This Week in Dermatology — Sep 18, 2026

Welcome to This Week in Dermatology. This week we're covering 10 notable papers spanning the comparative safety and durability of biologics in inflammatory skin disease, the real-world performance of our immunomodulatory workhorses in severe and rare conditions, and a group of studies on comorbidity screening and risk stratification. Let's dive in.

We start with biologic safety, where the British Journal of Dermatology has published what is probably the most useful infection dataset we've had in psoriasis for some time. Bright and colleagues analysed the British Association of Dermatologists Biologic and Immunomodulators Register, covering nearly 41,000 treatment episodes in just over 18,600 patients, with about 118,000 person-years of follow-up from 2007 to 2024 [1]. The headline for anyone who still worries reflexively about granulomatous infection is reassuring: there were 22 cases of tuberculosis and 29 cases of meningitis across the entire cohort, giving incidence rates of roughly two tuberculosis cases and two and a half meningitis cases per ten thousand person-years. Most of those tuberculosis and meningitis cases clustered around TNF-alpha inhibitors, adalimumab in particular, the meningitis was predominantly viral rather than bacterial, and the tuberculosis was largely pulmonary. Fungal infection, by contrast, was not rare at all, at around seven and a half cases per thousand person-years, and here the signal is clean and clinically actionable. Interleukin-17 inhibitors, and only the interleukin-17 inhibitors, carried an elevated risk of candidiasis against every other systemic comparator, ranging from roughly two and a half times the rate seen with apremilast to more than four times the rate seen with interleukin-12/23 inhibitors. Importantly, the individual interleukin-17 agents did not differ meaningfully from one another, so switching within the class is not a mitigation strategy, and for fungal infections other than candida there were no significant differences between treatment groups at all. The practical message is to counsel patients starting an interleukin-17 inhibitor explicitly about oral, genital and intertriginous candidiasis, and to treat it as an expected, manageable event rather than a reason to abandon an effective drug. The authors are appropriately cautious that follow-up on the newer agents remains short for slow events like tuberculosis.

That candida signal gets an incidental echo in a smaller comparative study in Dermatology, where du and colleagues report a single-centre retrospective cohort of 79 Chinese adults with moderate-to-severe hidradenitis suppurativa treated with either a TNF-alpha inhibitor or an interleukin-17 inhibitor [2]. At week 12, response rates were broadly similar between the two classes, at around two thirds to three quarters of patients. By week 16, though, the TNF group had drifted down to just over half of patients responding, while the interleukin-17 group held steady at about two thirds. The single discontinuation for adverse events was a fungal infection in the interleukin-17 arm, which is exactly what the register data would predict. This is a small, non-randomised, single-centre study with unbalanced groups, so it cannot settle the sequencing question, but it does add to the impression that interleukin-17 blockade may hold its response better over the medium term in hidradenitis suppurativa.

Durability is also the theme of an important paediatric paper in JAMA Dermatology. Vroman and colleagues report the Dutch BioDay registry experience with dupilumab in 309 children aged 16 and under with moderate-to-severe atopic dermatitis, followed for up to three years across seven hospitals [3]. Effectiveness was well maintained: mean Eczema Area and Severity Index scores stayed low at three years, in the mild range, and three-year drug survival was about 80 percent. The most common adverse event was dupilumab-associated ocular surface disease, reported in just over a third of children, which is higher than trial data would lead you to expect and worth flagging at consent. The genuinely new clinical insight is the age gradient. Children aged six months to five years consistently reported higher itch scores and greater quality-of-life impairment over time than older children, and discontinuations in that youngest group were driven disproportionately by administration problems rather than by failure of the drug. Among those who stopped, the reasons were roughly split between ineffectiveness, adverse events and administration difficulties, and most stopping happened within the first eighteen months. So if you are starting a toddler on dupilumab, the injection experience itself deserves as much attention as the eczema score.

The second theme this week is how our older immunomodulatory tools perform when they leave the trial setting. In the Journal of the American Academy of Dermatology, Wu and colleagues report a multicentre Chinese retrospective cohort of 276 patients with pemphigus treated with rituximab plus glucocorticoids [4]. Over 52 weeks, close to half OF PATIENTS achieved complete remission on minimal therapy, and about one in eight relapsed. Three independent predictors of remission emerged: receiving three rituximab infusions rather than fewer, a higher baseline IgM level, and the absence of baseline herpes simplex infection. Relapse, meanwhile, was predicted by higher body weight, prior immunosuppressant use and prior cyclophosphamide exposure. Adverse events, mostly infections, affected just under a quarter of patients. This is retrospective and lacks dynamic biomarker data, but the predictors are all available at the bedside on day one, which makes them usable for risk stratification and for arguing the case for a fuller infusion course in the patients most likely to benefit.

Alongside that, Clinical and Experimental Dermatology reports twenty years of intravenous immunoglobulin use at a single tertiary centre — 285 patients, six in ten of whom had autoimmune bullous disease, with the remainder including the Stevens-Johnson syndrome and toxic epidermal necrolysis spectrum [5]. Aydogan and colleagues describe favourable outcomes overall, and adverse events in about one in six patients. Immediate reactions were mostly hypertension and flu-like symptoms; the delayed events that matter clinically were renal impairment and thromboembolism. Crucially, adverse events tracked with patient comorbidity, not with the underlying dermatological diagnosis — which argues for individualising infusion rate, hydration and osmolarity based on cardiovascular and renal risk rather than on the skin disease you are treating.

Two more papers round out this therapeutic theme. Also in Clinical and Experimental Dermatology, Yücel and colleagues looked at omalizumab updosing in 57 patients with chronic spontaneous urticaria, roughly half of whom also had symptomatic dermographism, all of whom had responded poorly to or lost response at the licensed 300 milligram dose [6]. Escalating to 450 milligrams every four weeks achieved disease control in just over seven in ten patients over six months, and of the ten who still weren't controlled and went on to 600 milligrams, nine got there. Concomitant dermographism, body mass index, total IgE and anti-thyroid peroxidase levels did not predict response — notably, a low baseline IgE did not preclude benefit. The only predictor was a higher baseline Urticaria Control Test score. The practical point is that our conventional poor-response biomarkers lose their usefulness once you are in the updosing space, so escalate on clinical grounds. And in the Journal of the European Academy of Dermatology and Venereology, Bellinato and colleagues systematically reviewed 182 reported cases of interstitial granulomatous dermatitis [7]. Around half of patients had an associated rheumatological or autoimmune disease, nearly one in five had a haematological or solid tumour, and a drug trigger was identified in a third of cases — cardiovascular drugs, biologics and targeted therapies. Where a culprit drug was withdrawn, almost all evaluable patients cleared completely or partially, which makes drug review the single highest-yield intervention. Topical and systemic corticosteroids each produced complete response in a little over half of treated cases, with TNF-alpha and JAK inhibitors reserved for refractory disease. Recurrence occurred in just over a quarter of patients with follow-up.

The final theme is comorbidity and screening. A meta-analysis in the Journal of the European Academy of Dermatology and Venereology pooled eight cohort studies covering more than 278,000 pregnant women with atopic dermatitis against over 2.7 million controls [8]. Liu and colleagues found modest but consistent increases in premature rupture of membranes, low birth weight, gestational hypertension and pre-eclampsia — each on the order of ten to fifteen percent higher relative risk, so small in absolute terms. The more striking signal, from a single study and therefore tentative, was a roughly two and a half fold increase in neonatal staphylococcal septicaemia. That is biologically plausible given maternal staphylococcal colonisation, and it is worth mentioning when you counsel pregnant patients with active eczema. In Pediatric Dermatology, Chiramel and colleagues pooled 37 studies of 6,291 children with vitiligo and found thyroid disease or abnormal thyroid testing in roughly nine percent overall, most commonly positive antithyroid antibodies in about one in seven tested and raised thyroid-stimulating hormone in about one in sixteen [9]. Most affected children had non-segmental disease, and no clinical feature — age, sex, disease duration, activity or family history — reliably identified who to test, though reporting heterogeneity was substantial. The authors support baseline and periodic screening with antithyroid antibodies and thyroid-stimulating hormone in paediatric vitiligo. Finally, a review in the British Journal of Dermatology maps the shift in vascular anomalies from empiric intervention to genotype-directed therapy, with PIK3CA mutations in lymphatic and venous malformations, KRAS and MAP2K1 in arteriovenous malformations, and mTOR, PI3K-alpha and MEK inhibitors delivering pathway-specific efficacy [10]. Resistance and drug dependency remain unsolved, and the authors look towards cell-free DNA monitoring for longitudinal disease tracking.

If you only have time for one paper this week, make it the BADBIR infection cohort in the British Journal of Dermatology [1]. It gives you numbers you can actually quote to a patient during a biologic consent conversation, and it settles the candidiasis question for the interleukin-17 class with a sample size nothing else comes close to.

Here are the key takeaways from this week in Dermatology. Tuberculosis and meningitis on modern psoriasis systemics are genuinely rare, and where they occur they sit mainly with TNF inhibitors; candidiasis, by contrast, is a class effect of interleukin-17 blockade that you should pre-empt rather than be surprised by. Dupilumab holds up in children over three years with about four in five still on drug, but the under-fives itch more, suffer more quality-of-life impairment, and stop because of injection difficulties — so plan the administration, not just the dose. In pemphigus, completing three rituximab infusions predicts remission, while higher body weight and prior immunosuppressant exposure predict relapse. For chronic spontaneous urticaria not controlled at the licensed omalizumab dose, escalate on clinical grounds — IgE and anti-thyroid peroxidase will not tell you who responds. And when you see interstitial granulomatous dermatitis, review the drug chart first and screen for associated autoimmune and malignant disease, because withdrawal of a culprit agent resolves almost all cases in which one is identified.

That's your roundup for This Week in Dermatology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

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This is an automated summary generated by artificial intelligence, which can make mistakes. Always review the original source materials.