ObjectiveTo investigate the clinical features, diagnosis, treatment and prognosis of pulmonary tumor thrombotic microangiopathy (PTTM).MethodsA patient with PTTM was reported. Literatures about PTTM searched by WanFang databases and PubMed were reviewed for its clinical characteristics.ResultsA 62-year-old female was admitted with chief complaint of dry cough, dyspnea and hemoptysis. Progressive dyspnea, pulmonary hypertension and hypoxemia occurred during hospitalization. Computed tomography angiography (CTA) of the lung excluded pulmonary embolism. Peripheral blood appearing a large number of late erythroblasts and erythrocyte debris and progressively decreasing platelets suggested that the patient suffer from thrombotic microvascular disease. CT showed widely metastatic lesions at the vertebrae and sternum. On the basis of above clinical characteristics, PTTM was diagnosed clinically. Although the patient accepted respiratory support therapy, anticoagulation therapy and resuscitation, she still died 5 days later after hospitalization. Literatures about PTTM with complete clinical information were reviewed. A total of 92 PTTM cases were reviewed and the main reasons of these patients admitted were progressive dyspnea and chronic cough. During hospitalization, they all suffered varying degrees of hypoxia, while radiological findings of the lungs lack specificity. No abnormal sighs were found by lung CTA. The results of ultrasonic cardiography or the Swan–Ganz catheter indicated varying degrees of pulmonary hypertension, some patients were proved with disseminated intravascular coagulation and/or microangiopathic hemolytic anemia. The definite diagnosis of PTTM depended on the histologic evidence which were often obtained from post-mortem examination, because many patients couldn’t tolerate the lung biopsy due to rapid aggravation. The treatment of PTTM included respiratory support therapy, anticoagulation therapy, antipulmonary hypertension and the chemotherapy of primary or metastatic tumour. The prognosis of PTTM was poor and almost all of the patients died in a short term, ranged from 48 hours to 3 months.ConclusionIf a patient with a history of cancer or evidence of cancer metastasis has hypoxemia and pulmonary hypertension but without abnormal lung CTA signs, PTTM should be considered.
ObjectivesTo detect expressions of trefoil factor 1 (TFF1) and TFF3 in the mice with acute allergic airway disease (AAD) after different interventions, and explore primitively the effect of recombinant TFF3 on airway inflammation and mucous secretion.MethodsForty BALB/c mice were randomly divided into 5 groups, each group with 8 mice, ie. a normal saline control group (group A), an AAD group (group B), a budesonide intervention group (group C), a recombinant TFF3 intervention group (group D), and a budesonide+recombinant TFF3 intervention group (group D). The BALB/c mice were sensitized and challenged with ovalbumin to induce AAD. Lung tissue sections were stained with hematoxylin-eosin staining for assessment of airway inflammation, and immunohistochemistry was used for detecting TFF1/TFF3 expression in the airway. Alcian blue stain was applied to determine mucous secretion.ResultsAirway inflammation score and airway mucous secretion: Group B was significantly more than group A (P<0.01); Group C was less than group B (P<0.05), and there was no significant difference between group D and group B (P>0.05); There was no significant difference between group C and group E (P>0.05). Expression of TFFs: TFF1 and TFF3 were expressed in epithelial cells, goblet cells and submucosal gland cells of bronchi and bronchioles in all groups; The expressions of TFF1 and TFF3 in group B were significantly higher than those in group A (P<0.01), while the expressions of TFF1 and TFF3 in group C were lower than those in group B (P<0.05). TFF1 expression in airway epithelium was positively correlated with inflammatory score (r=0.876, P=0.000) and mucin expression (r=0.807, P=0.000). TFF3 level was positively correlated with inflammatory score (r=0.654, P=0.006) and mucin expression (r=0.666, P=0.005).ConclusionsOvalbumin-induced acute allergic airway inflammation significantly increases TFF1/TFF3 expression. Intranasal TFF3 treatment may not influence airway inflammation and mucus secretion. Inhaled corticosteroids to some extent inhibit expressions of TFF1 and TFF3, simultaneously suppress airway inflammation and mucus secretion in the mouse model of acute AAD .
Objective To reveal the differences in gene expression levels between Th2-driven classical asthma (CA) and Th2-driven cough variant asthma (CVA) in order to investigate the pathogenesis of asthma further. Methods Clinical data were collected from asthmatic patients in the Department of Respiratory and Critical Care of Sichuan Provincial People's Hospital from June 1, 2018, to December 31, 2019. The healthy control (HC) group was healthy adults from the physical examination center. Gene expression of peripheral blood mononuclear cells (PBMCs) in the CA group, CVA group, and HC group was determined by full-length transcriptome sequencing. Differential genes were screened by GO, KEGG analysis, and protein-protein interaction (PPI) network analysis. The results of interaction network analysis were visualized by Cytoscape. Finally, the candidate genes were verified by real-time quantitative polymerase chain reaction (RT-PCR). ResultsA total of 31 patients with asthma were included in the study, including 20 patients in the CA group and 11 patients in the CVA group. According to serum total IgE > 60 IU/mL and fractional exhaled nitric oxide (FeNO) > 40 ppb as the screening condition, 9 cases of Th2-driven CA and 5 cases of Th2-driven CVA were screened for analysis. Gene expression analysis showed 300 differentially expressed genes between the Th2-driven CA group and the Th2-driven CVA group, among which 155 genes were up-regulated, and 145 were down-regulated. GO enrichment analysis showed that differential genes were mainly enriched in drug response, nitrogen compound biosynthesis, cytoplasmic matrix, protein binding, ATP binding, etc. KEGG pathway analysis showed that differential genes were mainly concentrated in 2-oxy-carboxylic acid metabolism and cytotoxic signaling pathways mediated by natural killer cells. PPI analysis revealed extensive protein interactions between different genes. Ten candidate genes were screened for RT-PCR verification and finally found that CLU, GZMB, PPBP, PRF1, PTGS1, and TMSB4X were significantly differentially expressed between the Th2-driven CA group and the Th2-driven CVA group. Conclusions Asthma's occurrence results from the interaction of many genes and pathways. CLU, GZMB, PPBP, PRF1, PTGS1, and TMSB4X genes may be essential in developing Th2-driven CVA to Th2-driven CA.