Abstract Background/Objectives Surgical deroofing is an essential part of ongoing management of Hidradenitis Suppurativa, including persistent lesions non‐responsive to medical therapy. The variables associated with delayed wound healing after surgical deroofing are contradictory within the literature due to the inclusion of heterogeneous surgical intervention methods. We aimed to assess the predictors of time to wound healing after surgical deroofing in HS. Methods Patients who underwent in‐office surgical deroofing between 2020 and 2024 at a single tertiary HS referral centre were included in analysis. Demographic, disease and blood variables were collected as per standard of care. Statistical analysis was performed using univariate correlation, with multiple regression performed to explore the interactions between variables and identify variables predictive of time to wound healing. Results A total of 270 individuals were included in the analysis. The median time to wound healing was 9.6 weeks with a range from 4 to 22 weeks. Kaplan–Meier curves demonstrated significant differences with the log rank test when comparing biologic use versus no use, normal versus abnormal CRP and normal versus abnormal haemoglobin. Cox regression analysis identified biologic use with a significant hazard ratio compared to no biologic therapy (HR = 2.512, p < 0.0001) along with baseline CRP (HR = 0.968, p < 0.0001) and baseline haemoglobin (HR = 1.052, p < 0.001). Conclusions Time to wound healing after in‐office deroofing can be decreased with prior biologic therapy and markers of systemic inflammation in blood are also significantly associated with delays in healing. This correlates well with the existing literature promoting concurrent medical and surgical therapy to improve patient outcomes in HS.
Abstract Sarcoidosis is a non‐infective granulomatous disorder of unknown aetiology, with cutaneous involvement affecting up to 30% of patients. Drug‐induced sarcoidosis has been reported secondary to modern melanoma therapies including immune‐checkpoint inhibitors and first generation BRAF inhibitors such as vemurafenib and dabrafenib. Herein, we report a case of cutaneous micropapular sarcoidosis that first developed on immune‐checkpoint inhibition with ipilimumab and nivolumab for metastatic melanoma, which was exacerbated and further complicated by pityriasis rubra pilaris‐like palmar plaques upon transition to a next‐generation BRAF‐dimerisation inhibitor. Both the micropapular eruption and palmar plaques rapidly resolved after cessation of the novel BRAF‐inhibitor and concurrent commencement of hydroxychloroquine. It is unclear how inhibition of BRAF‐dimerisation results in granuloma formation, though upregulation of T H 1/T H 17 T‐cells and impairment of T‐reg cells may be responsible. Clinicians should be aware of the potential for exacerbation of sarcoidosis when transitioning from immune‐checkpoint inhibitors to these novel BRAF‐dimerisation inhibitors, particularly as their uptake in treating cancers increases beyond clinical trials. Further studies are required to assess whether these next‐generation agents can trigger sarcoidosis de‐novo, or simply exacerbate pre‐existing sarcoidosis.
Abstract Introduction Rheumatoid arthritis (RA) may predispose patients to opportunistic infections—either from innate immune dysregulation, or as a result of immunosuppressant use to treat the RA. Particularly concerning opportunistic infections are those caused by non‐tuberculous mycobacterial (NTM) organisms, the incidence of which has been increasing in epidemiological studies. Despite this, guidelines on the management of patients with RA who develop NTM infections are scarce, particularly with respect to immunosuppressant regimen modulation and duration of antibiotic therapy. Case Report Herein, we present a case of disseminated Mycobacterium chelonae infection, manifesting as arthralgia and cutaneous nodules. Discussion In addition, a review of the literature was conducted to Preferred Reporting Items for Systemic Reviews and Meta‐Analyses guidelines to identify similar cases in the literature—revealing that all RA‐associated M. Chelonae infections occurred in immunosuppressed patients (the majority with corticosteroids or tumor necrosis factor inhibitors), and considerable heterogeneity in management approaches. Further research regarding risk factors, preventative approaches and best management of such NTM infections in vulnerable patients with RA is required in order to establish consensus guidelines and consistency.
Abstract Purpose of Review In the preceding decade, the management of metastatic cutaneous melanoma has been revolutionised with the development of highly effective therapies including immune checkpoint inhibitors (specifically CTLA-4 and PD-1 inhibitors) and targeted therapies (BRAF and MEK inhibitors). The role of chemotherapy in the contemporary management of melanoma is undefined. Recent Findings Extended analyses highlight substantially improved 5-year survival rates of approximately 50% in patients with metastatic melanoma treated with first-line therapies. However, most patients will progress on these first-line treatments. Sequencing of chemotherapy following failure of targeted and immunotherapies is associated with low objective response rates and short progression-free survival, and thus, meaningful benefits to patients are minimal. Summary Chemotherapy has limited utility in the contemporary management of cutaneous melanoma (with a few exceptions, discussed herein) and should not be the standard treatment sequence following failure of first-line therapies. Instead, enrolment onto clinical trials should be standard-of-care in these patients.
Pilonidal sinus disease (PSD) has been proposed as an intergluteal variant of Hidradenitis suppurativa (HS),1 given their clinical similarities and commonalities as disorders of follicular occlusion. Emerging evidence suggests early intervention with multimodal approaches combining surgical and medical therapies provides benefits in long-term disease control.2, 3 Limited real-world evidence exists as to the time-to-uptake of medical or surgical treatment after diagnosis of HS and/or PSD. We aimed to quantify and compare the demographic characteristics, prevalence of surgical and biologic therapy and time to surgical intervention/biologic therapy in HS and PSD in a real-world cohort. De-identified data using the TriNEtX database using ICD-10 codes were used to select for HS and PSD between 2014 and 2024. Propensity matching was based on age, sex, race, ethnicity, smoking status, use of oral antibiotics and BMI. Incidence of surgical intervention (defined as those requiring admission specifically for HS/PSD) after diagnosis as well as the time-to-surgery or commencement of biologic therapy was calculated. Subgroup differences between curves were quantified using the log rank test with p < 0.05 considered significant after adjustment for multiple comparisons using the Benjamini–Hochberg procedure. In total, 206,328 HS patients and 155,880 PSD patients were identified in the raw data. In total, 2413 (2.5%) of HS patients had biologic exposure compared with 1552 (1.6%) of the PSD cohort (p = 0.01). In total, 34,462 (18%) HS patients underwent surgical intervention compared with 21,097 (37.6%) for PSD (p = 0.07). Individuals with HS were significantly older (35.9 years vs. 27 years p < 0.0001), more likely female (72.0% vs. 39.1% p < −0.001), have higher BMI (34.2 vs. 29.4, p < 0.001) and more likely to have exposure to antibiotics (34% vs. 24% p < 0.001) than individuals with PSD. Additionally, significant differences between baseline haemoglobin levels (130 g/L vs. 137 g/L p < 0.001) and inflammatory markers such as ESR (25.5 vs. 19.4, p < 0.0001) were identified between individuals with HS and PSD. After 1-to-1 propensity matching, cohorts of 97,949 HS and PSD patients each were constructed. In total, 2405/97,949 (2.46%) HS patients received biologics compared with 1544/97,949 (1.58%) for PSD. A total of 15,559/97,949 (15.91%) HS patients underwent surgery compared with 16,787/97,949 (17.1%) of PSD patients. Only 1879 HS patients (1.9%) and 964 PSD patients (0.98%) underwent both biologic and surgical therapy within the same 12-month period. A sensitivity analysis limited to 2016–2024 (after FDA approval of adalimumab for HS) maintained these differences with similar biologic uptake rates for both HS and PSD (data not shown). Cumulative incidence curves are presented in Figure 1. The median time to biologic therapy was 3457 days after diagnosis in HS and greater than 3560 days in PSD (Figure 1). Individuals with HS had a 96% increase in the hazard of receiving biologic therapy compared to PSD (hazard ratio = 1.96; p < 0.0001). The median time to surgical intervention was 557 days after diagnosis in HS and 508 days in PSD. Individuals with HS had a 3% decrease in the hazard of surgical intervention compared to PSD (hazard ratio = 0.97; p < 0.005). These results indicate that patients with HS are more likely to receive biologics compared to PSD, while PSD patients are more likely to undergo surgical intervention compared to HS. Given recent randomized controlled trials and real-world studies identifying the benefits of early biologic intervention and concurrent biologic and surgical therapy,3-5 increased integration of these findings into guidelines and models of care is needed. Additionally, further work is required to establish the efficacy of biologic therapy in PSD particularly combined with surgical therapy. As epithelialized tunnels in HS are known to be immunologically active,6 surgical procedures which address these structures such as deroofing or wide excision may modulate local and systemic inflammatory profiles and increase efficacy of biologics, requiring further investigation. Access to this data was provided by TriNETx. J.W.F. has conducted advisory work for Janssen, Boehringer-Ingelheim, Pfizer, Kyowa Kirin, LEO Pharma, Regeneron, Chemocentryx, Abbvie and UCB, participated in trials for Pfizer, UCB, Boehringer-Ingelheim, Eli Lilly, CSL and received research support from Ortho Dermatologics, Sun Pharma and La Roche Posay. JPP is supported by an Australian Government Research Training Program (RTP) scholarship. TS, RI, KB and CK have no relevant disclosures. Not applicable. The data that support the findings of this study are available from the corresponding author upon reasonable request.
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