Background Psoriasis is a chronic immune‐mediated inflammatory disorder that also occurs in the setting of human immunodeficiency virus (HIV). Biological therapy has transformed the treatment landscape for psoriasis; however, individuals with HIV are excluded from clinical trials. The impact of biological therapy on blood parameters in HIV is unclear and is only observed in small case series. Objective The aim of this study was to assess the effect of biological therapy in psoriasis vulgaris in individuals with well‐controlled HIV on CD4+ cell counts, CD4+ proportion and HIV viral load over 12 months. Methods This retrospective cohort study was conducted at a tertiary referral centre in Sydney, Australia and included 36 HIV‐positive individuals with psoriasis treated with biological therapy, compared with 144 age‐, gender‐ and HAART‐matched individuals without psoriasis seen between 2010 and 2022. Outcomes of interest included HIV viral load, CD4+ cell count and incidence of infections. Results No statistically significant difference was seen in baseline HIV viral load and CD4+ count between individuals with and without psoriasis. No significant change in CD4+ count or HIV viral load was seen over the 12‐month period of analysis in the HIV cohort without psoriasis. The HIV cohort treated with biological therapy for psoriasis also did not demonstrate any significant change in HIV viral load and CD4+ counts over the 12‐month period examined. Stratification by type of biological therapy used did not identify any significant changes in these parameters. Rates of infections and adverse events were also not significantly different between cohorts. It is possible that minor blips seen in the biologics cohort may be a risk factor for future virological failure, and future prospective longitudinal studies are required. Conclusions In individuals with well‐controlled HIV, the use of biological therapy for psoriasis does not significantly impact HIV viral load, CD4+ cell count, CD4+ proportion and rates of infection over the first 12 months of therapy.

Hidradenitis suppurativa (HS) is a complex, heterogeneous inflammatory disease in need of novel therapies. 1 Currently, adalimumab is the sole licenced biologic therapy for HS, and only achieves clinical response (as measured by the hidradenitis suppurativa clinical response outcome measure) in 60% of patients. 2 Mechanistically, HS is associated with significant polarization of the Th17 immune axis with significant dysregulation of cytokines including IL-17A, 3 IL-17C, 4 IL-17F 3,[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] Agents targeting the Th17 immune axis have been explored in HS 6 including clinical trials, 7 but further development has been halted due to lack of positive results. 8 Two separate IL-23 antagonists (risankizumab and guselkumab) have been withdrawn from further development after a lack of positive results

The utility of Strongyloidiasis screening in the setting of Dupilumab therapy is unknown. Our retrospective cohort study identifies a low prevalence of Strongyloidiasis with no cases of disseminated disease in the setting of Dupilumab therapy. Baseline IgE and Eosinophil levels were not associated with Strongyloidiasis and screening is likely of low utility.

Background: Hidradenitis Suppurativa is a complex inflammatory disease in which predicting therapeutic response remains challenging. IL-23 interacts with sex hormones but the relationships between the two in HS remains uninvestigated. Objectives: To assess whether baseline clinical, hormonal, or molecular markers are associated with clinical response to IL-23 antagonism with Risankizumab in Hidradenitis Suppurativa. Methods: 26 individuals with Hurley Stage 2/3 disease were administered Risankizumab 150mg Week 0,4,12. Baseline sex hormones and skin biopsies were taken. Clinical response at Week 16 assessed by the HiSCR, and differences between responders and non-responders assessed. Results: 18 of 26 participants achieved HiSCR50 at week 16 (69.2%). Clinical response to IL-23 antagonism was associated with male gender, elevated total serum testosterone, and decreased levels of FSH. Stratification by clinical responders/non responders identified differentially expressed genes including PLPP4 and MAPK10. Immunohistochemistry identified elevated numbers of CD11c, IL-17A and IL-17F positive cells compared to non-responders. CD11c+ cells significantly correlated with serum levels of total testosterone and inversely correlated with serum FSH. Conclusions: Clinical response to IL-23 antagonism in HS is associated with serum sex hormones, Th17 polarized inflammation in lesional tissue and CD11c+ cells. These potential therapeutic biomarkers require further validation in larger cohorts but may suggest potential targeted HS therapy.