus erythematosus.

Rheumatology

Rheumatology condition center page is a comprehensive resource for clinical news and insights on rheumatologic disease. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for arthritis, gout, nr-AxSpA, and more.

Lupus

Alex Hillenbrand is an assistant editor for 

. She earned her BA in English from Lafayette College in 2023 and went on to write for pop culture, entertainment, and sports media outlets before joining MJH Life Sciences in 2025. In her free time, Alex enjoys cooking, going on walks, and meeting new people. Contact her at mjhlifesciences.com.

 shows slow disease progression over 5 years, increased rates of complete kidney remission, and a common pattern of recurrence, supporting extended follow-up and improved predictive models.

The silent progression of IgAN in children stems from persistently active kidney injury, which can lead to irreversible sclerotic damage. A 20-year study of early-onset IgAN found about 20% of children experienced kidney function decline or reached a combined renal endpoint, including end-stage kidney disease, doubling of serum creatinine, or death.

The retrospective cohort study evaluated poor prognosis, estimated glomerular filtration rate (eGFR), and the patterns of kidney remission and relapse in children, aiming to identify reliable prognostic markers to guide clinical management.

“IgAN is one of the major causes of chronic kidney disease (CKD) and kidney failure among pediatric glomerulopathies, with marked heterogeneity in clinical course and prognosis,” wrote Liru Qiu, MD, PhD, department of pediatrics at Tongju Hospital, and colleagues. “We systematically analyzed baseline characteristics, clinicopathological features at biopsy, and follow-up data.”

The study included 224 patients 3-18 years of age with biopsy-proven IgAN and ≥ 3 years of follow-up. Poor prognosis was defined as persistent eGFR < 90 mL/min/1.73 m2 for ≥ 3 months, kidney failure, or a ≥ 30% reduction in eGFR from baseline. Complete kidney remission was defined as the absence of hematuria and proteinuria with eGFR ≥ 90 mL/min/1.73 m2 for ≥ 1 year, and recurrence.

During a 5.41 year median follow-up, investigators observed poor prognosis in 12.05% of patients. Notable independent risk factors were found in males, older age at biopsy, Oxford classification E1 and S1 lesions, absence of gross hematuria, and no remission of proteinuria during follow-up, whereas those with elevated birth weight had reduced risk of adverse outcome (

Investigators also noted an association between age at biopsy, gross hematuria, and proteinuria remission status had significant time-dependent effects on eGFR slope. Patients < 12 years of age at biopsy demonstrated a decreased rate of kidney function decline compared to an increased eGFR rate for those ≥12 years of age, suggesting age of diagnosis might affect progression. When compared with isolated gross hematuria and no gross hematuria, patients with recurrent gross hematuria had an increased eGFR slope. Those with complete remission of proteinuria had a slower decline in kidney function than the non-remission group, suggesting a protective effect.

Investigators observed complete kidney remission in 70.98% of patients. The cumulative incidence of complete kidney remission at 2, 5, and 10 years post-biopsy was 23.21% (95% confidence interval [CI],17.67-28.76), 64.33% (95% CI, 57.58-71.08), and 84.03% (95% CI, 76.64-91.43), respectively. Among those in remission, 39.62% (63/159) remained relapse-free, while 60.38% (96/159) relapsed, including hematuria (29.17%), proteinuria (38.54%), or both (32.29%), underscoring the particularly elastic and variable nature of disease progression in pediatric patients with IgAN.

“Future research should leverage multicenter cohorts and integrate multi-omics approaches—including genomic, metabolic, and inflammatory profiling—to enhance prognostic accuracy and guide precision therapy in pediatric IgAN,” concluded investigators.

Liang W, He Y, Ma X, et al. Prognosis and predictive factors in pediatric IgA nephropathy. 

. Published online November 13, 2025. doi:

https://doi.org/10.1007/s00467-025-06988-8

Peruzzi L, Coppo R. IgAN Across the Age Spectrum: The Pediatric Perspective. 

. Published online March 2025:151569. doi:

https://doi.org/10.1016/j.semnephrol.2025.151569

Articles

Pediatric IgA nephropathy (IgAN) exhibits slow progression over five years, with increased complete kidney remission rates and common recurrence patterns, necessitating extended follow-up and improved predictive models. A 20-year study revealed that 20% of children with early-onset IgAN experienced kidney function decline or reached severe renal endpoints. A retrospective cohort study identified prognostic markers, highlighting risk factors such as male gender, older age at biopsy, and specific pathological lesions. Complete kidney remission was observed in 70.98% of patients, with a significant portion experiencing relapse, emphasizing the disease's variable progression.

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New Evidence on Pediatric IgAN Progression Supports Need for Extended Follow-Up

Evan Stein, MD, PhD, is the COO and CSO of LIB Therapeutics.

Lerodalcibep Efficaciously Reduces LDL-C Lastingly and Long-Term, With Evan Stein, MD, PhD

Lerodalcibep, an investigative oral PCSK9 inhibitor, has demonstrated substantial long-term efficacy in reducing LDL-C in patients at high or very high risk for 

 drug therapy, according to data from an open-label extension of the LIBerate-VI trial.

American Heart Association’s Scientific Sessions 2025

 in New Orleans, Louisiana, by Evan Stein, MD, PhD, chief operating officer and chief scientific officer of LIB Therapeutics.

“This is the first study to combine 2 different mechanisms for inhibiting PCSK9, and demonstrates that we gain synergy with this drug, which binds PCSK9 in the bloodstream,” Stein told 

 in an exclusive interview. “Only about 60 to 70% of PCSK9 in the bloodstream comes from hepatic synthesis; the rest comes from the gut, kidney, and other tissues. So this is a novel combination therapy which has never been tried before.”

LIBerate-VI was a randomized, open-label phase 3 study comparing lerodalcibep 300 mg to inclisiran 284 mg. For inclusion, patients were required to have a weight of ≥88 lbs and a body mass index (BMI) ≥16 and ≤42 kg/m2, a very high or high risk for CVD, high-intensity statin without other acceptable oral lipid lowering treatment plus diet stable for >4 weeks with LDL-C ≥85 mg/dL and triglycerides ≤400 mg/dL. Patients were excluded if they had homozygous familial hypercholesterolemia, severe renal dysfunction, NYHA class III or IV heart failure, or active liver disease, among other criteria.

The study’s primary outcome was percent change in LDL-C from baseline at day 270. Secondary outcomes included the frequency and severity of injection site reactions, the percent change in free PCSK9, the percent change in ApoB and Lp(a), and the percent of patients reaching ESC/EAS treatment goals. A total of 166 patients were included in the trial and subsequently randomly assigned to either lerodalcibep 300 mg administered subcutaneously monthly or inclisiran 284 mg, subcutaneously administered at days 1 and 90.

A total of 117 patients entered the open-label extension – of these, 107 completed the full 72-week extension period. These patients received lerodalcibep 300 mg subcutaneously monthly for the duration. They were dosed and monitored in clinic for 12 weeks, after which investigators aw them in clinic once monthly. Primary and secondary endpoints for the extension were LDL-C changes at week 72 and other lipids, achievement of LDL-C guidelines, and safety, respectively.

At the 72-week primary endpoint, mean and absolute LDL-C reductions were 59.2% and 66.6 mg/dL, respectively. Time average reductions across all visits were 63.4% and 71.4 mg/d,L respectively. Mean ApoB was reduced by 45.3% and median Lp(a) was reduced by 35.5%. Ultimately, investigators found consistency between the LDL-C response over 72 weeks and that of patients previously on lerodalcibep.

Additionally, patients who were switched from inclisiran had substantial reductions of 30-35% through week 24, which remained 22% lower through week 72. Similar additional reductions were noted across ApoB and Lp(a), and patients achieving guideline goals rose significantly. The team also found no treatment-related serious adverse events.

“Basically, what we’re looking at is a more available drug that lasts longer, because there’s less PCSK9 in the bloodstream to bind to our drug, and therefore the effect lasts longer,” Stein said. “And now we can explore whether, in these different types of patients, we can look at less frequent dosing than once a month, maybe every two months, maybe three, depending on the hepatic suppression of synthesis.”

Asprusten EA, Licka M, Cariou B, et al. Long-term Efficacy and Safety of Lerodalcibep in the Open-label 72-week Extension Study of Subjects Previously on Inclisiran or Lerodalcibep in the LIBerate-VI Trial. Presented at the American Heart Association’s Scientific Sessions 2025. New Orleans, Louisiana. November 8-10, 2025.

LIB Therapeutics LLC. Trial to Evaluate Efficacy and Safety of LIB003 and Inclisiran in High-risk CVD Patients (LIBerate-VI). ClinicalTrials.gov Identifier: NCT05004675. Updated October 23, 2024. Accessed November 24, 2025. 

https://www.clinicaltrials.gov/study/NCT05004675

Stein discusses the results of a groundbreaking open-label extension, which indicates the efficacy and safety of this investigative oral PCSK9 inhibitor.

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Atherosclerotic Cardiovascular Disease

Abigail Brooks is an assistant managing editor for 

She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

New research is shedding light on a significant association between social determinants of health (SDH) and 

metabolic dysfunction–associated steatotic liver disease (MASLD)

Study findings show children with MASLD were more likely to live in neighborhoods with greater socioeconomic and environmental disadvantage than their peers with overweight or obesity but without MASLD. Specifically, children with MASLD were more likely to reside in neighborhoods with lower socioeconomic advantage, reduced access to education and economic resources, poorer housing conditions, and greater environmental risks, including higher air pollution exposure.

MASLD is the leading cause of liver disease among children, affecting up to 38% of children with obesity in the US. However, known risk factors like genetic predisposition, diet, and physical activity levels do not fully explain the variability in disease development.

“Emerging evidence highlights the role of SDH in shaping disparities in pediatric liver disease,” Jeffrey Schwimmer, MD, a professor of pediatrics at UC San Diego School of Medicine and the director of the Fatty Liver Clinic at Rady Children’s Hospital San Diego, and colleagues wrote.

 “Identifying specific SDH linked to MASLD in children could inform strategies for early intervention and risk mitigation.”

To assess the association between neighborhood-level SDH and MASLD in children with overweight or obesity, investigators conducted a cross-sectional study of children evaluated in pediatric gastroenterology clinics, stratified by the presence of MASLD. For inclusion, patients were required to be < 18 years of age at their first visit, reside in California, and have a clear determination of the presence or absence of MASLD based on clinical evaluation.

Cases were defined as children who were clinically suspected of having MASLD and subsequently underwent liver biopsy, which confirmed macrovesicular steatosis in ≥5% of hepatocytes, with exclusion of other liver diseases through comprehensive clinical assessment, including medical history, laboratory testing, and histopathological review. Controls were defined as children with overweight or obesity who were evaluated for MASLD but determined not to have the disease, based on normal alanine aminotransferase (ALT) levels and absence of hepatic steatosis on imaging, confirmed through either magnetic resonance imaging–proton density fat fraction (MRI-PDFF) or ultrasound, depending on availability. Children initially referred for suspected MASLD or obesity but found to have no SLD on liver imaging and normal liver enzymes were included as controls.

In addition to clinical measures, neighborhood-level SDH were assessed using the California Healthy Places Index (HPI) 3.0.

Of 1206 children initially screened for eligibility, a potential study cohort of 988 children whose presence or absence of SLD was evaluated were assessed. Among these, 310 had liver imaging without any steatosis; however, 15 were excluded for an invalid address for geocoding, leaving 295 children with overweight or obesity without SLD as the control group. The remaining 678 children had a liver biopsy performed, confirming hepatic steatosis. After excluding ineligible patients, 593 children with overweight or obesity were diagnosed with MASLD.

Investigators did not observe any significant differences in age between children with and without MASLD (12.7 years vs 12.9 years; 

= .32) but noted a greater proportion of children with MASLD were male compared with those without MASLD (65.9% vs 56.9%; 

= .009). Race and ethnicity distributions also varied, with children in the MASLD group being more likely to identify as Hispanic (80.8% vs 65.8%; 

<.001) and less likely to identify as White (20.7% vs 44.1%; 

<.001). However, BMI did not differ significantly between groups, with a mean BMI of 30.9 kg/m2 in children with MASLD and 29.9 kg/m2 in those without MASLD (

Children in the study cohort, regardless of MASLD status, had lower HPI scores than the general population of San Diego County, with scores of −0.16±0.46 compared with 0.10±0.47 (

<.001). Further analysis revealed study participants without MASLD had a mean HPI of −0.03±0.48, approximating the 49th percentile, while those with MASLD had a mean HPI of −0.22±0.43, corresponding to roughly the 41st percentile (

Investigators also pointed out children with MASLD were more likely to live in neighborhoods with lower socioeconomic advantage across multiple HPI subdomains compared with those without MASLD, including the economic (

Further analysis of HPI subdomains showed that greater economic (

= .04) scores were associated with lower AST levels, while increased education (

= .04) scores were associated with lower ALT levels. However, none of the HPI subdomains were significantly associated with histologic disease severity.

This study provides further evidence that socioeconomic and environmental factors contribute to MASLD risk in children,” investigators concluded.

 “Future longitudinal studies should investigate whether specific SDH factors influence long-term MASLD outcomes, potentially guiding targeted public health interventions to improve the health trajectories of children at risk for MASLD.”

Venkatesh A, Thai N, Ugalde-Nicalo P, et al. Neighborhood disparities and metabolic dysfunction-associated steatotic liver disease in children with overweight or obesity. 

Mayo Clinic. Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD). October 4, 2023. Accessed November 24, 2025. 

https://www.mayoclinic.org/medical-professionals/pediatrics/news/pediatric-metabolic-dysfunction-associated-steatotic-liver-disease-masld-formerly-known-as-nonalcoholic-fatty-liver-disease-nafld/mac-20555493

Research highlights a link between social determinants of health (SDH) and metabolic dysfunction–associated steatotic liver disease (MASLD) in children with obesity. Children with MASLD often live in socioeconomically disadvantaged neighborhoods with environmental risks. The study found no significant age or BMI differences between children with and without MASLD, but noted gender and ethnic disparities. Lower Healthy Places Index (HPI) scores were observed in children with MASLD. The study suggests socioeconomic and environmental factors contribute to MASLD risk, advocating for future research to guide public health interventions.

Children with MASLD were more likely to live in neighborhoods with greater socioeconomic and environmental disadvantage than those with overweight or obesity but without MASLD.

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MASH / MASLD

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Latest News

Discussing Granuloma Annulare, Lichenoid Disorders, and Social Media, With Shannon Trotter, DO

Polygenic Risk Scores Reveal Genetic Drivers of Lupus Heterogeneity, With Matthew Dapas, PhD

New Evidence on Pediatric IgAN Progression Supports Need for Extended Follow-Up

Lerodalcibep Efficaciously Reduces LDL-C Lastingly and Long-Term, With Evan Stein, MD, PhD

Socioeconomic, Environmental Disadvantage Linked to Pediatric MASLD Risk