Background Pulmonary embolism (PE) is a life‐threatening condition requiring rapid diagnosis and accurate risk stratification. Biomarkers reflecting thromboinflammatory processes may improve early clinical assessment. Glycoprotein VI (GPVI), a key receptor involved in platelet activation, has been implicated in thrombus formation; however, its clinical relevance in PE remains unclear. Objective To examine the association of serum GPVI with radiological thrombus burden and clinical risk indicators in acute PE, while retaining the original PE‐versus‐control comparison only as a secondary exploratory case–control discrimination analysis, not as a diagnostic‐accuracy analysis. Methods In this cross‐sectional study, the analytic cohort comprised 50 patients with CTPA‐confirmed acute PE and 25 control participants. Serum soluble GPVI (sGPVI) was measured by a colorimetric sandwich ELISA. The study‐recorded CTPA thrombus‐burden categories were analyzed as lower, intermediate, and higher radiological burden and separately from an exploratory ESC‐aligned risk reconstruction. For ICU admission, parsimonious multivariable and incremental analyses evaluated GPVI beyond PESI with internal validation. A PE‐versus‐control ROC comparison with D‐dimer was retained only as a secondary exploratory case–control discrimination analysis and was not treated as an estimate of diagnostic accuracy. Results Among patients with PE, GPVI differed across the study‐recorded radiological burden categories (lower, n = 16: 192.95 [185.80–215.39]; intermediate, n = 13: 258.54 [238.60–276.29]; higher, n = 21: 307.90 [285.92–321.95] ng/L; p < 0.001). In the exploratory ESC‐aligned analysis, GPVI differed across risk categories (Kruskal–Wallis p = 0.045) and showed an ordinal association with increasing risk category (Spearman ρ = 0.331, p = 0.02). GPVI was higher in patients admitted to the ICU than in those not admitted (298.24 [278.42–315.89] vs. 206.17 [191.15–238.33] ng/L, p < 0.001) and had an ICU‐admission AUC of 0.969. In a parsimonious model adjusted for PESI, GPVI remained associated with ICU admission (OR per 10 ng/L, 2.31; 95% CI, 1.36–3.92; p = 0.002), although the magnitude should be interpreted cautiously given the small sample size, limited number of ICU events, and strong separation. These effect estimates are exploratory and should not be interpreted as stable clinical effect sizes. Adding GPVI to PESI increased the apparent AUC from 0.885 to 0.968 (ΔAUC, 0.083; bootstrap 95% CI, 0.013–0.200); the optimism‐corrected AUC was approximately 0.954, and repeated stratified 5‐fold cross‐validation yielded a mean AUC of approximately 0.916. In the secondary PE‐versus‐control analysis, GPVI was higher in PE (268.12 [215.39–298.47] vs. 114.07 [89.10–136.80] ng/L, p < 0.001) and showed an AUC of 0.968 versus 0.884 for D‐dimer (ΔAUC, 0.084; bootstrap 95% CI, 0.008–0.168; p = 0.03); this case–control estimate is susceptible to spectrum bias and is not an estimate of real‐world diagnostic accuracy. Conclusion Serum GPVI was associated with radiological thrombus burden and severity‐related clinical indicators in acute PE. These exploratory findings support further evaluation of GPVI as a potential risk‐stratification biomarker but do not establish diagnostic utility. Confirmation in larger, clinically representative prospective cohorts with hard clinical outcomes is required.
Background Obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS) are strongly linked to pulmonary hypertension and left ventricular abnormalities, driving cardiovascular issues. OHS, with daytime hypercapnia, affects 10%–20% of OSA patients. Continuous positive airway pressure (CPAP) is the first‐line therapy, but its cardiac effects are inconsistent. Methods We conducted a systematic review and meta‐analysis adhering to the PRISMA 2020 statement. Risk of bias was assessed using RoB 2 (RCTs) and the Newcastle–Ottawa Scale (NOS; cohort studies). Continuous outcomes were pooled as mean differences (MDs) with 95% CIs using random‐effects models (restricted maximum likelihood) with Hartung–Knapp adjustment. Results Eight studies (574 participants; 2 RCTs, 6 cohorts) were included, showing that CPAP significantly reduced pulmonary arterial pressure (MD = −2.32 mmHg, 95% CI: −3.88 to −0.76, p = 0.004) versus controls. Secondary analyses indicated improved left ventricular diastolic function (early‐to‐late diastolic mitral inflow velocity [E/A] ratio: MD = 0.29, 95% CI: 0.09 to 0.48, p = 0.004). No significant effects on left ventricular mass index (LVMi) (MD = −2.31 percentage points, 95% CI: −6.38 to 1.77, p = 0.27) or left ventricular ejection fraction (LVEF) (MD = 0.53 percentage points, 95% CI: −1.49 to 2.55, p = 0.61) were found. Sensitivity analyses confirmed robustness. Funnel plot analysis suggested potential publication bias for pulmonary artery systolic pressure (PASP)/mean pulmonary artery pressure (mPAP), E/A ratio, and LVEF, while LVMi showed low bias. Conclusions In adults with OSA or OHS, CPAP reduces pulmonary arterial pressure and improves LV diastolic function, but it does not significantly alter LVMi or ejection fraction. These findings support CPAP as a key intervention to mitigate pulmonary hemodynamic burden and diastolic dysfunction in this high‐risk population, while its potential to reverse structural cardiac remodeling requires further study.
Background Silicosis is a preventable occupational lung disease caused by inhalation of respirable crystalline silica. Although traditionally associated with mining, it is increasingly recognized among workers who fabricate engineered stone, also referred to as artificial stone, for kitchen and other countertops. In Canada, updated surveillance data are limited, and no published case series have characterized engineered stone–associated silicosis. Methods We report a retrospective case series of 20 patients diagnosed with silicosis following occupational exposure to engineered stone in Ontario, Canada, between November 2015 and September 2025. Demographic, occupational, clinical, radiologic, and functional data were extracted from medical records. Continuous variables are reported as median and interquartile range (IQR). Results The median age at diagnosis was 52 years (IQR: 41.5–64.5), and all patients were male, predominantly immigrants from Southeast Asia. Median occupational exposure to silica was 19 years (IQR: 10.5–27.5). Although 80% reported respirator use, adherence was inconsistent, and workplace controls were often inadequate. Cough and dyspnea were the most common presenting symptoms (60% each), with a median diagnostic delay of 13.5 months. Imaging showed simple silicosis in 70% and progressive massive fibrosis in 30%. Pulmonary function tests demonstrated predominantly restrictive impairment with reduced diffusion capacity. Outcomes were significant, including 15% mortality, median age at death of 43 years, chronic hypoxia in 35%, and lung transplant referral in 30%. Conclusions Engineered stone–associated silicosis in Ontario is characterized by prolonged silica exposure, inadequate workplace protections, delayed diagnosis, and severe disease at presentation. These findings underscore the urgent need for strengthened regulatory measures to protect engineered stone workers: more effective occupational silica exposure controls, systematic respiratory health surveillance of workers at risk, and earlier recognition and diagnosis of silicosis.
Background Pulmonary papillary adenoma is currently considered a benign tumor; however, a few cases have been reported in the past with potential for malignancy. Therefore, the histological nature of papillary adenomas remains controversial. This article presents a rare case of a multifocal papillary adenoma with uncertain malignant potential, featuring an ERBIN–BRAF gene fusion and an APC mutation, along with a literature review, to enhance understanding of this tumor. Case Description The patient sought medical consultation due to symptoms of cough and sputum production. Imaging showed a high‐density, lobulated nodule in the posterior basal segment of the left lower lobe, surrounded by multiple smaller nodules. Postpulmonary lobectomy, histopathological examination revealed a large nodule composed of a single papillary structure, with the papillary surface covered by a single layer of cuboidal or low‐columnar epithelium. Local areas showed transition to surrounding alveolar epithelium, and well‐formed glands were observed in the proliferative fibrous tissue, with local stromal fibrosis. Some tumor cells in the surrounding small nodules grew in a lepidic fashion, with cellular morphology similar to that of the large nodule. Immunohistochemical staining showed that tumor cells were positive for TTF‐1, CK, CK7, and Napsin A, with a few cells expressing P53 and a Ki‐67 index of approximately 8%. Next‐generation sequencing (NGS) identified an APC gene mutation (Exon 16, p.E1306∗) and an ERBIN exon3–BRAF exon11 fusion. Given that BRAF alterations have been implicated in lung carcinogenesis, a similar BRAF‐mediated tumorigenic pathway may be active in this tumor; therefore, complete resection of the adenoma may be indicated. The tumor’s multifocal distribution and molecular alterations suggest that this case represents a papillary adenoma with uncertain malignant potential. Conclusions Currently, there is no established standard treatment for such tumors, and the tumor in this case underwent pulmonary lobectomy. Future studies should accumulate more cases to clarify the prognosis and treatment guidelines for this type of tumor.
BACKGROUND:Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial lung disease with a poor prognosis. Honeycombing on high-resolution computed tomography (HRCT) is a defining feature of the usual interstitial pneumonia (UIP) pattern and has traditionally been considered a marker of advanced disease. However, in the era of antifibrotic treatment (AFT), the prognostic significance of the UIP pattern in IPF remains uncertain. This study aimed to evaluate the association between HRCT UIP pattern and long-term prognosis in patients with IPF receiving AFT. METHODS:This retrospective multicenter study investigated consecutive patients with IPF who initiated AFT between 2009 and 2019 at seven institutions in Japan. HRCT patterns were classified as UIP or non-UIP by multidisciplinary assessment. The primary outcome was IPF-related events, defined as IPF-related death or first acute exacerbation (AE) after initiating AFT. Event-free survival was analyzed using Kaplan-Meier methods with stratification by gender-age-physiology (GAP) stage. Propensity score matching (PSM) was performed to adjust for age, sex, GAP score, and antifibrotic agent. RESULTS:Of the 139 patients included, 99 had a UIP pattern, and 40 had a non-UIP pattern. In the overall cohort, event-free survival did not differ significantly. Stratified analyses showed no significant survival difference between UIP and non-UIP patterns among GAP Stage I patients (median survival time [MST]: 2050 vs. 1104 days; p = 0.90). Similarly, among patients with GAP Stages II-III, MST did not differ significantly. After PSM, 34 matched pairs were analyzed, and no significant differences in event-free survival were observed between UIP and non-UIP patterns. CONCLUSIONS:In patients with IPF treated with AFT, the radiological UIP pattern on HRCT was not independently associated with long-term prognosis. Multidimensional risk assessment incorporating physiological impairment and disease behavior may provide more accurate prognostic stratification in treated UIP populations.
