Citations

Background Corticosteroid injections (CSIs) are widely employed in facet and sacroiliac joint pain. Similar to CSIs at other sites (peripheral nerve blocks, joints, epidural), these injections are associated with potential adverse events. These multisociety consensus recommendations aim to develop evidence-based statements and recommendations on the safe use of CSIs in facet joint and sacroiliac joint injections. Methods Development of the consensus recommendations was approved by the American Society of Regional Anesthesia and Pain Medicine Board of Directors and several other societies that agreed to participate. The scope of statements and recommendations was agreed on to include safety of the injection technique (landmark-guided, ultrasound, or radiology-aided injections); effect of the addition of the corticosteroid on effectiveness (vs local anesthetic or saline); and adverse events related to the injection. Experts were assigned topics to perform a comprehensive literature review and draft statements and recommendations, which were refined and voted for consensus (>75% agreement) using a modified Delphi process. A modified version of the US Preventive Services Task Force grading of evidence and strength of recommendation was followed. Results All statements and recommendations were approved by all participants after four rounds of discussion. The Practice Guidelines Committees and Boards of Directors of the participating societies also approved all statements and recommendations. Injection of corticosteroid into the facet joint in patients with joint inflammation may relieve pain and improves function. Intra-articular, extra-articular (periarticular), and combined administration are effective for sacroiliac joint injections. No dose-response studies exist, but CSIs containing 10 mg of methylprednisolone or triamcinolone per facet joint and 40 mg per sacroiliac joint (SIJ) (or their respective pharmacologic equivalents) are reasonable. Conclusions In this practice recommendation, we provide statements and recommendations on facet and sacroiliac joint CSIs, the optimal doses, and intervals and criteria for repeating the CSIs in patients with facet joint and sacroiliac joint pain.

Background: Studies in the past have demonstrated an association between sarcoidosis and pulmonary embolism (PE), but little is known about its impact, especially in young adults. We aim to determine the burden and impact of PE in young adults hospitalized with sarcoidosis. Methods: This study investigates the prevalence and consequences of PE in young adults aged 18–44 years hospitalized with sarcoidosis using data from the National Inpatient Sample (2016–2020) with relevant International Classification of Diseases (ICD)-10 codes. This study aims to address the primary outcomes of the burden and trends of PE and its associated impact on in-hospital mortality. Additionally, it explores secondary outcomes such as healthcare resource utilization and discharge patterns. Results: Among 50,385 young adults (median age 37 years) hospitalized with sarcoidosis, 1120 had PE, showing a linear increase from 2% in 2016 to 2.9% ( P < 0.001) in 2020. The sarcoidosis–PE+ group, predominantly in young blacks, exhibited a higher prevalence of comorbidities such as obesity, smoking, drug use, peripheral vascular disease, hypothyroidism and prior history of venous thrombus embolism. In contrast, the sarcoidosis–PE− group had a higher prevalence of diabetes (with/without chronic complication), hyperlipidemia and chronic pulmonary disease. Multivariable regression analysis adjusted for all potential sociodemographic and comorbid variables showed higher odds of all-cause mortality (odds ratio [OR]: 2.92, 95% confidence interval [CI]: 1.18–7.24, P < 0.02) in the sarcoidosis–PE+ group as compared to the sarcoidosis–PE− group. The sarcoidosis–PE+ group also had higher hospital costs and length of stay. Conclusion: The higher odds of in-hospital mortality with an increased length of stay and hospital cost observed in the sarcoidosis–PE+ group highlight the often underreported complications of sarcoidosis, particularly in a younger demographic. The relevance of this study stems from its potential to uncover trends that could lead to improved diagnostic and therapeutic strategies.

Abstract Introduction Histiocytic neoplasms (HN) are a rare, heterogeneous group of hematologic disorders derived from myeloid-dendritic cell lineages. The most common forms include Langerhans cell histiocytosis (LCH), Erdheim-Chester disease (ECD), and Rosai-Dorfman disease (RDD). These disorders are driven by recurrent activating mutations in the MAPK pathway, most frequently involving BRAF, MAP2K1, PIK3CA, KRAS, and NRAS. This discovery enabled a major therapeutic advance with the use of BRAF and MEK inhibitors, resulting in durable responses. For patients harboring KRAS mutations, MEK inhibitors (MEKi) remain the primary therapeutic approach. However, the impact of KRAS mutation subtypes on treatment response remains poorly understood. Our study aimed to characterize the spectrum of KRAS mutations in LCH, ECD, and RDD and evaluate the responses to MEKi, providing insights to guide future treatment strategies. Methods We conducted a retrospective review of patients with LCH, ECD, and RDD who were evaluated at Mayo Clinic or University of Alabama at Birmingham. Patients were included if next-generation sequencing identified a KRAS mutation. The response assessment was based on radiographic evaluation under the most recent Histiocyte Society consensus guideline. Results We identified 23 patients with a KRAS mutation: 17 females (73.9%) and 6 males (26.1%), with a median age at diagnosis of 61 years (range, 20–78). RDD accounted for 73.9% (17/23) and ECD for 26.1% (6/23); no KRAS mutations were detected in LCH patients. The most frequent KRAS variants were p.K117N (34.8%), p.G12D (17.4%), p.A146T (13.0%), p.G13C (8.7%), and p.G13D (8.7%), with additional variants including p.T58I, p.A59G, p.A146P, and p.A146V. Mutation distribution differed by disease group: p.G12D was more common in ECD (50%) than RDD (5.9%) (p=0.01), whereas p.K117N occurred in 47.1% of RDD and was absent in ECD. Regarding treatment, 57% (13/23) received MEKi, all initially cobimetinib, with 1 patient switched to trametinib due to progression. Of the 10 patients who did not receive MEKi, 1 was treated with vemurafenib for a concurrent BRAF p.V600E mutation; 3 remained on observation; 2 underwent surgery without recurrence; 3 received other systemic therapies including corticosteroid, methotrexate, rituximab, lenalidomide, or sirolimus; and 1 developed diffuse large B-cell lymphoma, treated with R-CHOP. The overall response rate in the 12 patients on MEKi (excluding 1 patient too early for assessment) was 75%—3 (25%) CR and 6 (50%) PR (including 1 who initially progressed on cobimetinib but responded to trametinib). All 3 non-responders had RDD. Among the 5 patients with p.K117N, 3 had no response to cobimetinib, 1 achieved PR, and 1 achieved CR; notably, 1 non-responder switched to trametinib and achieved PR in 2 months. All 3 patients with codon 146 mutations achieved PR. Of the 2 patients with p.G12D, 1 achieved CR with a co-occurring MAP2K1 mutation, and 1 had no response. No additional genotype–response patterns were observed. Similar heterogeneity has been reported in prior studies. In a phase II cobimetinib trial, an ECD patient with p.R149G achieved PR, whereas another ECD patient with p.G12R and an LCH patient with p.G13C achieved CR in the presence of co-occurring ARAF and NRAS mutations, respectively. A retrospective cohort described an ECD patient with p.K117N achieving PR on dabrafenib and trametinib with a concurrent BRAF mutation and another with p.G12A achieving PR on trametinib. In a multicenter analysis of trametinib, a patient with p.A59T (co-occurring BRAF and NRAS mutations) had no response, whereas another with p.A146P achieved PR. Collectively, these findings, together with our data, underscore that KRAS-mutated histiocytoses exhibit heterogeneous responses to MEKi, likely influenced by variant type and co-mutations. Discussion KRAS mutations represent an important subset of MAPK pathway alterations in HN, although their prevalence varies by disease type and appears extremely rare in LCH, with no cases identified in our cohort. The most common variants include p.K117N and p.G12D, which may be linked to suboptimal response to MEKi in the absence of concurrent MAPK pathway alterations. As MEKi acts downstream, efficacy likely depends on the level of pathway activation conferred by specific KRAS variants. Larger studies are needed to confirm these observations and identify mutation-specific predictors to guide personalized treatment.

Abstract Introduction: Targeted therapy yields deep and durable response in histiocytic neoplasms.However, relapse rate following interruption is high at 75-77%, with a median time to relapse 6-9 months in previous studies. Outcomes after discontinuation in those who have already achieved a durable response are not well understood and are the focus of this study. Methods: We performed a multicenter retrospective study, including 4 US centers, including patients with histiocytic disorders treated with BRAF inhibitor (BRAFi), MEK inhibitor (MEKi), or combination BRAF/MEKi, and whose therapy was interrupted after ≥12 months of therapy following a best response of partial (PR) or complete response (CR). Progression-free survival (PFS) and overall survival (OS) were analyzed with Kaplan-Meier method. Cox regression was performed to identify clinical and molecular factors that are associated with PFS. Results: 26 patients were included (median age 55 [range 12-72]; male 53.8%; Caucasian 69.2%). Most predominant histology was Erdheim-Chester Disease (ECD) (n=15, 57.5%), followed by mixed histiocytosis (n=5, 19.2%). Rosai-Dorfman Disease (RDD) (n=4, 15.4%), and Langerhans Cell Histiocytosis (LCH) (n=2, 7.7%). All had BRAF V600E analysis and 10 (38.5%) were positive. 19 patients underwent additional molecular testing; alternative mutations identified included MAP2K1/2 (n=6, 23.1%), NRAS (n=1, 3.8%), RAF1 (n=1, 3.8%), ASXL1 (n=1, 3.8%), and SRSF2 (n=1, 3.8%). Targeted therapy was given as frontline therapy (n=8, 30.8%) or in the relapsed refractory setting (n=18, 69.2%) with median 1 prior line of therapy (range 0-7). Targeted therapies include BRAFi (n=5, 19.2%; 2 dabrafenib, 3 vemurafenib), MEKi (n=17, 65.4%; 14 cobimetinib, 3 trametinib), and BRAF/MEKi (n=4, 15.4%; 3 dabrafenib/trametinib, 1 vemurafenib/cobimetinib). PR and CR occurred in 8 (30.8%) and 18 (69.2%) patients, respectively. The median duration of treatment was 32 months (range 13-60) (12-24 months: 9 [34.6%]; 24-36 months: 7 [26.9%]; &gt;36 months: 10 [38.5%]). Median time from initiation of targeted therapy to best response was 6 months (&lt;6 months: 14 [53.8%]; 6-12 months: 5 [19.2%]; &gt;12 months: 7 [26.9%]). Median duration from best response to drug discontinuation was 19 months (12-24 months: 14 [53.8%]; 24-36 months: 7 [26.9%]; &gt;36 months: 5[19.2%]). Reasons for drug discontinuation include toxicity (n=8, 30.8%), patient preference (n=13, 50.0%), cost prohibition (n=1, 3.8%), and other critical medical conditions (n= 4,15.4%). Eleven patients (42.3%) experienced disease progression after discontinuation of targeted therapy, 5 patients progressed within 6 months. Systemic and CNS progression were captured by PET/CT and MRI brain, respectively. At median follow-up of 33.0 months (95%CI 24.3-47.1), median PFS, defined by time from targeted therapy discontinuation to progression or death, was 29 months (95% confidence interval [CI] not estimable). Median OS was not reached. In Cox regression model, BRAF V600E mutation (hazard ratio [HR] 4.16, 95% CI 1.10-15.70, p 0.036) and CNS involvement (HR 4.64, 95% CI 1.21-17.67, p 0.025) were associated with inferior PFS. MEKi containing regimen trended toward improved PFS (HR 0.35, 95%CI 0.10-1.21, p 0.097). There was no difference in PFS when assessing demographics, histology, prior therapies, best response to targeted therapy, treatment duration, or time from best response to discontinuation. Of the 11 patients with progression, 9 were re-challenged with targeted therapy (7 switched class), 2 did not receive next line therapy (1 transitioned to hospice and passed from progression, 1 has pending evaluation for next line therapy). Of 6 with response assessments, all recaptured response (1 CR, 5 PR), and none had progressed by data cutoff. Conclusions: In patients with histiocytic neoplasm and prior durable response to targeted therapy, ~40% experienced disease progression after treatment discontinuation. BRAF V600E mutation and CNS disease are associated with inferior PFS, suggesting these subgroups may not be appropriate for limited duration of treatment. Novel approaches are needed in these high-risk patients.

Abstract Introduction: Langerhans Cell Histiocytosis (LCH) is a rare histiocytic neoplasm, with approximately 90% of patients exhibiting alterations in the MAPK pathway. BRAF and MEK inhibitors have shown promising results in treating MAPK pathway-altered LCH. However, treatment interruptions due to adverse effects are common, and limited access to targeted therapies complicates care globally. While chemotherapy remains a common treatment for LCH, the outcomes for patients with MAPK pathway-altered LCH specifically receiving chemotherapy are still unclear. Methods: This multi-institutional international retrospective cohort study analyzed adult patients with BRAF or MAP2K (gain-of-function, GOF) altered LCH that were consecutively seen at Mayo Clinic, MN, AZ, and FL, University of Alabama at Birmingham, and Peking Union Medical College Hospital in China between 2007 and 2024. All patients who were included in this study were treated with chemotherapy, and those who have received targeted therapies or other modalities of frontline treatment were excluded. All time-to-event analyses were performed from the frontline therapy initiation, using the Kaplan-Meier method. Progression-free survival (PFS) included death and progression as events and was measured from the time of treatment initiation. The response assessment was based on radiographic evaluation in accordance with the most recent Histiocyte Society consensus guideline. Risk organ involvement was defined as disease involving the liver, spleen, bone marrow or central nervous system. Results: A total of 63 patients with LCH were included. The median age of the population was 34 years (range: 27-43), and males were 59%. Risk organ involvement was seen in 44 (70%) of patients and multisystemic LCH was observed in 48 (76%) patients. Among the 63 patients, BRAF gain-of-function alterations were observed in 79%, MAP2K mutations in 19%, and BRAF fusions in 2%. Of the BRAF gain-of-function alterations, BRAFV600E mutation was seen in 64% patients and [p.N486_P490del] deletion in 36%. There was no significant difference in organ involvement (single-system versus multisystem) or risk organ involvement between patients with BRAF and MAP2K alterations. All 63 patients received systemic therapy with chemotherapy and the regimens included Cytarabine (n=43), Cladribine (n=5), Etoposide (n=1), Methotrexate (n=1), and combined Methotrexate and Cytarabine (n=13). The median follow-up for the entire cohort was 3.8 years (range 3.2–5.0 years), with similar durations observed in patients with single-system vs. multisystem involvement and those with risk-organ involvement vs. no risk-organ involvement. The overall response rate among patients who received chemotherapy was 89%, with complete responses in 15 patients (26%) and partial responses in 40 patients (64.5%). The median progression-free survival (PFS) for the entire cohort was 2.61 years (95% CI: 2.06–NA). The 3-year PFS did not significantly differ based on risk organ involvement: 50.6% (95% CI: 36–71) for patients with risk organ involvement versus 47.4% (95% CI: 28–81) for those without, p=0.52. Patients with single-system disease experienced longer PFS compared to those with multisystem disease; the 3-year PFS was 80.2% (95% CI: 58.7–100) versus 42.2% (95% CI: 29–61.5), respectively, p=0.04. Conclusions: Our results indicate that LCH patients with a GOF alteration in the MAPK pathway derive significant clinical benefit from chemotherapy, achieving deep and durable responses. Therefore, patients should not be excluded from treatment due to the absence of targeted therapies, as they can still attain substantial responses and clinical improvement with chemotherapy, even in the context of MAPK pathway-driven disease.

Abstract Background:Erdheim-Chester Disease (ECD) is a rare, incurable histiocytic neoplasm. Since its recognition in 1930, our understanding of ECD's pathophysiology has evolved. The identification of its clonal nature after 2015 established ECD as a cancer, prompting increased disease awareness and treatment advances. Targeted therapies show promising responses, but changes in ECD mortality over time have not been extensively documented. Methods:A multi-institutional retrospective cohort study analyzed adults with ECD consecutively seen at Mayo Clinic MN, AZ, and FL and the University of Alabama at Birmingham between 2007 and 2024. Clinical and prognostic data were abstracted. Overall survival was estimated using the Kaplan-Meier method and compared to expected survival using U.S. Census data, based on age at diagnosis (by calendar year), date of diagnosis, and sex. Standardized mortality ratios (SMRs) were calculated by dividing the number of observed deaths in the study population by the expected number of deaths using U.S. population data. Risk of death was compared by date of diagnosis (pre- and post-2015) using Cox proportional hazards analysis. Statistical analysis was performed with R software. Results:A total of 159 ECD patients were included (median age 58 years [range 19-82], 65% male). Forty-nine patients were diagnosed between 1990-2014 and 110 between 2015-2024. Median follow-up for the entire cohort was 4.0 years (95% CI: 3.2-4.4). Median follow-up for those diagnosed between 1990-2014 was 10.4 years (CI: 3.2-16.8), compared to 3.5 years (CI: 3.0-4.2) for those diagnosed between 2015-2024. The 5-year overall survival rate was 80% (95% CI: 72-88). Patients with ECD had an increase in mortality over expected, with 28 deaths compared to an expected 11.2, an SMR of 2.5 (95% CI: 1.7-3.6, p&lt;0.001). Of 17 patients with an identified cause of death, death was attributable to ECD in 11 (65%), secondary malignancy in 1 (7%), and unrelated causes in 5 (29%). Cause of death was unknown in 11 patients. Among deaths, 11 (39%) were treated with targeted therapy, 8 (29%) with chemotherapy, and 1 (4%) received both. One patient (4%) received steroids, 1 received immunomodulator and targeted therapy (4%), and 6 (21%) received no disease-directed therapy. Of the patients whose death was related to ECD, 10 (91%) had multisystem disease. For 49 patients diagnosed pre-2015, 14 deaths occurred during the follow-up, significantly higher than the expected 5.2 deaths based on U.S. population data (SMR of 2.7 [95% CI: 1.5-4.4, p=0.001]). Among those diagnosed between 2015 and 2024, 14 deaths occurred, compared to expected 6.1 (SMR of 2.3 [95% CI: 1.3-3.8, p=0.006]). In an age- and sex-adjusted Cox proportional hazards model, diagnosis after 2015 vs. diagnosis prior to 2015 yielded a hazard ratio of 0.59 (95% CI: 0.27-1.31, p=0.19). Conclusion:The mortality rate of ECD patients remains higher than the general population, despite advancements in disease recognition and development of targeted therapies. While our data suggest a possible trend toward improved survival among patients diagnosed after 2015, we did not find statistically significant evidence of decreased mortality compared to those diagnosed prior to 2015. Larger cohorts with longer follow-up periods are needed to draw definitive conclusions regarding mortality.

ABSTRACT Objective We sought to characterize the sixth most common finding in our neuroimmunological laboratory practice (tissue assay‐observed unclassified neural antibodies [UNAs]), combining protein microarray and phage immunoprecipitation sequencing (PhIP‐Seq). Methods Patient specimens (258; 133 serums; 125 CSF) meeting UNA criteria were profiled; October 2022–September 2023. Top‐ranking candidate antigens were validated in silico, by dual‐staining confocal microscopy, and ≥ 1 protein‐specific assay. Clinical data were reviewed. Results Among 21 patients, 11 autoantibodies were characterized (serum, 19; CSF, all 9 available). Autoantigens were CACNA1I, 1; CAMK2B, 2; CLIP2, 1; FMN2, 2; MAP1A, 2; MAP2, 5; NECAB1, 1; SNAP91, 3; SRCIN1, 1; SYNJ1, 1; SYT3, 2. Analytical validation was by confocal TIIFA (all), western blot (10/10 available), and cell‐based assay (5/5 performed). Clinical accompaniments were: encephalitis, 6; brainstem encephalitis, 2; encephalomyelitis, 2; cerebellar ataxia, 2; longitudinally extensive transverse myelitis (LETM), 2; sensory neuronopathy, 1; peripheral neuropathy, 4, and movement disorders, 2. Inflammatory MRI abnormalities were identified in 5/16 patients (31%) with CNS disorders: T2 signal change (2), LETM (2), leptomeningeal enhancement (1). Seven of 8 (88%) had inflammatory CSF (pleocytosis, 5 [median 25.5 cells, range 7–294]; elevated IgG index/synthesis rate, 4; CSF‐exclusive oligoclonal bands, 4). Six had paraneoplastic causation (lung cancer, 2; other, 4); 3 were postinfectious (1 each of COVID‐19, HSV‐1, and post‐Group A streptococcal infection). Of 9 immunotherapy‐treated patients, 5 improved. Interpretation UNAs are partly accounted for by a repertoire of diverse mostly intracellular synaptic antigens. Their characterization is expedited by protein arrays and PhIPSeq. Further individual studies are needed to assess them as disease biomarkers.

Abstract Glioblastoma (GBM) is a highly aggressive brain tumor characterized by invasive growth, genetic heterogeneity and resistance to therapy. Alterations in the epithelial growth factor receptor (EGFR) are frequently detected in GBM, including gene amplifications, mutations and exon deletions, exemplified by the expression of EGFR variant III (EGFRvIII). To target both wild-type and EGFRvIII, we generated the humanized antibody A10, which reacts with the 287-302 loop that is fully exposed on the extracellular domain of EGFRvIII and conditionally exposed on cells expressing gene-amplified EGFR. However, A10 showed little or no reactivity for cells expressing normal levels of wild type EGFR. We engrafted antibody fragments derived from A10 on to ARTEMIS® Cell Receptor Platform, which introduces two separate receptors into engineered T cells to provide activation and co-stimulatory signals. Specifically, the A10 antigen-binding fragment (Fab) was fused to the N-terminus of a γδTCR-signaling domains (A10-AbTCR) while the A10 single chain variable fragment (scFv) was fused to a costimulatory signaling receptor (A10-CSR). The resulting A10 ARTEMIS® T cells were cytotoxic for tumor cell lines displaying amplified or overexpressed EGFR and EGFRvIII. Further, glioblastoma PDXs were sensitive to A10 ARTEMIS® T cell killing. This prompted an in vivo evaluation in EGFR-driven cancers. GBM39 PDX tumors (expressing amplified EGFRvIII) were implanted into the brains of NSG mice. Mice received one or two infusions. Treatment with one infusion of A10 ARTEMIS® cells resulted in prolonged survival of tumor bearing mice with 40 % of mice were long-term survivors (74 days) compared to a median survival of 32 days (control) or 52 days (mock T-cells). For mice receiving two A10 ARTEMIS® T cell infusions, there was 100% survival of mice beyond 60 days, while all control and mock treated mice were dead by 28 days. Further, treatments of EGFR-amplified MDA-MB-468 tumors resulted in complete tumor regression with one treatment of A10 ARTEMIS® cells. Thus, this new format of A10 engineered T-cells appears to be a particularly promising for treating cancers with high levels of EGFR or EGFRvIII including GBM. Citation Format: Antonella Antignani, Danielle Burgenske, Guangyan Xiong, Hongbing Zhang, Cheng Liu, Jann Sarkaria, David FitzGerald. Engineered T-cells, targeting overexpressed EGFR and EGFRvIII, produce complete remissions in a PDX model of human glioblastoma [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2025 Oct 22-26; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2025;24(10 Suppl):Abstract nr B056.

Minimally invasive esophageal cellular collection devices such as the Capsule Sponge may offer the potential for targeted screening of high-risk patients. The capsule sponge has been shown to be a safe, accurate and effective means of detecting Barrett’s esophagus. Here, we explore two potential real-life scenarios that could occur in a future screening or case finding programme. Firstly, when the capsule sponge test result is positive but confirmatory endoscopy demonstrates <1cm of columnar epithelium and secondly when subsequent endoscopy identifies gastric intestinal neoplasia. We discuss the clinical implication of the result and suggest how these patients could potentially be followed up in the future.

ABSTRACTObjectivesTo achieve consensus among expert laser surgeons on standards for the prevention and management of adverse events from fully ablative laser resurfacing of the face.Materials and MethodsDelphi study with two rounds of ratings and revisions until consensus was achieved. The draft set of statements was developed by a steering committee based on expert clinical experience. This was followed by two rounds of rating and revisions completed by an expert panel, then a virtual consensus meeting. In both rounds, respondents rated the draft statements on a 9‐point Likert scale (1 = strongly disagree; 9 = strongly agree) and optionally provided comments. The consensus meeting was supplemented by the results of a systematic review of the literature (from 2000 to 2023).ResultsTwo rounds of Delphi survey were completed by 34 participants across four countries. Represented specialties were dermatology, facial plastic surgery, plastic surgery, and oculoplastic surgery. The initial 105 statements from round 1 expanded to 112 in round 2, with 96 statements achieving consensus. These included possible adverse events (11 statements); absolute and relative contraindications to treatment (5 statements); preoperative care and antimicrobial prophylaxis precautions (16 statements); intraoperative precautions (17 statements); postoperative care (21 statements); monitoring for and management of infection (16 statements); management of pigmentation changes (6 statements); and management of scarring and incipient scarring (4 statements).ConclusionAn international consensus statement was developed for the prevention and management of complications associated with fully ablative laser resurfacing of the face. While expert practices vary, key factors for optimizing outcomes include careful patient selection, counseling, and meticulous pre‐ and postoperative care. Further research will improve our understanding of this treatment technique.