BACKGROUND: Transplant recipients have an increased risk of skin cancer and related death compared to the general population. How demographics or geography impact mortality is unclear. Understanding these will help ident...BACKGROUND: Transplant recipients have an increased risk of skin cancer and related death compared to the general population. How demographics or geography impact mortality is unclear. Understanding these will help identify groups at highest risk of skin cancer death. OBJECTIVES: To estimate skin cancer mortality rates among kidney transplant recipients in Australia and New Zealand and describe excess mortality by demographics and geography, relative to the general population, and change over time. METHODS: We linked kidney transplant recipients from the Australia and New Zealand Dialysis and Transplant Registry with National Death Registers in Australia and New Zealand from 1990 to 2019. We identified deaths from melanoma (ICD-10 code C43), keratinocyte cancer (KC) (C44) and carcinoma in situ (D04) and estimated absolute mortality per 100,000 person-years (py) of follow-up. We used indirect standardisation to estimate standardised mortality ratios (SMR) with 95% confidence intervals (CI) for kidney transplant recipients compared to the general population by sex, age at death, decade of death, and New Zealand or Australian state. RESULTS: We included 21,503 individuals who received their first kidney transplant between 1990-2019. There were 251 deaths from skin cancer, 82 from melanoma and 169 from KC, in 212,317 person-years of follow-up (py). Absolute skin cancer mortality rate was 118.2 per 100,000py (95% CI 104.1-134.2); 38.6 per 100,000py for melanoma (95% CI 31.1-48.0), and 79.6 per 100,000py for KC (95% CI 68.5-92.6). Skin cancer mortality was 11.1-times higher in kidney transplant recipients compared to the general population (SMR) overall, 4.5-times higher for melanoma and 34.5-times higher for KC. Excess skin cancer mortality relative to the general population was observed in both sexes, across all age groups, residential areas and decades of follow-up. Excess mortality was highest in regions with high ultraviolet radiation (UV) indices - Australian states of Queensland (SMR 14.8; 95% CI 11.7-18.8), Western Australia (SMR 13.1; 95% CI 8.7-19.7) and in New Zealand (SMR 11.0; 95% CI 8.3-14.6). CONCLUSIONS: Kidney transplant recipients are at increased risk of skin cancer death, especially from KC, in all demographics and regions, especially those with high UV indices. Enhanced surveillance and rapid treatment entry are warranted.
Catalán E, Dianta B, Koplow N
… +10 more, Tiozzo-Lyon P, Faune G, Morandé P, Palisson F, Soto-Montandon C, Ravasio A, South AP, Rebolledo-Jaramillo B, Nyström A, Fuentes I
BACKGROUND: ABP 654 is a biosimilar to ustekinumab reference product (RP). It is approved for the treatment of patients with moderate-to-severe plaque psoriasis and other autoimmune disorders. OBJECTIVES: To demonstrate...BACKGROUND: ABP 654 is a biosimilar to ustekinumab reference product (RP). It is approved for the treatment of patients with moderate-to-severe plaque psoriasis and other autoimmune disorders. OBJECTIVES: To demonstrate the interchangeability of ABP 654 and ustekinumab RP following multiple switches. METHODS: In this randomized, double-blinded study that evaluated pharmacokinetics (PK), efficacy, immunogenicity, and safety, patients with moderate-to-severe plaque psoriasis received a subcutaneous injection of ustekinumab RP 45 mg or 90 mg (baseline body weight ≤100 kg or >100 kg, respectively) on day 1 (week 0), week 4, and week 16 (Run-in Period). At week 28, patients with a 50% improvement in Psoriasis Area and Severity Index (PASI) or better response were randomized in a 1:1 ratio to the Continued-Use group or Switching group. Those in the Continued-Use group received ustekinumab RP at the same dose as in the Run-in Period at weeks 28, 40, and 52, while the Switching group received ABP 654 at week 28, ustekinumab RP at week 40, and ABP 654 at week 52. The primary endpoints were area under the curve over the dosing interval (AUCtau) and maximum concentration (Cmax) between weeks 52 and 64. Secondary endpoints included time to maximum concentration between weeks 52 and 64, trough concentration at steady state between weeks 28 and 52, PASI percent improvement from baseline at week 64, PASI 75 and PASI 100 responses at week 64, incidence of antidrug antibodies (ADAs), and incidence and severity of adverse events (AEs). RESULTS: Of the 494 enrolled patients, 453 successfully completed the Run-in period and were randomized to the Continued-Use (n = 225) or Switching (n = 228) groups. The point estimates and 90% confidence intervals (CIs) of the geometric mean ratios (GMRs) for AUCtau and Cmax between weeks 52 and 64 were 0.93 (0.89, 0.98) and 0.95 (0.90, 1.00), respectively. As both 90% CIs fell within the prespecified similarity margin of 0.8 to 1.25, PK similarity was demonstrated between the Switching and Continued-Use groups. In addition, efficacy, incidence of ADAs, and AEs were also similar between the groups. CONCLUSION: These results support interchangeability of ABP 654 and ustekinumab RP.
BACKGROUND: Evidence regarding the role of hematopoietic mosaic loss of chromosome Y (mLOY) in incident dermatitis and eczema (DE) risk, and its contribution to male susceptibility remains limited. OBJECTIVE: To evaluate...BACKGROUND: Evidence regarding the role of hematopoietic mosaic loss of chromosome Y (mLOY) in incident dermatitis and eczema (DE) risk, and its contribution to male susceptibility remains limited. OBJECTIVE: To evaluate the associations of mLOY with incident DE and to assess whether mLOY may contribute to sex differences in DE susceptibility. METHODS: This prospective study included 189,572 UK Biobank men free of DE at baseline, recruited between 2006 and 2010. Hematopoietic mLOY was derived from genotyping intensity data and analysed as both categorical mLOY status and continuous mLOY percentage (mLOY%). Cox proportional hazards models were used to estimate associations with incident DE. Sex susceptibility was evaluated in a 1:1 propensity score-matched male-female cohort. Genetic modification was assessed using a DE polygenic risk score (PRS), and mediation by circulating metabolites was explored in the Metabolomics analyses. RESULTS: During follow-up, 9,608 men developed DE. In fully adjusted models, both low mLOY (8-20%) and high mLOY (>20%) were associated with increased DE risk, with the strongest association observed for high mLOY [adjusted hazard ratio (aHR) 1.44, 95% CI 1.26-1.66; P <0.001]. Compared with females, males without detectable mLOY had a similar DE risk, whereas males with low mLOY and high mLOY had progressively higher risks (aHR 1.14, 95% CI 1.07-1.21; and aHR 1.52, 95% CI 1.32-1.74, respectively), supporting a contribution of mLOY to male susceptibility. In age-mLOY discordance analyses, younger men with high mLOY showed a DE risk approaching that of older men without high mLOY, consistent with accelerated biological ageing. The greatest risk was observed in men with both high mLOY and high PRS (aHR 1.85, 95% CI 1.49-2.31; P <0.001). In metabolomic analyses, 98 circulating metabolites significantly mediated the mLOY-DE association, predominantly lipoprotein-related traits. CONCLUSION: Hematopoietic mLOY was associated with an increased risk of incident DE and may contribute to late-life sex differences in DE susceptibility. Lipoprotein-centric mediation signals implicate modifiable metabolic pathways and support integrating mLOY status and lipid profiling into risk assessment for older men.
Carapeba M, Pereira C, Pereira F
… +16 more, Michalany A, Pilar E, Talarico A, da Silva A, Ferreira C, de Oliveira I, de Moraes J, Saueiro F, Lellis R, Christensen T, Gomes I, Cohlmia G, Olsson S, Duarte Neto A, de Araujo L, DaCosta A
T cells are central to inflammatory skin diseases, but legacy subset labels often blur migration, localization, function, differentiation state and antigen context. That problem is amplified in dermatology because skin i...T cells are central to inflammatory skin diseases, but legacy subset labels often blur migration, localization, function, differentiation state and antigen context. That problem is amplified in dermatology because skin is a compartmentalized barrier organ, clinically important questions often concern persistence or relapse, and tissue studies commonly infer key properties such as residency from proxy markers rather than direct assays. The 2025 consensus guidelines for T-cell nomenclature offer a practical foundation: define subset terms operationally in the Methods, use standardized legacy definitions transparently, and apply modular nomenclature when needed to separate measured from inferred properties. Here, we propose a dermatology-specific reporting overlay built on, but not part of, the published modular nomenclature v1.0; this is not a competing skin-specific nomenclature, but a practical reporting aid intended to preserve cross-tissue comparability while making skin-specific sampling context explicit. This overlay foregrounds tissue source, tissue state, location or niche, lineage, assay-defined functional programme, and the strength of evidence supporting any residency or trafficking claim. Using psoriasis, atopic dermatitis, and allergic contact dermatitis as exemplar diseases, and extending the logic to selected additional inflammatory dermatoses, we show how more conservative and auditable reporting can improve transparency, cross-study comparability, and clinical interpretability in skin research without necessarily requiring additional experiments.