BMC Pulmonary Medicine最新文献

Background: Alterations in the central nervous system of patients with asthma have been reported. However, the intricate relationship between asthma and cortical structure remains unclear and challenging to determine. To determine the association between asthma and changes in brain cortical structure, we conducted a two-sample Mendelian randomization study.

Methods: Genome-wide association studies summary data of asthma in 408,442 participants from the UK Biobank were used to identify genetically predicted asthma. Uncorrelated (r² < 0.001) single nucleotide polymorphisms (SNPs) were selected as instrumental variants. Cortical thickness and surface area were obtained from 51,665 patients from the ENIGMA Consortium as outcomes in this study. Inverse-variance weighted was employed as the primary estimate whereas MR Pleiotropy RESidual Sum and Outlier, MR-Egger, and weighted median were used to detect heterogeneity and pleiotropy.

Results: At the global level, no statistically significant association was observed between asthma and global surface area or cortical thickness. In region-specific analyses, nominal significant associations were identified between asthma and the surface area of the parahippocampal gyrus, both with global weighting (β = 5.07 mm², 95% CI: 0.80 to 9.33, P = 0.0198) and without global weighting (β = 5.92 mm², 95% CI: 0.77 to 11.07, P = 0.0242), as well as with the cortical thickness of the caudal anterior cingulate gyrus, both with global weighting (β = -0.01 mm, 95% CI: -0.02 to -0.001, P = 0.0243) and without global weighting (β = -0.01 mm, 95% CI: -0.02 to -0.001, P = 0.0259). However, none of these associations remained statistically significant after adjustment for multiple comparisons.

Conclusions: This two-sample Mendelian randomization analysis did not identify a statistically significant association between asthma and global cortical metrics. While nominal associations were observed between asthma and changes in parahippocampal and caudal anterior cingulate, these findings did not remain significant after correction for multiple comparisons and should be interpreted as exploratory. Further research is needed to elucidate potential neuroanatomical alterations associated with asthma.

Objective: To explore the clinical and pathological characteristics and the diagnosis and differential diagnosis of primary pulmonary follicular dendritic cell sarcoma (FDCS).

Methods: Clinical and pathological data from 2 cases of primary pulmonary FDCS were collected, and sections were prepared for haematoxylin-eosin (H&E) staining, immunohistochemistry (IHC) staining, and in situ hybridization (ISH). The relevant literature was reviewed. In both cases, the lesions presented as pulmonary masses.

Results: The tumour cells demonstrated diffuse sheets, delicate eosinophilic cytoplasmic staining, oval nuclei and small nucleoli, and occasionally showing multinucleated or giant cells in some areas. Another important histological feature was the abundant infiltration of small lymphocytes among the tumour cells. The tumourcells were positive for one or more follicular dendritic cell (FDC) markers, including CD21, CD23, CD35 and podoplanin (D2-40). ISH revealed negative EBER expression. Both patients underwent surgical resection, and no recurrence or metastasis was observed.

Conclusion: FDCS has a unique histological morphology and immunophenotype for FDCS. It is rare for FDCS to occur in the lungs. However, owing to the lack of experience among doctors and the limitations of small biopsy specimens, FDCS can easily be misdiagnosed as lung cancer. When tumour cells exhibit the above histological features, additional immunostaining for FDC markers should be performed. The Clinical Trial Number is ChiCTR2400090730 and Reg Date is October 12, 2024.