An 81-year-old man was incidentally found to have multiple bilateral pulmonary nodules on chest computed tomography. Bronchoscopy revealed Mycobacterium intracellulare, and partial spontaneous regression of several nodules initially supported a diagnosis of nontuberculous mycobacterial lung disease. However, other nodules showed progressive enlargement during antimicrobial therapy. Surgical lung biopsy revealed diffuse large B-cell lymphoma (DLBCL), and subsequent evaluation demonstrated gastric involvement. The patient achieved complete remission after systemic chemotherapy. This case highlights the diagnostic challenge of pulmonary lymphoma presenting with heterogeneous radiological behaviour and emphasizes the importance of histological confirmation when the clinical course is atypical.

With increasing environmental pollution and a high incidence of respiratory infections, pulmonary nodules (PN) are being detected more frequently. Although most are benign, they are often accompanied by chronic inflammation and localized fibrosis, which may predispose patients to progression toward idiopathic pulmonary fibrosis (IPF). However, the biological relationship between benign pulmonary nodules (BPNs) and IPF remains poorly understood. Therefore, this study aims to investigate the shared molecular mechanisms and identify potential biomarkers linking BPN and IPF, with the goal of elucidating the pathogenic transition from BPN to IPF. In this study, microarray data from GEO datasets were systematically analyzed to explore shared molecular mechanisms, immune infiltration characteristics, and potential early intervention strategies linking BPN and IPF. Differential expression analysis, protein-protein interaction (PPI) networks, weighted gene co-expression network analysis (WGCNA), and integrative machine learning approaches identified MME and ANKRD23 as key hub genes associated with the transition from BPN to IPF. Both genes demonstrated strong diagnostic performance, with Area Under the Curve (AUC) values exceeding 0.7, and were significantly correlated with immune cell infiltration, particularly effector memory CD8[+] T cells. Functional enrichment and gene set enrichment analyses indicated that these genes were mainly involved in immune-related processes in BPN, while in IPF, ANKRD23 was linked to cytoskeletal organization and genomic stability, and MME was enriched in profibrotic pathways such as TGF-β signaling. The diagnostic value of these biomarkers was further validated in a bleomycin-induced IPF mouse model using quantitative polymerase chain reaction (qPCR). In addition, drug-gene interaction prediction and molecular docking analyses highlighted several naturally derived compounds with favorable binding affinity and anti-inflammatory properties, among which folic acid, curcumin, and arbutin emerged as promising candidates for safe early intervention. Collectively, these findings identify MME and ANKRD23 as potential biomarkers for early identification of BPN patients at risk of developing IPF and provide a theoretical basis for early diagnosis and targeted preventive strategies.

Dedifferentiated chondrosarcoma is a rare, high-grade malignant bone tumor distinguished by its highly aggressive clinical course. This primary bone malignancy is characterized by the coexistence of a low-grade cartilaginous component and an abrupt transition to a high-grade non-cartilaginous sarcoma. Although pulmonary metastases are common, pleural involvement presenting as malignant effusion is exceedingly rare and poorly documented in cytology literature. We report a case of a 49-year-old man with previously diagnosed pelvic dedifferentiated chondrosarcoma who presented with massive pleural effusion and multiple pulmonary nodules. Cytologic examination of the pleural fluid revealed scattered large pleomorphic malignant cells with moderate cytoplasm, irregular nuclear membranes, and prominent nucleoli, admixed with reactive mesothelial cells. Immunocytochemistry on cell block sections showed tumor cells positive for vimentin and negative for cytokeratin (AE1/AE3), calretinin, S-100, WT1, and IDH1 (R132H). Correlation with the prior histopathologic findings of the iliac bone lesion confirmed metastatic dedifferentiated chondrosarcoma involving the pleural cavity. To the best of our knowledge, this is the first reported case of cytology of DDCS in effusion cytology. This case highlights the exceptional metastatic potential of DDCS and underscores the critical role of cytology, supported by clinicoradiologic and immunocytochemical correlation, in diagnosing rare metastatic presentations in serous effusions.

Psoriasis vulgaris (PV), a chronic immune-mediated inflammatory dermatosis, is associated with a significant burden of systemic comorbidities. Traditional comorbidity research methods struggle to reveal its complex interconnectedness. Based on large-scale retrospective cohort data, we constructed a PV comorbidity network using the Ising model from statistical physics. Weighted network centrality analysis was used to identify core and hub nodes and elucidate shared molecular mechanisms at the multiomics level (nontargeted proteomics and lipid peroxidation metabolomics). Finally, the impact of IL-17A inhibition (IL-17Ai) on PV and atherosclerosis (assessed by carotid Doppler color ultrasound) was evaluated using a prospective intervention study. The Ising model identified atherosclerosis- coronary heart disease (CHD) as the core comorbidity (degree centrality >10), with pulmonary nodules, hypertension, and fatty liver serving as key hub nodes (betweenness centrality >60). Multiomics analysis revealed a core molecular mechanism in PV, involving immune inflammation, oxidative stress, lipid metabolism disorder, and coagulation abnormalities, where the oxidative stress molecule GPX3 acts as a critical hub. Following IL-17Ai intervention, both skin lesions and early atherosclerosis markers significantly improved, accompanied by downregulation of the proinflammatory peripheral blood factor S100A9 and upregulation of anti-inflammatory lipid peroxidation metabolites (e.g., 17(R)-RVD1). This study systematically revealed the modular hierarchical structure of PV comorbidities at the network topology and molecular mechanism levels, confirming the central role of the IL-17 signaling pathway in driving the comorbidity network. This conclusion was further clinically validated by IL-17Ai intervention outcomes. This research provides theoretical and clinical evidence for early identification, prioritized management, and "one drug, multiple targets" therapeutic strategies for treating PV comorbidities.

Pulmonary metastasis remains the leading cause of death in osteosarcoma; however, the pronounced and long-recognized subpleural predominance of metastatic nodules remains mechanistically unexplained. Contemporary "seed-and-soil" and pre-metastatic niche frameworks emphasize microenvironmental conditioning and spatial heterogeneity, but they do not explain why metastatic seeding consistently localizes to the peripheral 1-2 cm of the lung. Likewise, modern mechanical perspectives acknowledge that circulating tumor cells can be retained at multiple sites within the pulmonary microvasculature (including capillaries and pre-capillary arterioles), yet they do not account for a reproducible intra-organ, subpleural spatial bias.

ObjectiveHeat shock protein 90α is involved in tumorigenesis; however, its concentration-dependent relationship and threshold with pulmonary nodules remain unclear. This study aimed to explore the association and critical threshold of plasma heat shock protein 90α levels with the prevalence of pulmonary nodules in males aged ≥40 years.MethodsThis study included 968 male participants (aged ≥40 years) undergoing low-dose computed tomography and plasma heat shock protein 90α measurement from January 2022 to June 2024. Restricted cubic splines and segmented logistic regression were used to identify were the inflection point of the concentration-response relationship. Multivariable models were adjusted for age, smoking index, high-density lipoprotein cholesterol, triglycerides, and family history of lung cancer.ResultsPulmonary nodules were detected in 40.2% (389/968) of participants. The prevalence of pulmonary nodules increased from 28.7% to 51.0% across heat shock protein 90α quartiles (P for trend <0.001). A threshold was identified at 89.5 ng/mL (95% confidence interval: 87.2-93.1). Above this level, each 1 ng/mL increase in the heat shock protein 90α levels was associated with a 3% higher prevalence of pulmonary nodules (adjusted odds ratio = 1.03, 95% confidence interval: 1.01-1.05). The adjusted odds ratio for the highest versus lowest quartile was 1.88 (95% confidence interval: 1.26-2.80).ConclusionsElevated plasma heat shock protein 90α levels are associated with an increased prevalence of pulmonary nodules in asymptomatic males aged ≥40 years, with a critical threshold of 89.5 ng/mL.

Lung nodule evaluation is a vital practice in pulmonary medicine. While biopsy remains the diagnostic gold standard, it carries procedural risks. In regions endemic for fungal disease, low-cost, noninvasive testing may help reduce unnecessary procedures.

Choriocarcinoma is a rare and aggressive gestational trophoblastic neoplasm that often arises after a molar pregnancy or miscarriage and is characterized by rapid metastatic potential. Diagnosis is typically based on clinical presentation, history of antecedent pregnancy, markedly elevated β-hCG levels, and supportive imaging and histopathologic findings. Early recognition and prompt initiation of multi-agent chemotherapy are crucial, as they markedly improve survival, with remission achievable even in advanced disease. We report the case of a 24-year-old woman who presented with persistent vaginal bleeding, severe pelvic pain, and progressive dyspnea one month after a molar pregnancy treated with dilation and curettage. Examination revealed pallor and mild abdominal tenderness. Laboratory studies showed a β-hCG level >250,000 mIU/mL (reference range: 0-5 mIU/mL) and profound anemia with a hemoglobin of 2 g/dL (reference range: 12-15.3 g/dL). Contrast-enhanced abdominal and pelvic computed tomography demonstrated metastatic lesions in the liver and gastrointestinal tract, while chest CT revealed multiple pulmonary nodules consistent with metastases. The patient was promptly initiated on multi-agent chemotherapy, resulting in normalization of β-hCG levels after several treatment cycles. This case highlights the importance of vigilant follow-up in patients with molar pregnancies and persistently elevated β-hCG, as timely diagnosis and treatment can lead to curative outcomes despite widespread metastasis.

Background: Granulomatosis with polyangiitis (GPA) is an antineutrophil cytoplasmic antibody (ANCA)-associated necrotizing vasculitis primarily affecting small and medium-sized vessels. The typical presentation commonly includes upper and/or lower respiratory tract and renal involvement. GPA has a particularly strong association with proteinase-3 (PR3) ANCA. Though well defined, GPA may be clinically difficult to recognize, particularly in early disease. Initial presentations may include nonspecific symptoms, including but not limited to fatigue, fever, and sinus congestion or sinusitis, which may be mistaken for infection. Though initial ANCA testing is useful, it is not definitive as early stages of disease may be negative, thus delaying diagnosis; Clinical Significance: This case highlights the importance of including GPA in the differential diagnosis of patients with unremitting upper or lower respiratory and constitutional symptoms despite negative ANCA testing. Though atypical, GPA cases may lack renal involvement and even have negative ANCA serologies, leading to a delay in diagnosis and increased morbidity. ANCA positivity can be as low as 60% in limited GPA cases, and less than 20% of individuals have renal involvement at presentation. If GPA suspicion is high, repeat testing and biopsy are warranted; Case Presentation: A woman in her 50s initially presented to the emergency department with recurrent/persistent fever with nonspecific sinus symptoms that remained unresolved despite multiple outpatient treatments and tests. Infectious work-up was negative. She was found to have multiple pulmonary nodules on various scans. Initial testing on admission was unremarkable or nondiagnostic, including anti-neutrophil cytoplasmic antibody (ANCA) serologies. The patient's hospital course was complicated by acute hypoxic respiratory failure with distributive shock during bronchoscopy. Repeat serological testing was positive for PR3-ANCA, and lung biopsy demonstrated necrotizing granulomatous vasculitis consistent with a diagnosis of granulomatosis with polyangiitis (GPA). The patient demonstrated clinical improvement with avacopan, glucocorticoids, and rituximab; Conclusions: The diagnosis of GPA should be suspected in all patients with nonspecific constitutional symptoms along with clinical evidence of upper/lower respiratory tract involvement, regardless of renal function. Physicians with a strong suspicion of an autoimmune disease, such as GPA, should utilize a thorough clinical history, physical exam, and other labs in the setting of a negative autoimmune marker and/or negative imaging. Clinical judgment is required to not rule out GPA despite a negative workup when other more serious causes have been excluded, as the diagnosis may be life-threatening.

We report the case of a 64-year-old man with chronic liver disease who presented with abdominal discomfort, anorexia, and progressive weight loss, initially suspected to have hepatocellular carcinoma based on a large hepatic mass lacking definitive radiologic hallmarks. Multiphase CT demonstrated heterogeneous peripheral enhancement without classical washout, while thoracic imaging revealed numerous bilateral pulmonary nodules surrounded by ground-glass halos, indicating hemorrhagic metastases. These thoracic findings proved pivotal in directing diagnostic suspicion toward a vascular neoplasm. Ultrasound-guided liver biopsy confirmed high-grade hepatic angiosarcoma, with tumor cells showing ERG positivity and weak CD31 expression, and lacking hepatocellular or epithelial markers. The patient experienced rapid clinical deterioration with intrapulmonary hemorrhage, multiorgan dysfunction, and refractory shock, culminating in death shortly after diagnosis. This case highlights the diagnostic complexity of hepatic angiosarcoma and underscores the importance of integrating thoracic imaging with hepatic evaluation, particularly when liver findings are atypical.