Objectives Mesothelioma mortality continues to reflect asbestos exposure because of its long latency. While previous Spanish studies focused primarily on pleural disease, this study assessed mesothelioma mortality across the ICD-10 C45 category in Spain from 1999 to 2024.Materials and methods:A population-based time-trend study was conducted using mortality data (ICD-10 C45) from the Spanish National Statistics Institute. Age-standardised mortality rates (ASMRs) were calculated using the 2013 European Standard Population. Temporal trends and sex-specific parallelism were evaluated using Joinpoint regression. Results Among 9733 recorded mesothelioma deaths (7311 men, 2422 women), ASMRs were consistently higher in men, although temporal trends were parallel by sex. Overall mortality increased until 2016 (annual percentage change [APC] 2.3%, 95% CI 1.5–3.0) and subsequently declined non-significantly, yielding an average annual percentage change (AAPC) of 1.0% (95% CI 0.2–1.7) for 1999–2024. Pleural mortality increased until 2011 before declining non-significantly, whereas recorded peritoneal mortality increased throughout the study period (AAPC 2.0%, 95% CI 0.7–3.2). Deaths coded as unspecified site (C45.9) showed the largest increase in ASMR (AAPC 2.1%, 95% CI 1.1–3.1) and accounted for 43.5% of male and 31.8% of female mesothelioma deaths in 2024. Conclusions Absolute mesothelioma deaths increased in Spain while age-standardised rates attenuated after 2016. The continued increase in recorded peritoneal mortality and the substantial contribution of unspecified-site deaths indicate that surveillance should not rely solely on pleural mesothelioma, highlighting the need for comprehensive monitoring of the complete ICD-10 C45 category and improved anatomical classification.
Background Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. However, comprehensive population-level data describing etiologic patterns, treatment exposure, healthcare utilisation, and survival remain limited in many countries. This study aimed to characterise the national burden, care patterns, and outcomes of HCC in Turkey. Methods We performed a nationwide, real-world analysis of adult patients diagnosed with HCC between 2016 and 2024 using administrative health data. Cases were identified by an administrative case definition requiring at least three separate records of ICD-10 codes C22, C22.0, or C22.9; at least one C22.0 code was not required, so HCC could not be confirmed at the individual level. Baseline comorbidities were restricted to conditions recorded on or before the date of diagnosis. Demographic characteristics, underlying liver disease, etiologic factors, treatment exposure, and the level and type of diagnosing institution were assessed. Overall survival (OS) was estimated using the Kaplan–Meier method. To reduce immortal-time bias, treatment exposure was analysed in a three-month landmark cohort; because treatment dates were unavailable, this reduces but does not eliminate the bias. Multivariable Cox regression was performed within the same cohort. Results A total of 13,674 patients (64.6% male; median age 64 years, IQR 55–73) were included, of whom 61.4% had died at the data cutoff; median follow-up was 53.0 months. The median OS was 13.2 months (95% CI 12.1–14.5), with 1-, 3-, and 5-year OS of 50.9%, 41.1%, and 36.9%; because patients dying before three qualifying records accumulated could not enter the cohort, these estimates apply to patients meeting the case-identification algorithm and are likely to overstate population survival. OS was markedly longer in women than in men (median 50.9 vs 8.2 months), and longer in patients without cirrhosis recorded at diagnosis than in those with cirrhosis (18.5 vs 9.0 months; both P < 0.001). Hepatitis B was the most frequently recorded specific etiology (29.4%); among mutually exclusive categories, NAFLD-associated HCC had the most favourable survival (5-year OS 61.0%) and alcohol-related HCC the least (median 8.8 months), while HBV–HDV co-infection was associated with longer survival than HBV mono-infection (58.2 vs 12.0 months; P < 0.001), a difference that persisted after adjustment for age, sex, and cirrhosis; no specific etiology could be assigned in 56.1% of patients. Sensitivity analyses restricting etiologic ascertainment to codes recorded within 3 months before to 3 months after diagnosis, or incorporating viral serology, attenuated the survival of the specific viral etiologies, indicating survival-dependent ascertainment. In a multivariable Cox model fitted in the three-month landmark cohort (n = 8958), older age, male sex, cirrhosis, and systemic therapy were associated with higher mortality (all P < 0.001), with time-varying associations for age, cirrhosis, and systemic therapy. The association of local therapy with mortality was not constant over follow-up (HR 0.78, 95% CI 0.72–0.85 during 0–24 months after the landmark and 1.22, 1.04–1.43 thereafter); the overall association was no longer evident after liver transplantation was excluded from the local-therapy category. Care was highly centralised within secondary and tertiary institutions. Conclusions In this nationwide analysis, HCC in Turkey was characterised by limited OS and pronounced sex-based disparities, with survival differing by cirrhosis status and recorded etiology; etiologic ascertainment was itself survival-dependent, so these contrasts describe recorded categories. Hepatitis B was the most frequently recorded specific etiology, underscoring the continued importance of HBV prevention, screening, and surveillance, while HCV, HDV, alcohol-related and metabolic liver disease accounted for smaller recorded proportions; temporal trends in etiology were not analysed. Because tumour stage and liver function were unavailable, the treatment–survival associations are descriptive and subject to confounding by indication. Efforts focused on HBV control, earlier detection, risk-based surveillance of patients with cirrhosis, and improved referral pathways may improve population-level outcomes.
Background Head and neck cancer (HNC) imposes a substantial burden in Aotearoa New Zealand (AoNZ), yet contemporary population-level data on incidence and early mortality across sociodemographic groups remain limited. Methods This population-based retrospective cohort study used New Zealand Cancer Registry to identify all primary HNC diagnoses from 2009 to 2020 (n = 6980). The cases were classified according to ICD-10 subsites. Incidence rates (IRs), age-standardised IRs, and age-standardised rate ratios were estimated by age, sex, ethnicity, socioeconomic deprivation, and rurality. Regression models were used to estimate annual percentage change in IRs and to estimate adjusted risk ratios for two-year all-cause mortality. Results In total 6980 people were diagnosed with HNC; an overall incidence rate of 13.5 per 100,000 person-years (PY). Oropharyngeal cancer (OPC), the most common subsite, increased from 3.4 per 100,000 PY in 2009–2011–4.9 per 100,000 PY in 2018–2020, whereas IRs for oral cavity cancer (OCC), the second most common, were more stable. HNC IRs were higher among males, older adults, Māori, Pacific Peoples and people living in the most socioeconomically deprived areas, with subsite-specific differences: Māori experienced higher OPC incidence rates, while Pacific Peoples experienced higher OCC IRs. Within two years of diagnosis, 25.2% of patients had died. Two-year all-cause mortality was 44.4% for hypopharyngeal cancer, 30.9% for OCC, and 22.7% for OPC. Among people diagnosed with HNC, after adjusting for available sociodemographic factors and treatment timing, two-year all-cause mortality was higher for Māori, Pacific Peoples, and those in the most deprived quintile. Rurality showed no consistent association with incidence or two-year mortality. Conclusions These findings indicate an OPC-driven shift in HNC epidemiology in AoNZ and a persistent inequitable burden of both disease occurrence and early mortality, supporting stronger surveillance and equity-focused cancer-control responses.
Background The effects of intermittent, high-dose cholecalciferol supplementation on circulating vitamin D metabolites and related biomarkers remain unclear. The ProsD randomised controlled trial evaluated the effects of monthly oral supplementation with 50,000 IU cholecalciferol in males with prostate cancer and assessed longitudinal changes in vitamin D metabolite responses. Objective To characterise vitamin D metabolites and ratios after a monthly dose of 50,000 IU cholecalciferol supplementation and to assess the effects on biochemical markers. Methods ProsD recruited and randomised 123 men with prostate cancer; 118 participants (placebo n = 40; vitamin D n = 78) provided blood samples at baseline, and from remaining participants at 0, 6, 12, and 24 months, at follow-up visits. Plasma vitamin D metabolites—25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, and 3-epi-25(OH)D3—and vitamin D metabolite ratios (VMRs) were quantified. Longitudinal changes and between-group differences were evaluated using age-adjusted generalised estimating equations with estimated marginal means. Routine biochemical markers were also assessed. Results Compared with placebo, monthly cholecalciferol supplementation increased peak between-group difference at 24 months for 25(OH)D3 (+30.10 nmol/L; p < 0.01), 1,25(OH)2D3 (+12.44 pmol/L; p = 0.11), 24,25(OH)2D3 (+3.95 nmol/L; p < 0.01), and 3-epi-25(OH)D3 (+5.94 nmol/L; p < 0.01). The 25(OH)D3:24,25(OH)2D3 VMR increased in the placebo group but remained constant in the intervention group, and between-group analysis showed consistently lower ratios in the vitamin D group. All routine biomarkers remained within normal ranges throughout follow-up. Conclusions Monthly oral supplementation of 50,000 IU cholecalciferol in men with prostate cancer produced sustained increases across multiple vitamin D metabolites over 24 months, accompanied by adaptive shifts in metabolite ratios consistent with regulated catabolic activation, with no clinically meaningful abnormalities in biochemical markers. Trial registration Australian New Zealand Clinical Trials Registry (ACTRN12616001707459), Date: 13 December 2016.
