The pathogenetic mechanisms of thrombosis in cancer involve a complex interaction between tumour cells, activation of blood coagulation such as in acute-phase reactions, paraprotein production, inflammation, necrosis and haemodynamic disorders. Malignant cells can activate blood coagulation by releasing proinflammatory and proangiogenic cytokines and by interacting with vascular and blood cells. 4 It has been thought that patients with idiopathic or primary VTE are at higher risk of occult cancer than patients with a venous thrombotic event secondary to a provoking factor. 5 However, several studies have shown that VTE in patients with chronic diseases like psoriasis may also be a marker for occult cancer. 6 Comprehensive research has shown that extensive screening for occult cancer in patients with VTE in general will lead to a higher rate of cancer detection, but these strategies have not been associated with improved cancer-related mortality. 7 It is not clear from existing literature whether some subgroups of patients, like those with psoriasis, may benefit from extensive diagnostic investigations for cancer. Therefore, patients with psoriasis with a VTE should follow the same guidelines for occult cancer screening as other patients with VTE, until more evidence becomes available. 8

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