Welcome to this month's journal review, covering the August 2026 issue of Dermatologic Surgery. We've got four pieces on tap today — a workforce trends analysis on gender representation in Mohs fellowship training, a technique case series on retroauricular transposition flaps for anterior ear defects, a case report on surgical management of interferon-induced calcinosis, and a case series linking hyaluronidase injections to xanthelasma. Let's get into it.

First up is a communications piece — essentially a data-driven brief — on gender representation in Mohs micrographic surgery and dermatologic oncology fellowship training. The background here is something most of us have observed anecdotally: dermatology residency has skewed female for years, but Mohs and dermatologic oncology fellowship, one of the most competitive and surgically-oriented tracks in the specialty, hasn't followed that trend. The authors wanted to quantify that gap and track it over time.

Methodologically, this is a descriptive analysis of publicly available workforce data — pulling gender composition figures from the ACGME Data Resource Book from 2007 to 2023, for both dermatology residents overall and Mohs and dermatologic oncology fellows specifically. This is about as straightforward as a methods section gets: no modeling, no adjustment, just aggregated proportions compared across two training pathways, with basic hypothesis testing to see whether the observed gender splits differed significantly from parity or from each other. Worth noting they excluded the ACGME's newer nonbinary and other category, simply because there wasn't enough data reported in it to analyze meaningfully — a pragmatic, if imperfect, choice.

The results are pretty stark. Across that seventeen-year window, women made up roughly six in ten dermatology residents, while men made up under four in ten — a statistically significant and clinically obvious gap in the other direction. Flip over to Mohs and dermatologic oncology fellowship, and it essentially reverses: women were under half of fellows, at about forty-seven percent, versus roughly fifty-two percent for men. That's a smaller absolute gap than the residency figure, but it was still statistically significant. And there's a texture to this worth mentioning out loud: female representation in fellowship actually climbed nicely from 2018 to 2021, going from about forty-five percent up to fifty-eight percent, which would have been a genuinely encouraging trend — except it then reversed completely by 2023, sliding back down to that same forty-five percent starting point. So this isn't a steady linear climb toward parity; it's a wobble that erased itself.

The discussion leans into the "why," acknowledging the data can't actually answer that question — this is purely descriptive, no causal analysis possible. But they layer in some suggestive context: a burnout survey showing meaningfully higher burnout in female Mohs surgeons compared with male colleagues, attributed partly to work-home conflict; a leadership analysis showing about seven in ten current fellowship program directors are male, which the authors frame as a plausible mentorship bottleneck; and a separate cross-sectional study showing substantial productivity and Medicare reimbursement gaps for women in mixed-gender practices specifically, with smaller productivity gaps but persistent reimbursement gaps even in single-gender practices. None of this is causally linked to the fellowship gender gap in this paper — it's associative scaffolding the authors use to argue the issue is likely multifactorial.

Limitations are inherent to the design: this is registry-level, aggregate data with no ability to look at individual trainee decision-making, no adjustment for confounders, and reliance on a database category structure that already excludes nonbinary trainees from meaningful analysis.

Practically, this isn't practice-changing in the sense of altering how you operate on Monday morning, but it is actionable at the program and mentorship level. If you direct or teach in a fellowship, or sit on a selection committee, this is a nudge to look at your own mentorship pipeline and parental leave flexibility as concrete levers, rather than treating this as an intractable, self-correcting trend — because the data suggest it very much is not self-correcting.

Next, a technique-focused case series on the retroauricular transposition flap, sometimes called the buttonhole or pull-through flap, for reconstructing anterior auricular defects after Mohs surgery.

The clinical rationale up front is one you already live daily: full-thickness auricular defects involving cartilage, especially in the concha or triangular fossa, are a real reconstructive puzzle. Second intention healing risks contour distortion that can compromise glasses or hearing aid fit, and skin grafts carry their own necrosis and secondary scarring risk with similar functional consequences. The authors present their case series to reinforce this flap as a workhorse option.

This is a retrospective single-surgeon case series, pulled from one academic Mohs practice between 2021 and 2025, so there's no comparative statistics here — just descriptive outcomes, which fits fine for a technique-validation piece like this.

The technique itself: a template of the defect is transposed to the posterior ear, the flap is elevated preserving a muscular pedicle for blood supply, a full-thickness cartilage window is created, and the flap is tunneled through to resurface the anterior defect — hence "pull-through." The posterior donor site is usually closed primarily, though the senior author notes he'll deliberately leave it to heal by second intention in larger defects or ones involving the superior crus of the antihelix, specifically to avoid tethering the posterior ear.

Results across fourteen cases: mostly older male patients, basal cell carcinoma as the dominant indication, most requiring two Mohs stages, average final defect size around two-and-a-half by two centimeters, concentrated in the concha and adjacent antihelix. Zero infectious or hemorrhagic complications, and all flaps were viable at one week — a clean safety signal, albeit in a small series.

Discussion frames the flap's reliability around its robust musculocutaneous vascular supply from the posterior auricular and superficial temporal vessels, and flags the one real technical caveat: pedicle-related tethering of the posterior ear, particularly a risk with larger defects or ones extending into the superior crus, which the senior author manages by selectively allowing secondary intention healing at the donor site rather than forcing primary closure.

There's no formal limitations section since this isn't a comparative trial, but the obvious caveats are implicit — small single-surgeon series, no control group, no long-term follow-up beyond routine healing checks.

Practically, this is a nice technique reinforcement rather than a paradigm shift — most of you already have this flap in your reconstructive vocabulary for deep anterior auricular defects. The actionable pearl is the tethering management detail: for larger defects or ones creeping into the superior crus of the antihelix, deliberately leaving the posterior donor site to heal secondarily rather than closing it under tension is a concrete, exportable modification worth adopting.

Third, a case report on surgical management of plate-like subcutaneous calcinosis secondary to interferon-beta injections in a patient with multiple sclerosis.

The setup: interferon-beta is a mainstay disease-modifying therapy for relapsing-remitting multiple sclerosis, and while injection-site reactions like erythema and mild necrosis are well known, subcutaneous calcinosis is a rare, under-recognized late complication — case reports show it can surface up to a decade after the drug was stopped. The mechanism is murky, with vascular thrombosis, perivascular inflammation, and possibly subclinical metabolic derangement all proposed, though this patient had entirely normal calcium, phosphate, and parathyroid hormone levels preoperatively, so no systemic driver was identified here.

The patient was a woman in her late sixties with a multi-decade history of self-injected interferon-beta, first the 1a formulation, then the 1b formulation, rotated across both flanks, who presented years after stopping therapy with large, painful, ossified plaques exceeding ten centimeters on both flanks, confirmed radiographically and histologically as calcinosis cutis. She underwent staged en bloc excision in two sessions five months apart, tolerated it without complication, and reported complete symptomatic relief and cosmetic satisfaction at three-month follow-up.

There's no statistical analysis to teach here — this is a single case report — but the discussion does useful comparative work on why surgery was the right call for this patient specifically. The authors walk through the nonsurgical alternatives and their real-world drawbacks: intravenous sodium thiosulfate running near eighty-seven hundred dollars a month, extracorporeal shockwave therapy needing up to five sessions, colchicine and calcium channel blockers being well tolerated but slow — taking months to show any effect — and intravenous bisphosphonates helping only about half of patients while carrying an osteonecrosis risk. Against that backdrop, definitive excision for a well-localized, symptomatic case looks like the more efficient, lower-morbidity option, though the authors are careful to say surgery isn't the answer for diffuse or non-surgical candidates.

The limitation, implicit in any single case report, is generalizability — one patient, one surgeon's experience, no way to know how this extrapolates to less localized or more diffuse calcinosis presentations.

Practical takeaway: this is a useful pattern-recognition and referral pearl rather than a technique change for most of you — if you see a patient with a remote injection-drug history, whether interferon, or really any chronic subcutaneous injectable, presenting with firm plate-like masses years to decades later, calcinosis cutis should be on the differential, and for well-localized symptomatic disease, straightforward en bloc excision is a legitimate first-line option rather than routing patients through months of medical therapy first.

Last, a case series on xanthelasma palpebrarum occurring after hyaluronidase injections used to dissolve tear trough hyaluronic acid filler.

The clinical hook: hyaluronic acid filler in the tear trough is common, and hyaluronidase is the standard reversal agent when things go wrong — valued precisely because it's supposed to be a clean, reversible undo button. The authors report three normolipidemic patients who developed xanthelasma at the injection sites specifically after hyaluronidase treatment, not after the original filler. They note fifteen prior published cases of xanthelasma following filler itself, but say these are the first cases temporally linked specifically to the dissolving agent rather than the filler.

Across the three patients, the pattern is fairly consistent: all had prior tear trough hyaluronic acid filler, all received hyaluronidase — in some cases repeated sessions or unusually high cumulative doses — and then developed thin yellow periorbital plaques within weeks to about a year afterward. One notable detail: in the second patient, the side that was more resistant to enzymatic dissolution and needed higher hyaluronidase volumes was the same side that developed the plaque, which is a nice bit of internal dose-response signal within a single patient. All three declined biopsy, so these are clinical diagnoses only, not histologically confirmed.

There's no statistical analysis here — this is mechanistic case series reporting, so the bulk of the discussion is biological plausibility rather than data analysis. The proposed mechanism is that hyaluronidase cleaves the cross-linked filler HA into low molecular weight fragments, which are themselves proinflammatory and increase vascular permeability, theoretically allowing dermal lipoprotein extravasation and subsequent macrophage foam cell formation in a periorbital area already prone to capillary fragility. They cite prior bench work showing HA can complex with LDL and VLDL to promote foam cell uptake, and that oxidized LDL accelerates that process further. The relatively rapid onset in two of their patients, compared with the roughly ten-month latency typically described after filler alone, leads the authors to suggest hyaluronidase itself may accelerate the process rather than simply the antecedent filler exposure.

The clear limitation, which the authors state themselves, is that no patient consented to biopsy, so this remains a clinical, not histologic, diagnosis in all three cases — and obviously, three patients is far too few to establish anything beyond a plausible association worth watching for.

Practically, this isn't practice-changing, but it is a useful pattern to bank for anyone doing filler work or fielding referrals for filler complications: if a patient develops new periorbital yellow plaques in the weeks to months following hyaluronidase treatment, particularly at sites that required higher or repeated dosing, xanthelasma should be on your differential rather than assuming it's simply a delayed reaction to the original filler.

That wraps our four articles for this August 2026 issue — a workforce disparity that hasn't resolved on its own, a solid reconstructive workhorse for anterior ear defects with a practical tethering fix, a reminder to keep old injectable exposures on your differential for calcinosis, and a new twist linking hyaluronidase itself to xanthelasma. Thanks for listening, and we'll see you next month.