The efficacy and safety of continuous intravenous infusion of rh-endostatin combined with platinum-based doublet chemotherapy for advanced non-small-cell lung cancer.

BACKGROUND: Platinum-based doublet chemotherapy is commonly used in the treatment of non-small cell lung cancer (NSCLC). A growing body of evidence indicates that incorporating antiangiogenic agents into platinum-based chemotherapy may enhance the survival outcomes for NSCLC patients. However, the optimal administration protocol for intravenous recombinant human endostatin (rh-endostatin), an antiangiogenic agent, remains uncertain at present. AIM: This study aims to investigate the efficacy and safety of 5-d continuous intravenous infusion of rh-endostatin in combination with chemotherapy for patients with advanced NSCLC. The predictive biomarkers for this treatment regimen were further probed. METHODS: This prospective, single-arm multicenter study enrolled a total of 48 patients with advanced NSCLC who were histologically or cytologically confirmed but had not received any prior treatment from January 2021 to December 2022. Prior to the chemotherapy, these patients received a continuous intravenous infusion of rh-endostatin (210 mg) over a period of 120 h, using an infusion pump. The chemotherapy regimen included a combination of platinum with either pemetrexed or paclitaxel, given in 21-day cycles. The primary endpoint of the study was median progression-free survival (mPFS), and the secondary endpoints included median overall survival (mOS), objective response rate (ORR), disease control rate (DCR), and assessment of adverse events (AEs). RESULTS: The mPFS was 6.5 months (95% confidence interval (CI): 3.8-9.1 m) while the mOS was 12.3 months (95% CI: 7.6-18.5 m). The ORR and DCR was 52.1% and 75.0%, respectively. Leukopenia (52.1%), anemia (33.3%), and thrombocytopenia (20.8%) were the most common adverse effects and these toxicities were deemed acceptable and manageable. In addition, a correlation was noted between elevated serum carcinoembryonic antigen (CEA) levels and decreased PFS and OS. CONCLUSIONS: The incorporation of a 5-day continuous intravenous infusion of rh-endostatin into platinum-based doublet chemotherapy has demonstrated both safety and efficacy in the treatment of advanced NSCLC. Furthermore, the baseline serum levels of CEA may potentially function as a predictor for the efficacy of rh-endostatin when combined with chemotherapy in NSCLC patients. CLINICALTRIALS: GOV: NCT05574998.

Discovery of Multiple Effects of Reactive Oxygen Species on Lung Adenocarcinoma at the Single-cell and Bulk Tissue Levels.

BACKGROUND: Reactive oxygen species (ROS) are potential targets for treating malignant tumors. AIMS: The aim of this study was to probe into the mechanisms of disease development and treatment in lung adenocarcinoma (LUAD). OBJECTIVE: This study investigated the impact of ROS on the progression of LUAD at different transcriptomic levels and analyzed key molecules involved in the regulation of LUAD. METHODS: Single-cell RNA-seq (scRNA-seq) data of LUAD were clustered and annotated to determine cell types. Scissor cells based on LUAD bulk transcriptome and epithelial scRNA-seq data were used to classify subsets associated with ROS phenotypes. Least absolute shrinkage and selection operator (LASSO) and stepwise multivariate regression analyses were performed between the Scissor-positive and Scissor-negative epithelial cells to select key differentially expressed genes (DEGs) for developing a ROS-related signature. RESULTS: The ROS score was significantly negatively correlated with the overall survival (OS) of LUAD. Seven cell types from the LUAD tissues were identified. The ROS-related gene signature was significantly correlated with metabolism, tumor microenvironment (TME) indicators, and the half-maximal inhibitory concentration (IC50) values of 10 drugs. The gene signature was verified as an independent indicator for LUAD prognosis. CONCLUSION: The current study provided novel insights into the impact of ROS on LUAD pathology at both single-cell and bulk-tissue levels, facilitating the prognostic evaluation and drug therapy development for patients with LUAD.

Multiple pulmonary cavities in an immunocompetent patient: a case report and literature review.

Legionella pneumonia (LP) is a relatively uncommon yet well-known type of atypical community-acquired pneumonia (CAP). It is characterized by a rapid progression to severe pneumonia and can be easily misdiagnosed. In most patients, chest computed tomography (CT) showed patchy infiltration, which may progress to lobar infiltration or even lobar consolidation. While pulmonary cavities are commonly observed in immunocompromised patients with LP, they are considered rare in immunocompetent individuals. Herein, we present a case of LP in an immunocompetent patient with multiple cavities in both lungs. Pathogen detection was performed using metagenomic next-generation sequencing (mNGS). This case highlights the unusual radiographic presentation of LP in an immunocompetent patient and emphasizes the importance of considering LP as a possible diagnosis in patients with pulmonary cavities, regardless of their immune status. Furthermore, the timely utilization of mNGS is crucial for early pathogen identification, as it provides multiple benefits in enhancing the diagnosis and prognosis of LP patients.

Machine learning-based radiomics strategy for prediction of acquired EGFR T790M mutation following treatment with EGFR-TKI in NSCLC.

The epidermal growth factor receptor (EGFR) Thr790 Met (T790M) mutation is responsible for approximately half of the acquired resistance to EGFR-tyrosine kinase inhibitor (TKI) in non-small-cell lung cancer (NSCLC) patients. Identifying patients at diagnosis who are likely to develop this mutation after first- or second-generation EGFR-TKI treatment is crucial for better treatment outcomes. This study aims to develop and validate a radiomics-based machine learning (ML) approach to predict the T790M mutation in NSCLC patients at diagnosis. We collected retrospective data from 210 positive EGFR mutation NSCLC patients, extracting 1316 radiomics features from CT images. Using the LASSO algorithm, we selected 10 radiomics features and 2 clinical features most relevant to the mutations. We built models with 7 ML approaches and assessed their performance through the receiver operating characteristic (ROC) curve. The radiomics model and combined model, which integrated radiomics features and relevant clinical factors, achieved an area under the curve (AUC) of 0.80 (95% confidence interval [CI] 0.79-0.81) and 0.86 (0.87-0.88), respectively, in predicting the T790M mutation. Our study presents a convenient and noninvasive radiomics-based ML model for predicting this mutation at the time of diagnosis, aiding in targeted treatment planning for NSCLC patients with EGFR mutations.

IgG4-related diseases involving pleura: a case report and literature review.

Immunoglobulin G4-related disease (IgG4-RD) is a systemic fibro-inflammatory disease with the potential to involve virtually all organs, including the pancreas, kidneys, lungs, and pleura, amongst others. IgG4-RD pleural involvement may cause diverse complications such as pleural effusion, pleural thickening, pleural nodules, and additional lesions, which can be presented in many clinical diseases. However, isolated cases of pleurisy are still rare in IgG4-RD. We report a 72-year-old patient who was admitted to our hospital with cough, expectoration, and fatigue. He had a right-sided pleural effusion, and the tissue evaluation of the pleural biopsy by medical thoracoscopy met the diagnostic criteria of IgG4-RD. His serum IgG4 levels were elevated and he was finally diagnosed with IgG4-RD pleural involvement. He was subsequently started on prednisone 40 mg daily and his pleural effusion was almost disappeared 2 weeks later. This paper reported a case of IgG4-RD who had exclusive involvement of the pleura and highlighted the significance of considering IgG4-RD as a potential diagnosis in patients with unexplained pleural effusion.

Semaphorin 7a aggravates TGF-ß1-induced airway EMT through the FAK/ERK1/2 signaling pathway in asthma.

Background: TGF-ß1 can induce epithelial-mesenchymal transition (EMT) in primary airway epithelial cells (AECs). Semaphorin7A (Sema7a) plays a crucial role in regulating immune responses and initiating and maintaining transforming growth factor ß1 TGF-ß1-induced fibrosis. Objective: To determine the expression of Sema7a, in serum isolated from asthmatics and non-asthmatics, the role of Sema7a in TGF-ß1 induced proliferation, migration and airway EMT in human bronchial epithelial cells (HBECs) in vitro. Methods: The concentrations of Sema7a in serum of asthmatic patients was detected by enzyme-linked immunosorbent assay (ELISA). The expressions of Sema7a and integrin-ß1 were examined using conventional western blotting and real-time quantitative PCR (RT-PCR). Interaction between the Sema7a and Integrin-ß1 was detected using the Integrin-ß1 blocking antibody (GLPG0187). The changes in EMT indicators were performed by western blotting and immunofluorescence, as well as the expression levels of phosphorylated Focal-adhesion kinase (FAK) and Extracellular-signal-regulated kinase1/2 (ERK1/2) were analyzed by western blot and their mRNA expression was determined by RT-PCR. Results: We described the first differentially expressed protein of sema7a, in patients with diagnosed bronchial asthma were significantly higher than those of healthy persons (P<0.05). Western blotting and RT-PCR showed that Sema7a and Integrin-ß1 expression were significantly increased in lung tissue from the ovalbumin (OVA)-induced asthma model. GLPG0187 inhibited TGF-ß1-mediated HBECs EMT, proliferation and migration, which was associated with Focal-adhesion kinase (FAK) and Extracellular-signal-regulated kinase1/2 (ERK1/2) phosphorylation. Conclusion: Sema7a may play an important role in asthma airway remodeling by inducing EMT. Therefore, new therapeutic approaches for the treatment of chronic asthma, could be aided by the development of agents that target the Sema7a.

Pleural involvements in pulmonary sarcoidosis: A case report and review of the literature.

As a chronic and multisystemic granulomatosis of unknown origin, sarcoidosis can affect multiple organs throughout the body with variable progression and prognosis. Sarcoidosis may present with a battery of symptoms and signs, such as dyspnea, non-productive cough, uveitis, and erythema nodosum. Although the lungs and mediastinal lymph nodes are almost affected in sarcoidosis, involvements of the pleurae remain uncommon. Herein, we report a case of sarcoidosis with both pleural effusions and pleural nodules as confirmed by thoracoscopic pleural biopsy.

IL-27 attenuates airway inflammation and epithelial-mesenchymal transition in allergic asthmatic mice possibly via the RhoA/ROCK signalling pathway

Background: Asthma is an airway disease characterized by airflow limitation and various additional clinical manifestations. Repeated inflammatory stimulation of the airways leads to epithelial-mesenchymal transition (EMT) which aggravates subepithelial fibrosis during the process of airway remodelling and enhances resistance to corticosteroids and bronchodilators in refractory asthma. There is growing evidence that IL-27 modulates airway remodelling, however, the molecular mechanisms involving IL-27 and EMT are poorly understood. The objective of this study was to investigate the effects of IL-27 on ovalbumin (OVA)-challenged asthmatic mice in vivo and TGF-ß1-induced EMT in 16HBE cells in vitro. Methods: Airway inflammation, mucus secretion, and collagen deposition were analysed by conventional pathological techniques. The ratio of Th17 and Th9 cells in the spleen of mice was measured using flow cytometry, ELISA was performed for cytokine analysis to identify EMT-related molecules and signalling pathways, and other molecular and cellular techniques were used to explore the functional mechanism involving IL-27 and EMT. Results: Airway inflammation in asthmatic mice was significantly alleviated by IL-27, with downregulation of RhoA and ROCK, upregulation of E-cadherin, and a decrease of vimentin and α-SMA expression, compared to asthmatic mice. Moreover, the frequency of Th17 and Th9 cells in the spleen of asthmatic mice decreased following treatment with IL-27. In TGF-ß1-induced 16HBE cells, the addition of IL-27 was shown to inhibit EMT, based on the expression of E-cadherin, vimentin, and α-SMA. Conclusion: Intranasal administration of IL-27 attenuates airway inflammation and EMT in a murine model of allergic asthma possibly by downregulating the RhoA/ROCK signalling pathway.

Interleukin­27 ameliorates allergic asthma by alleviating the lung Th2 inflammatory environment.

Interleukin (IL)­27 can inhibit the differentiation of Th2 cells and plays a role in the development of asthma. However, whether the therapeutic administration of IL­27 in a mouse model of asthma can inhibit allergic responses remains a matter of debate. Additionally, the mechanisms through which IL­27 ameliorates inflammatory responses in asthma are not yet fully understood. Thus, the aim of the present study was to examine the effects of IL­27 on asthma using a mouse model and to elucidate the underlying mechanisms. For this purpose, mice received an intranasal administration of IL­27 and the total and differential cell counts, levels of cytokines and type 1 regulatory T (Tr1) cells in the lungs were detected. The protein and mRNA levels of signal transducer and activator of transcription (STAT)1 and STAT3 were analyzed and airway remodeling was assessed. The results indicated that IL­27 did not ameliorate airway inflammation, airway hyperresponsiveness, and airway remolding when administrated therapeutically. Preventatively, the administration of IL­27 decreased the concentrations of Th2 cytokines and increased the number of Tr1 cells. The protein and mRNA levels of STAT1 and STAT3 were increased. Taken together, these findings demonstrate that the prophylactic administration of IL­27 ameliorates asthma by alleviating the lung Th2 inflammatory environment through the restoration of both the STAT1 and STAT3 pathways. IL­27 may thus prove to be useful as a novel agent for the prevention of asthma.

Machine Learning-Based Radiomics for Prediction of Epidermal Growth Factor Receptor Mutations in Lung Adenocarcinoma.

Identifying an epidermal growth factor receptor (EGFR) mutation is important because EGFR tyrosine kinase inhibitors are the first-line treatment of choice for patients with EGFR mutation-positive lung adenocarcinomas (LUAC). This study is aimed at developing and validating a radiomics-based machine learning (ML) approach to identify EGFR mutations in patients with LUAC. We retrospectively collected data from 201 patients with positive EGFR mutation LUAC (140 in the training cohort and 61 in the validation cohort). We extracted 1316 radiomics features from preprocessed CT images and selected 14 radiomics features and 1 clinical feature which were most relevant to mutations through filter method. Subsequently, we built models using 7 ML approaches and established the receiver operating characteristic (ROC) curve to assess the discriminating performance of these models. In terms of predicting EGFR mutation, the model derived from radiomics features and combined models (radiomics features and relevant clinical factors) had an AUC of 0.79 (95% confidence interval (CI): 0.77-0.82), 0.86 (0.87-0.88), respectively. Our study offers a radiomics-based ML model using filter methods to detect the EGFR mutation in patients with LUAC. This convenient and low-cost method may be of help to noninvasively identify patients before obtaining tumor sample for molecule testing.

IL­27 suppresses airway inflammation, hyperresponsiveness and remodeling via the STAT1 and STAT3 pathways in mice with allergic asthma.

Type 2 cytokine­associated immunity may be involved in the pathogenesis of allergic asthma. Although interleukin 27 (IL­27) has been reported as an initiator and suppressor of T­helper 1 (Th1) and T­helper 2 (Th2) responses, respectively, its effects on the development of asthma remain unclear. In the present study, mice were induced and challenged with ovalbumin and received subsequent intranasal administration of IL­27. Total and differential cell counts were determined from Wright­Giemsa­stained cytospins, whereas the cytokine levels were detected using ELISA. In addition, the expression levels of signal transducer and activator of transcription (STAT) 1, STAT3, GATA­binding protein­3 (GATA3) and T­bet (T­box transcription factor) were analyzed in T cells by western blot analysis. Their corresponding mRNA expression levels were determined by quantitative PCR. Airway remodeling was assessed by conventional pathological techniques. The results indicated that intranasal administration of IL­27 ameliorated airway inflammation and hyperresponsiveness in an acute model of asthma. Furthermore, IL­27 prevented airway remodeling in a chronic model of asthma. Following administration of IL­27, the mRNA expression levels of STAT1 and T­bet were upregulated, while those of GATA3 were downregulated. Moreover, the phosphorylation levels of STAT1 and STAT3 were increased. Taken together, these findings demonstrated that intranasal administration of IL­27 ameliorated Th2­related allergic lung inflammation and remodeling in mouse models of asthma by repairing both the STAT1 and STAT3 pathways.

Racial and Ethnic Disparities in Influenza Vaccination among Adults with Chronic Medical Conditions Vary by Age in the United States.

BACKGROUND: People living with chronic health conditions exhibit higher risk for developing severe complications from influenza according to the Centers for Diseases Control and Prevention. Although racial and ethnic disparities in influenza vaccination have been documented, it has not been comprehensively determined whether similar disparities are present among the adult population with at least one such condition. OBJECTIVE: To study if racial and ethnic disparities in relation to influenza vaccination are present in adults suffering from at least one chronic condition and if such inequalities differ between age groups. METHODS: The Medical Expenditure Panel Survey (2011-2012) was used to study the adult population (age ≥18) who had at least one chronic health condition. Baseline differences in population traits across racial and ethnic groups were identified using a chi-square test. This was conducted among various age groups. In addition, survey logistic regression was utilized to produce odds ratios of receiving influenza vaccination annually between racial and ethnic groups. RESULTS: The total sample consisted of 15,499 adults living with at least one chronic health condition. The numbers of non-Hispanic whites (whites), non-Hispanic blacks (blacks), and Hispanics were 8,658, 3,585, and 3,256, respectively. Whites (59.93%) were found to have a higher likelihood of self-reporting their receipt of the influenza vaccine in comparison to the black (48.54%) and Hispanic (48.65%) groups (P<0.001). When examining persons aged 50-64 years and ≥65 years, it was noted that the black (54.99%, 62.72%) and Hispanic (53.54%, 64.48%) population had lower rates of influenza vaccine coverage than the white population (59.22%, 77.89) (both P<0.0001). No significant differences between whites and the blacks or Hispanics were found among the groups among adults between 18 and 49 inclusive (P>0.05). After controlling for patient characteristics, the difference in influenza vaccine coverage between whites and the minority groups were no longer significant for adults aged 50-64 years. However, the difference were still statistically significant for those aged ≥65 years. CONCLUSIONS: In the United States, there are significant disparities in influenza vaccination by race and ethnicity for adults over 65 years with at least one chronic health condition. Future research is needed to help develop more targeted interventions to address these issues and improve influenza vaccination rates.

Racial and ethnic disparities in meeting MTM eligibility criteria among patients with asthma.

BACKGROUND: Asthma is one of the most frequently targeted chronic diseases in the medication therapy management (MTM) programs of the Medicare prescription drug (Part D) benefits. Although racial and ethnic disparities in meeting eligibility criteria for MTM services have been reported, little is known about whether there would be similar disparities among adults with asthma in the United States. METHODS: Adult patients with asthma (age ≥ 18) from Medical Expenditure Panel Survey (2011-2012) were analyzed. Bivariate analyses were conducted to compare the proportions of patients who would meet Medicare MTM eligibility criteria between non-Hispanic Blacks (Blacks), Hispanics and non-Hispanic Whites (Whites). Survey-weighted logistic regression was performed to adjust for patient characteristics. Main and sensitivity analyses were conducted to cover the entire range of the eligibility thresholds used by Part D plans in 2011-2012. RESULTS: The sample included 4,455 patients with asthma, including 2,294 Whites, 1,218 Blacks, and 943 Hispanics. Blacks and Hispanics had lower proportions of meeting MTM eligibility criteria than did Whites (P < 0.001). According to the main analysis, Blacks and Hispanics had 36% and 32% lower, respectively, likelihood of MTM eligibility than Whites (odds ratio [OR]: 0.64, 95% confidence interval [CI]: 0.45-0.90; OR: 0.68, 95% CI: 0.47-0.98, respectively). Similar results were obtained in sensitivity analyses. CONCLUSIONS: There are racial and ethnic disparities in meeting Medicare Part D MTM eligibility criteria among adult patients with asthma. Future studies should examine the implications of such disparities on health outcomes of patients with asthma and explore alternative MTM eligibility criteria.

Alterations of pulmonary function in patients with inflammatory bowel diseases.

AIM: The aim of this study was to investigate the alterations of pulmonary function tests (PFTs) and their relationship with disease activity in inflammatory bowel diseases (IBDs). METHODS: Sixty-four IBD patients (31 Crohn's disease [CD] and 33 ulcerative colitis [UC]) and thirty healthy individuals (controls) were studied with regard to the following parameters of PFTs: Forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), their ratio, mid-forced expiratory flow of 25-75% (FEF 25-75), residual volume, total lung capacity, and diffusing capacity of the lung for carbon monoxide (DLCO). The disease activity was calculated using the Crohn's Disease Activity Index for CD and Mayo Clinic Score for UC. Correlation analysis was performed between disease activity and sputum cytology and PFTs. RESULTS: Nineteen of the 31 CD patients (61.29%) and 17 of the 33 UC patients (51.52%) but none of the controls showed at least one abnormal PFTs (P < 0.05). Compared with controls, both CD and UC patients exhibited a significant reduction in FEV1 (P < 0.05), FVC (P < 0.05), FEF 25-75 (P < 0.05), and DLCO (P < 0.05). The majority with decreased measurements of PFTs were in the active phase of diseases (P < 0.05). IBD activity scores correlated negatively with some parameters of PFTs and positively with lymphocytosis and eosinophilia of sputum (P < 0.05). CONCLUSIONS: Pulmonary function disorders are significantly common in IBD patients. The impairment in active disease is significantly greater than in remission.

Primary extragastrointestinal stromal tumor of the pleura: A case report.

Gastrointestinal stromal tumors (GISTs) are the most common type of mesenchymal tumor of the gastrointestinal tract. The stomach and small intestine are the most common sites of occurrence. GISTs are mesenchymal neoplasms originating from the interstitial cells of Cajal (ICCs), and are characterized by positivity for cluster of differentiation (CD) 117, also known as proto-oncogene c-Kit. While the majority of GISTs develop in the alimentary tract, in rare cases they may also be found in extragastrointestinal tissues. This type of GIST is known as an extragastrointestinal stromal tumor (EGIST). Despite the fact that EGISTs have been reported in the mesentery, omentum and retroperitoneum, primary intrathoracic EGISTs, arising from the pleura or lungs, are rare. The patient presented in the current study was a 40-year-old man, who presented with a cough and pyrexia, with pleural effusion on the left side. Multiple nodules throughout the parietal pleura were identified by thoracoscopy and a diagnosis of primary GIST of pleura was established, since they were positive for CD117 and discovered on GIST-1 and there was no evidence of gastrointestinal tumors. Subsequently, the patient was administered with imatinib and had no signs of disease recurrence 2 years later.

A case of pulmonary sarcoidosis with endobronchial nodules.

Sarcoidosis is a multisystemic disorder of unknown cause that is characterized pathologically by noncaseating granulomas and predominantly affects the lungs and the lymphatic system, especially intrathoracically. Diagnosis is based on the association of a compatible clinical and radiological presentation, the presence of characteristic histopathological lesions and the exclusion of other potential causes of granuloma. Although the lungs and mediastinal lymph nodes are almost involved, endobronchial nodular lesions of sarcoidosis with lung involvements are rare. We report a case of sarcoidosis with lung involvements and endobronchial nodules as confirmed by bronchial biopsy.

Pulmonary manifestations of inflammatory bowel disease.

Extraintestinal manifestations of inflammatory bowel disease (IBD) are a systemic illness that may affect up to half of all patients. Among the extraintestinal manifestations of IBD, those involving the lungs are relatively rare and often overlooked. However, there is a wide array of such manifestations, spanning from airway disease to lung parenchymal disease, thromboembolic disease, pleural disease, enteric-pulmonary fistulas, pulmonary function test abnormalities, and adverse drug reactions. The spectrum of IBD manifestations in the chest is broad, and the manifestations may mimic other diseases. Although infrequent, physicians dealing with IBD must be aware of these conditions, which are sometimes life-threatening, to avoid further health impairment of the patients and to alleviate their symptoms by prompt recognition and treatment. Knowledge of these manifestations in conjunction with pertinent clinical data is essential for establishing the correct diagnosis and treatment. The treatment of IBD-related respiratory disorders depends on the specific pattern of involvement, and in most patients, steroids are required in the initial management. Corticosteroids, both systemic and aerosolized, are the mainstay therapeutic approach, while antibiotics must also be administered in the case of infectious and suppurative processes, whose sequelae sometimes require surgical intervention.

Pulmonary manifestations of Crohn's disease.

Crohn's disease (CD) is a systemic illness with a constellation of extraintestinal manifestations affecting various organs. Of these extraintestinal manifestations of CD, those involving the lung are relatively rare. However, there is a wide array of lung manifestations, ranging from subclinical alterations, airway diseases and lung parenchymal diseases to pleural diseases and drug-related diseases. The most frequent manifestation is bronchial inflammation and suppuration with or without bronchiectasis. Bronchoalveolar lavage findings show an increased percentage of neutrophils. Drug-related pulmonary abnormalities include disorders which are directly induced by sulfasalazine, mesalamine and methotrexate, and opportunistic lung infections due to immunosuppressive treatment. In most patients, the development of pulmonary disease parallels that of intestinal disease activity. Although infrequent, clinicians dealing with CD must be aware of these, sometimes life-threatening, conditions to avoid further impairment of health status and to alleviate patient symptoms by prompt recognition and treatment. The treatment of CD-related respiratory disorders depends on the specific pattern of involvement, and in most patients, steroids are required in the initial management.

Tracheobronchial nodules and pulmonary infiltrates in a patient with Crohn's disease.

Crohn's disease is a granulomatous systemic disorder of unknown etiology. Obvious pulmonary involvement is exceptional. Tracheal involvement in Crohn's disease is even more unusual, only a few cases have been reported to date. We herein report a rare case of tracheobronchial nodules and pulmonary infiltrates in both lungs as a complication of Crohn's disease. A 42-year-old man underwent pancolectomy for multiple broken colon caused by Crohn's disease. Forty days later pulmonary symptoms and radiologic abnormalities were noted. A search for bacterial (including mycobacteria) and fungal in the repeated sputum proved negative. The treatment consisted of intravenous antimicrobials for one month, but there was no improvement in pyrexia or cough and radiologic abnormalities. Fibreoptic bronchoscopy (FOB) was performed and revealed nodes in the trachea and the right upper lobe opening. Histopathology of tracheobronchial nodules and bronchial mucosa biopsy specimen both showed granulomatous inflammation with proliferation of capillaries and inflammatory cells. Oral steroid and salicylazosulfapyridine were commenced and led to marked improvement in symptoms and an almost complete resolution of his chest radiograph. Repeated FOB showed that nodes in the trachea disappeared and the ones in the right upper lobe opening diminished obviously. Crohn's disease can be associated with several respiratory manifestations. The form of tracheal and bronchopulmonary involvement in Crohn's disease is rare and responded well to steroids.