BackgroundThe systemic artery to pulmonary vessel fistula (SAPVF) is a vascular anomaly characterized by penetration of nonbronchial systemic chest wall arteries into the lung parenchyma. To our knowledge, about 150 cases of SAPVF have been reported to date. Fifteen percent of SAPVF are congenital and occur in the presence of cardiopathy or pulmonary artery hypoplasia. Secondary SAPVF are caused by pleural adhesions that occur subsequent to inflammatory changes associated with conditions such as pleuritis, empyema, trauma, and surgery. Though several cases of secondary SAPVF as a post coronary artery bypass graft (CABG) complication have been reported, secondary SAPVF especially following video-assisted thoracic surgery (VATS) are relatively rare.Case presentationA 19-year-old man was admitted to our hospital because of recurrence of left pneumothorax. His previous history included left and right pneumothorax at the ages of 15 and 16 years, respectively, which were treated by VATS. VATS was planned for the surgical indication of second postoperative recurrence. In the operation, the lingular segment with dilated pulsating pulmonary vessels adhered to the port scar of the chest wall, which was made at first VATS for pneumothorax. The computed tomography showed an abnormal connection between the branch of the systemic artery of the chest wall and the dilated pulmonary artery and pulmonary vein in the lingular segment. Left subclavian selective arteriography also showed hypertrophic blood vessels arose from the internal thoracic artery, the lateral thoracic artery, and the subscapular artery, which drained into the both the pulmonary artery and the pulmonary vein in the lingular segment. Despite of four sessions of embolization for aberrant arteries, the abnormal blood flow persisted. Partial resection of the left lingular segment was therefore performed. The patient has been disease-free about SAPVF for 2 years and 2 months after the last operation.ConclusionsWe described our experience with a case of secondary SAPVF that was associated with fistulas between a systemic artery and both the pulmonary artery and pulmonary vein, which was developed after first VATS for pneumothorax. Radical resection was safely performed and effective after four sessions of embolization.

A total of 297 resected Japanese non-small cell lung cancers (74 squamous cell carcinomas and 223 adenocarcinomas) were analyzed to evaluate the validity of the p53 mutation spectrum as a fingerprint for mutagenic substances as etiological factors. Frequencies of G→ → → →T transversions in smokers were significantly higher than in non-smokers (P = 0.003) and the average incidence of G→ → → →T at hot spot codons of adduct formation was higher than that in other codons in smokers and in the hot spots in non-smokers. Further, the mutation showed a marked strand bias. G→ → → →A transitions at CpG sites (CpG→ → → →CpA) were equally distributed in smokers and non-smokers, and on both strands. A→ → → →G transitions did not show any variation with smoking status in terms of frequency, but exhibited a marked strand bias. Taken together, the G→ → → →T may be a fingerprint of direct mutagenic action of tobaccorelated compounds, the A→ → → →G being a new marker for other environmental chemicals, while the CpG→ → → →CpA may be attributable to endogenous spontaneous mutation, for active in lung carcinogenesis. (Cancer Sci 2008; 99: 287-295)

Malignant pleural mesothelioma (MPM) is thought to arise from the mesothelial cells that line the pleural cavities. Most patients initially experience the insidious onset of chest pain or shortness of breath and have a history of asbestos exposure. MPM rarely presents as spontaneous pneumothorax. We report two male patients who presented with a spontaneous hydropneumothorax. One was exposed to asbestos and the other was not. Computed tomography showed tiny nodules with pleural thickness. They both underwent pleural effusion cytology and/or pleural biopsy. Therefore, the pathological diagnosis of MPM was obtained in both cases. We also reviewed 16 Japanese MPM cases with pneumothorax including our two patients. More than half of the patients suffered from pneumothorax repeatedly. We emphasize the need to obtain a pathological diagnosis of pleural effusion cytology and/or pleural biopsy in older patients presenting with a spontaneous hydropneumothorax.

The question of whether squamous cell carcinomas (SCCs) arising in different sites of lung are caused by different etiological factors is of obvious importance for prevention, early detection and effective treatment. We here subclassified a large series of resected SCCs (74 cases) into 3 tumor-sites, central (main to segmental bronchi), intermediate (subsegmental to sub-subsegmental) and peripheral (distal to sub-subsegmental bronchi), and examined relationships with p53 mutational spectra and smoking history to provide clues to etiological factors. The rate for GfiA transitions at CpG sites considered to be caused by endogenous mechanism was higher in central (40%) than in intermediate (0%) and peripheral (14%) lesions, in spite of highest percentage of heavy smokers. In contrast, GfiT transversions associated with tobacco smoke carcinogens were most frequent (50%) in the intermediate location, although proportions of heavy smoker's ratio were the same among the locations when confined to p53 mutation cases. In the periphery, other mutations were highest (67%) compared with 33 and 50% in the central and intermediate regions, respectively. Thus, different etiological factors may be playing causal roles in the development of SCCs in different locations of bronchial tree. Furthermore, the results suggest that more extensive study of the influence of tobacco smoke carcinogens on endogenous mechanisms is warranted.

A 70-year-old man with T1N3M1 stage IV squamous cell carcinoma in the right upper lobe of the lung developed chylothorax and chylopericardium as rare simultaneous complications. Intravenous hyperalimentation, repeated pleurodesis, and ligation of the thoracic duct were all ineffective. A pleuroperitoneal shunt was inserted into the right pleural cavity from the fifth intercostal space, and a peritoneal catheter was placed in the abdominal cavity. Chylothorax was markedly improved, and the quality of life of the patient increased. This case indicates that a pleuroperitoneal shunt can be used for lung cancer-related chylothorax, as well as for malignant pleural effusion.

An 86-year-old woman with a history of right breast cancer resected seven years ago had a small pulmonary nodule located in left S5. Diagnosis was made by bronchoscopy using the endobronchial ultrasonography-guided sheath (EBUS-GS) method, but a histological diagnosis was not obtained. Wedge resection was performed due to suspicion of a metastatic lesion from breast cancer based on radiological findings. The tumor was subsequently found to be malignant melanoma of the lung. An initial diagnosis of primary melanoma of the lung was made because a melanoma lesion at another site was not seen despite a detailed work up. However, 8 months after surgery, a malignant melanoma appeared at the tip of the right index finger. We rediagnosed the lung lesion as a metastatic malignant melanoma based on the low incidence of primary melanoma of the lung and on the pathological features.

We analyzed relationships between histological subtypes of pulmonary adenocarcinomas and three gene alterations (p53, K-ras, and epidermal growth factor receptor gene), or thyroid transcription factor-1 (TTF-1) expression, and also studied prognoses by the subtypes, with or without combined multiple gene mutation status. Our purpose was to clearly determine pathogenesis, along with the best predictive value for biology and therapy-related traits. A total of 223 consecutively resected pulmonary adenocarcinomas were sub-classified using either the World Health Organization (WHO) or our five-cell type (FCT) classification system (hobnail, columnar ⁄ cuboidal, mixed, polygonal ⁄ oval, and goblet cell types). DNAs extracted from frozen samples of the adenocarcinomas were examined for gene alterations, and TTF-1 expressions were determined using immunohistochemistry. Next, relationships among the various data and clinicopathological factors were analyzed. The most striking result was: while almost 70% of adenocarcinomas were sub-classified as a mixed subtype by WHO, the FCT classified many of them as other cell subtypes. The FCT closely reflected differences in etiological factors, cellular lineages, and frequencies of gene mutations; and whether the data from combined gene mutations were used or not, differences among the cell types in postoperative survivals appeared. In contrast, subtypes of WHO did not show any association with the gene alteration or prognosis, and the FCT more suitably indicated sensitivity to gefitinib therapy than did WHO. The FCT combined with multiple gene mutation status appears to be useful in indicating pathogenesis and predicting the biological nature of pulmonary adenocarcinomas, and it could facilitate development of new therapies for each subtype.

Background.Case. Conclusions.JJLC.