Objective:To investigate the clinicopathological features, pathological classification, and molecular characteristics of pulmonary hamartomas.Methods:A retrospective analysis was conducted on 316 cases of pulmonary hamartomas diagnosed at Nanjing Chest Hospital, Nanjing, China from January 2015 to June 2024. Next generation sequencing (NGS) was performed on 15 cases of this study. The clinical data, histopathological features, immunophenotypes, and molecular alterations were analyzed. Relevant literature was reviewed.Results:Among the 316 patients, there were 154 males and 162 females, with an average age of 56±10 years. Among the 316 cases, 310 were intrapulmonary hamartomas and 6 were intraluminal bronchial hamartomas. Microscopically, there were complex proliferative mesenchymal components and epithelial components, presenting various combinations and hamartomatous morphologies. These hamartomas were morphologically classified into mesenchymal-type hamartomas (cartilaginous, fibrous, smooth muscle, adipose tissue, and mixed types) and epithelial-mesenchymal mixed-type hamartomas (respiratory epithelial-mesenchymal mixed and mucosal gland-mesenchymal mixed types). The cartilaginous hamartomas accounted for 72.8% (230/316) of them, and the non-cartilaginous hamartoma accounted for 27.2% (86/316). Secondary changes such as calcification, ossification, collagenization, mucin degeneration, and cystic changes were commonly present. The immunophenotype was CK7 +/TTF1 + for respiratory epithelial cells, or TTF1 -/CK7 +/p40 + for interstitial cells. Interstitial cells might express desmin, SMA, S-100, caldesmon, etc, while CD34 +/CD10 +/ER + spindle-shaped interstitial cells were also commonly noted. Genetic variations were detected in 11 of the 15 cases that were subject to NGS, including HMGA2-related fusion genes, EP300 mutations, FLT1 mutations, JAK1 mutations, SETD2 and TAP2 mutations, and high-copy amplification of CDK4/PHF1/TSPAN31. The patients were followed up for 6 to 110 months without any known recurrence or metastasis. Conclusions:Pulmonary hamartomas mainly occur in the peripheral lung parenchyma, with the cartilaginous type being the most common. Their clinical pathological and molecular features of pulmonary hamartomas are characterized and the histological types are roughly ascertained in this study, with emphasis of the key points of diagnosis and differential diagnosis. Classification of pulmonary hamartomas is valuable for guiding future research. Pulmonary hamartomas overall have a good prognosis. However, those with cystic changes or intraluminal hamartomas in the bronchus may cause serious airway lesions and therefore require special attention.

Objective:To investigate the clinicopathological features, pathological classification, and molecular characteristics of pulmonary hamartomas.Methods:A retrospective analysis was conducted on 316 cases of pulmonary hamartomas diagnosed at Nanjing Chest Hospital, Nanjing, China from January 2015 to June 2024. Next generation sequencing (NGS) was performed on 15 cases of this study. The clinical data, histopathological features, immunophenotypes, and molecular alterations were analyzed. Relevant literature was reviewed.Results:Among the 316 patients, there were 154 males and 162 females, with an average age of 56±10 years. Among the 316 cases, 310 were intrapulmonary hamartomas and 6 were intraluminal bronchial hamartomas. Microscopically, there were complex proliferative mesenchymal components and epithelial components, presenting various combinations and hamartomatous morphologies. These hamartomas were morphologically classified into mesenchymal-type hamartomas (cartilaginous, fibrous, smooth muscle, adipose tissue, and mixed types) and epithelial-mesenchymal mixed-type hamartomas (respiratory epithelial-mesenchymal mixed and mucosal gland-mesenchymal mixed types). The cartilaginous hamartomas accounted for 72.8% (230/316) of them, and the non-cartilaginous hamartoma accounted for 27.2% (86/316). Secondary changes such as calcification, ossification, collagenization, mucin degeneration, and cystic changes were commonly present. The immunophenotype was CK7 +/TTF1 + for respiratory epithelial cells, or TTF1 -/CK7 +/p40 + for interstitial cells. Interstitial cells might express desmin, SMA, S-100, caldesmon, etc, while CD34 +/CD10 +/ER + spindle-shaped interstitial cells were also commonly noted. Genetic variations were detected in 11 of the 15 cases that were subject to NGS, including HMGA2-related fusion genes, EP300 mutations, FLT1 mutations, JAK1 mutations, SETD2 and TAP2 mutations, and high-copy amplification of CDK4/PHF1/TSPAN31. The patients were followed up for 6 to 110 months without any known recurrence or metastasis. Conclusions:Pulmonary hamartomas mainly occur in the peripheral lung parenchyma, with the cartilaginous type being the most common. Their clinical pathological and molecular features of pulmonary hamartomas are characterized and the histological types are roughly ascertained in this study, with emphasis of the key points of diagnosis and differential diagnosis. Classification of pulmonary hamartomas is valuable for guiding future research. Pulmonary hamartomas overall have a good prognosis. However, those with cystic changes or intraluminal hamartomas in the bronchus may cause serious airway lesions and therefore require special attention.

Objective To investigate the long-term outcome of children with recurrent wheeze and to determine the effectiveness of inhaled hormone therapy. Methods One thousand and thirty-five children with recurrent wheezing were followed up for more than 4 years and the data were retrospectively evaluated. Results Of 1035 cases, 751 (72.56%) patients outgrew their wheeze during the follow-up period, whereas the other 284 (27.44%) patients had recurrence wheeze during the last two years. The age of wheezing onset was<3 years in 542 (52.37%) cases, from 3 to 7 years in 386 (37.29%) cases, and from 7 to 12 years in 107 (10.34%) cases. There was significant difference in clinical control rate among groups with different wheezing ages onset (χ2=45.27, P<0.001). Children with wheezing age onset from 7 to 12 years had the lowest clinical control rate. Among 1035 wheeze children, 343 (79.95%) children in 429 cases who received inhaled hormone therapy for more than one year outgrew their wheeze. Whereas 408 (67.35%) in 606 cases who did not receive inhaled hormone therapy outgrew their wheeze. There was significant difference of clinical control rate between inhaled group and non-inhaled group (P<0.01). Con-clusions The age of wheezing onset is<7 years in 89.66%of children with recurrent wheeze. Most of them can be clinicalycon-trolled. The long term inhaled hoemone therapy for children with recurrent wheeze can reduce the risk of developing adulthood asthma.