[Pneumothorax caused by a ruptured emphysema bulla].
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Humans↗
Biomedical subjects
H Dienemann
Publications and source records attributed to H Dienemann.
Report from the first meeting of the 'European Network on Translational Research in Lung Cancer Amsterdam-Barcelona-Bialystok-Heidelberg'. Thoraxklinik Heidelberg, Germany, July 25, 2001.
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Antineoplastic Agents↗
Evidence-based medicine: lung volume reduction surgery (LVRS).
Lung volume reduction surgery (LVRS) was developed as a means of surgical treatment for severe pulmonary emphysema. To date, various studies have been designed to explain the mechanisms involved in pathophysiological changes after treatment, to define criteria for patient selection, to identify the surgical technique of choice and to propose appropriate follow-up care. Preliminary results of follow-up studies (up to five years) have already been published, indicating improved pulmonary function and quality of life after surgical treatment. However, the alarming results from the National Emphysema Treatment Trial (NETT) Research Group indicated a considerable risk for death in patients with homogenous emphysema and low forced expiratory volume in one second (FEV1) undergoing LVRS. This brief review summarizes the results of currently published studies to supply evidence for selection criteria in order to better define the subset of patients for which LVRS offers an effective and safe means of palliation from the symptoms of advanced COPD. Due to acceptable morbidity and mortality rates, stapler device wedge excision and closure has become the standard procedure for removing non-functioning, hyperinflated lung areas in heterogeneously affected organs. LVRS is carried out in two ways - using video-assisted thoracoscopic surgery (VATS) as well as thoracotomy/sternotomy-and performed in unilateral and bilateral procedures. In contrast, most clinics have found laser resection of emphysematous parenchyma to be unsuccessful. In some patients, LVRS was carried out as an alternative to lung transplantation, whereas in others, it served as a bridge-to-transplant procedure. LVRS has proven effective in the reduction of dyspnea, especially in patients with recovery options in both the circulatory and pulmonary system. In responders, recovery from labored breathing and O(2) dependency and increased physical capacity are usually accompanied by improved spirometric data. These results are mainly explained by a more regular breathing pattern and an increase in the maximum volume of ventilation in the affected lung. In most cases, functional improvement is maximized during the first six months postoperatively and decreases steadily thereafter indicating the need for a systematic postoperative patient care after surgical treatment. After indicating at-risk patients who should not be considered for LVRS, long-term results from the multicenter NETT research group will hopefully help clarify the impact of this treatment on survival of patients further.
Evidence-Based Medicine↗
Comparison of multiple DNA adduct types in tumor adjacent human lung tissue: effect of cigarette smoking.
Cigarette smokers inhale a broad range of carcinogens derived from tobacco and its pyrolysis products, including free radicals, which induce oxidative stress and subsequent lipid peroxidation (LPO). Miscoding carcinogen-DNA adducts are formed by cigarette smoke constituents and are thought to initiate lung carcinogenesis. The presence of various types of DNA damage was therefore analyzed in tumor adjacent uninvolved lung tissues of 13 smoking and 11 non-smoking operated lung cancer patients. O(4)-ethylthymidine (O(4)etT), 1,N(6)-ethenodeoxyadenosine ( epsilon dA) and 3,N(4)-ethenodeoxycytidine ( epsilon dC) were determined by immuno-enriched (32)P-postlabeling. Polycyclic aromatic hydrocarbon (PAH)-DNA adducts were measured as diagonal radioactive zones after nuclease P1 enriched (32)P-postlabeling. Mean O(4)etT and PAH-DNA adduct levels were higher in lung DNA of smokers than of non-smokers (O(4)etT/10(8) thymidine: 3.8 versus 1.6, P < 0.01; PAH-DNA adducts/10(8) nucleotides: 11.2 versus 2.2, P < 0.01). Pulmonary etheno-DNA adduct levels did not differ between smokers and non-smokers, but large inter-individual variations were observed (80- and 250-fold differences for epsilon dA and epsilon dC, respectively). As all smokers (except one) refrained from smoking at least for 1 week before surgery, our results demonstrate the persistence of O(4)etT and PAH-DNA adducts in human lung. A positive correlation obtained between O(4)etT and PAH-DNA adducts (R = 0.65, P < 0.01) suggests that both adducts are formed from cigarette smoke as the main exposure source. We conclude that in addition to the DNA adducts derived from PAH and tobacco-specific nitrosamines, miscoding O(4)etT lesions are formed by cigarette smoke that contribute to the increased genomic instability and increased lung cancer risk in smokers.
Aged↗
Surgical treatment of hepatic and pulmonary metastases from non-colorectal and non-neuroendocrine carcinoma.
BACKGROUND: Surgical resection is standard treatment for colorectal and neuroendocrine liver metases provided the tumor can be removed completely. The same is true for isolated pulmonary metastases. To date, only few reports have addressed the value of surgical resection of organ metastases from other solid tumors. METHODS: The literature was searched by Medline, conference proceedings and cross-referencing of published articles for information pertaining to the long-term results of surgical treatment of non-colorectal and non-neuroendocrine (NCNN) liver or lung metastases. RESULTS: Resection of hepatic and pulmonary metastases is increasingly performed in non-colorectal and non-neuroendocrine malignancies. Mortality and morbidity of hepatic and pulmonary resection are low and 5 year survival can be expected to reach some 20-30 percent, irrespective of the histological type of the primary tumor. CONCLUSION: Resection of hepatic or pulmonary metastasis should be considered in all patients with low operative risk provided that complete resection is possible.
Humans↗
Altered DNA repair capacity and bleomycin sensitivity as risk markers for non-small cell lung cancer.
DNA repair capacity in human peripheral blood lymphocytes was monitored by the repair rate of bleomycin-induced DNA damage using an alkaline single-cell gel electrophoresis assay (comet assay). DNA repair capacity, after 15 min repair time, in lymphocytes of non-small cell lung cancer patients (n = 160) and controls (n = 180) was 67% and 79.3%, respectively (p < 0.0004). Bleomycin sensitivity defined as the tail moment of bleomycin-treated peripheral blood lymphocytes, without allowing time for DNA repair, was significantly higher in lung cancer patients than in tumor-free hospital controls (p < 0.0001). There was no correlation, in either patient or control group, between the bleomycin sensitivity and DNA repair capacity with age or gender. The median values of DNA repair capacity and sensitivity in controls were used as the cut-off points for calculating odds ratios (OR). After adjustment for age, gender and smoking status, the cases vs. controls had reduced DNA repair capacity (OR = 2.1; 95% confidence limit [CL] 1.1-4.0) and increased bleomycin sensitivity (OR = 4; 95% CL 2.2-7.4). For current smokers, the adjusted risk associated with bleomycin sensitivity was 2.3 (95% CL 1.1-4.9). We conclude that our standard comet assay as a phenotypical repair test has sufficient sensitivity and rapidity allowing application to both native and cryopreserved lymphocytes. Bleomycin sensitivity and DNA repair capacity were found to be 2 independent susceptibility markers for non-small cell lung cancer, confirming similar investigations with different marker end points. The latter were much more time consuming than the method used in our study. Thus, the comet assay is more suitable for screening large numbers of individuals in epidemiological studies. Validation of this assay in large prospective studies for the identification of subjects at high risk for non-small cell lung cancer is now warranted.
Adult↗
[Benign, pulmonary metastatic leiomyoma of the uterus].
Pulmonary nodules resected in 10 patients were histologically classified as benign metastatic leiomyoma of the uterus. Hysterectomy because of myoma had been performed between 0 and 24 years earlier (median 14.9 years). Between 1 and 27 nodules were found in one or both lungs. Patients presenting with a single nodule had it resected with diagnostic intent and were followed up. Multiple nodules were resected if the loss of parenchyma was tolerable; otherwise, one lesion was resected for diagnosis. In some cases antihormonal therapy was performed postoperatively. The median duration of follow-up was 4.7 years. In this time, no local complication occurred, and no patient died of this disease. Apparently, benign metastatic leiomyoma of the uterus biologically shows benign behaviour. New manifestation or progressing growth of non-resected lesions does occur, however. Consequently, regular follow-up is required. Local complications indicate surgical intervention.
Adult↗
[Tracheobronchial injuries and fistulas].
In association with perforating or blunt trauma, isolated injuries of the trachea and the bronchi are rarely seen. More frequently, however, they occur when adjacent organs or structures are involved, thus creating very complex syndromes. Symptoms such as dyspnea, coughing attacks, hemoptysis, soft tissue emphysema, cyanosis, and pneumothorax should point to severe tracheobronchial injuries. Diagnosis is confirmed through an emergency tracheobronchoscopy; early surgical repair is mandatory. Iatrogenic injuries--most often due to intubation maneuvers--are infrequent but potentially life-threatening and demanding immediate repair except in cases with superficial tears. Leading symptoms of transmural lacerations are dyspnea, soft tissue emphysema, and pneumothorax. Tracheoesophageal fistulas result from decubital necrosis caused by long-term intubation. With spontaneous healing never occurring, surgical repair is carried out ideally by closing both openings in chronic fistulas, while simultaneous tracheal stenosis is treated by segmental resection. Tracheoarterial fistulas, mostly associated with tracheostomy, become fatal if not detected immediately. Definitive repair requires the resection of the vascular segment involved.
Aged↗
[Endobronchial juvenile hemangioma in infancy--removal by main bronchus cuff resection. Case report].
The rare case of a 3.5 month-old infant diagnosed with a endobronchial haemangioma is presented and discussed against a background of reference literary material. A main-bronchus sleeve resection with end-to-end anastomosis was performed without reduction of lung parenchyma. No complications were documented during the period of observation. The results of repeated bronchoscopy showed the post-operative period to be of a non-problematic nature.
Bronchi↗
Endobronchial juvenile hemangioma--a case report of a neonate including immunohistochemical monitoring and nuclear, cellular, and vascular morphometry.
A 3-month-old female child suffered from tachypnea and dyspnea with abnormal blood gas values. Chest X-rays revealed an increased transparency of the left lung and a mediastinal shift to the right side. High resolution computed tomography (CT) documented a narrowing of the left upper stem bronchus. Ensuing endoscopy detected an occlusive endobronchial tumor mass that did not infiltrate the bronchial cartilage as confirmed with endobronchial ultrasonic monitoring. Based on gross histological examination of the surgical specimen obtained using sleeve resection, the highly vascularized tumor exhibited an adenomatoid growth pattern with a rather homogeneous population of nuclei. The light microscopical presentation was consistent with a juvenile (infantile) hemangioma, which was confirmed using immunohistochemical examinations despite the display of neuroendocrine features. Although endobronchial juvenile hemangiomas are an extremely rare event in early childhood, this case underscores the necessity to not neglect its occurrence in differential diagnosis.
Biomarkers, Tumor↗
Principles of surgical treatment in localized non-small cell lung cancer.
Non-small cell cancer has become the leading cause of cancer-related deaths in women and men in the western hemisphere. Surgical resection remains the mainstay of therapy in stage I and II disease. Surgical therapy has an acceptable morbidity and mortality rate. Analysis of 5-year survival shows 70-75% in experienced centers for stage I and 40% for stage II, including tumors extending to the chest wall. Local and distant recurrence account for the disappointing survival rates after complete resection. In the future, appropriate selection of surgical procedures and effective use of systemic therapies might depend upon the elucidation of prognostic factors that predict recurrence and poor outcome. Thus, parameters need to be identified that characterize those patients preoperatively.
Biomarkers, Tumor↗
Rapid screening assay for mutagen sensitivity and DNA repair capacity in human peripheral blood lymphocytes.
Individual susceptibility to carcinogens, an important determinant of disease risk, is influenced by host factors such as the ability to repair DNA lesions. In order to identify subjects who are at high risk, we have developed a microgel electrophoresis assay for use in molecular epidemiological studies. The assay was validated in a pilot case-control study: Peripheral blood lymphocytes were collected from 100 patients with lung cancer and 110 control patients without cancer and from the same hospital, and stored at -80 degrees C. After thawing, phytohaemagglutinin-stimulated cells were treated with bleomycin at 20 microg/ml for 30 min and the extent of DNA damage and DNA repair capacity were determined by microgel electrophoresis. Peripheral blood lymphocytes from patients with lung cancer were significantly more sensitive to mutagens than those from controls and showed reduced DNA repair capacity (both P < 0.001). Both endpoints were independent risk factors for smoking-related lung cancer. Repeated analysis of peripheral blood lymphocytes from the same individual demonstrated good reproducibility of the assay. Cryopreservation of the lymphocytes for less than or = 12 months did not significantly affect their sensitivity. Our standardized microgel electrophoresis assay is suitable for determining individual sensitivity to mutagens and DNA repair capacity: it is sensitive and faster than cytogenetic assays, and can be applied to native and cryopreserved peripheral blood lymphocytes.
Adult↗
Relevance of N-acetyltransferase 1 and 2 (NAT1, NAT2) genetic polymorphisms in non-small cell lung cancer susceptibility.
The highly polymorphic N-acetyltransferases (NAT1 and NAT2) are involved in both activation and inactivation reactions of numerous carcinogens, such as tobacco derived aromatic amines. The potential effect of the NAT genotypes in individual susceptibility to lung cancer was examined in a hospital based case-control study consisting of 392 Caucasian lung cancer patients [152 adenocarcinomas, 173 squamous cell carcinomas (SCC) and 67 other primary lung tumours] and 351 controls. In addition to the wild-type allele NAT1*4, seven variant NAT1 alleles (NAT1*3, *10, *11, *14, *15, *17 and *22) were analysed. A new method based on the LightCycler (Roche Diagnostics Inc.) technology was applied for the detection of the polymorphic NAT1 sites at nt 1088 and nt 1095. The NAT2 polymorphic sites at nt 481, 590, 803 and 857 were detected by polymerase chain reaction-restriction fragment length polymorphism or LightCycler. Multivariate logistic regression analyses were performed taking into account levels of smoking, age, gender and occupational exposure. An increased risk for adenocarcinoma among the NAT1 putative fast acetylators [odds ratio (OR) 1.92 (1.16-3.16)] was found but could not be detected for SCC or the total case group. NAT2 genotypes alone appeared not to modify individual lung cancer risk, however, individuals with combined NAT1 fast and NAT2 slow genotype had significantly elevated adenocarcinoma risk [OR 2.22 (1.03-4.81)] compared to persons with other genotype combinations. These data clearly show the importance of separating different histological lung tumour subtypes in studies on genetic susceptibility factors and implicate the NAT1*10 allele as a risk factor for adenocarcinoma.
Aged↗
Glutathione-S-transferase M1, M3, T1 and P1 polymorphisms and susceptibility to non-small-cell lung cancer subtypes and hamartomas.
Polymorphic glutathione-S-transferase (GST) genes causing variations in enzyme activity may influence individual susceptibility to lung cancer. In this case-control study (consisting of 389 Caucasian lung cancer patients, including 151 adenocarcinomas (ACs) and 172 squamous cell carcinomas (SCCs), and 353 hospital control subjects without malignant disease, genotype frequencies for GSTM1, GSTM3, GSTP1 and GSTT1 were determined by polymerase chain reaction (PCR)/ restriction fragment length polymorphism (RFLP)-based methods. While adjusted odds ratios (ORs) indicated no significantly increased risk for lung cancer overall due to any single GST genotype, the risk alleles for GSTM1, GSTM3 and GSTP1 conferring reduced enzyme activity were present at higher frequency in SCC than in AC patients. This is consistent with a reduced detoxification of carcinogenic polycyclic aromatic hydrocarbons (PAHs) from cigarette smoke that are more important for the development of SCC than for AC. An explorative data analysis also identified statistically significantly increased ORs for the combinations GSTT1 non-null and GSTP1 GG or AG for lung cancer overall (OR 2.23, CI 1.11-4.45), and for SCC (OR 2.69, CI 1.03-6.99). For lung cancer overall, and especially among SCC patients, the GSTT1 null genotype was underrepresented (SCC 11.2% v. control subjects 19%, P = 0.026, OR 0.57, CI 0.30-1.06). Additionally, in 28 patients with hamartomas, the GSTT1 null genotype was also protective (P = 0.013), while GSTP1 variant allele carriers were overrepresented (OR 2.48, CI 1.06-6.51). In conclusion, GST genotypes may act differently, either by detoxifying harmful tobacco carcinogens and/or by eliminating lung cancer chemopreventive agents. The latter role for GSTT1 would explain the observed lower risk of SCC and hamartoma associated with GSTT1 null. Further confirmatory studies are required.
Adenocarcinoma↗
[Is minimally invasive technique suitable for surgery of lung metastases?].
Video-assisted thoracic surgery (VATS) for surgery of pulmonary metastases has to be defined with respect to technical as well as oncological aspects. Peripheral lesions up to 2 cm in diameter can easily be removed by wedge resection, but anatomical resection can also be safely accomplished. Since VATS does not allow for digital palpation of lung parenchyma, complete resection of all lesions can never be guaranteed. Thus, VATS is recommended only for diagnostic and palliative procedures but not for curative intention except in randomised studies.
Humans↗
[Thoracic surgery centers].
The term "center for thoracic surgery" needs to be defined with respect to "thoracic surgery" and "center". "Thoracic surgery" includes the knowledge, the technical skills, and the experience, which allows for a correct diagnosis and the surgical treatment of diseases of the chest (chest wall, pleura, lungs, trachea, bronchi, mediastinum, diaphragm and adjacent structures). The "center" is defined by the specific organisational structure facilitating interdisciplinary patients care according to international standards, education and training of surgeons and continuous clinical and experimental investigation in the field of thoracic surgery.
Germany↗
hOGG1 polymorphism and loss of heterozygosity (LOH): significance for lung cancer susceptibility in a caucasian population.
Oxidative damage is implicated in several chronic diseases including cancer. 8-Hydroxyguanine (8-oxoG) is one of the major promutagenic DNA lesions, which is produced by reactive oxygen species, causes G:C to T:A transversions and is excised by OGG1, an 8-oxoG specific DNA glycosylase/AP-Lyase. In a nested case-control study, gDNA from 105 Caucasian primary non-small cell lung cancer cases and 105 matched controls was screened for 6 possible new polymorphic sites in the human OGG1 gene, detected previously mainly in tumour tissue. The previously described Ser(326)Cys polymorphism was found to be common (allele frequency 0.22) in Caucasians. However, no major difference in Ser(326)Cys genotype distribution could be detected between cases and controls. Two 5;-end polymorphisms previously found in Japanese as well as Arg(131)Gln could not be detected in this population. An Ala(85)Ser polymorphism was found in 2 controls, whereas Arg(46)Gln was detected in only 1 case. As the hOGG1 gene is mapped (3p26.2) to a region frequently lost in primary lung tumours, the frequency of loss of heterozygosity (LOH) was investigated. Forty-three percent of the studied lung tumours exhibited loss of one of the hOGG1 alleles. The wt Ser(326) allele was not predominantly lost in our sample set, which suggests a minor role of this polymorphism in tumourgenesis. Our results show that LOH at the hOGG1 gene locus is a very common occurrence in lung tumourgenesis, possibly leading to increased mutational damage due to ROS in smokers. However, the hOGG1 polymorphisms studied are probably not major contributors to individual lung cancer susceptibility in Caucasians.
Adenocarcinoma↗
[Mesothelioma of the pleura and peritoneum. Diagnostic and therapeutic sequelae].
In patients with pleural or peritoneal mesothelioma, surgery is a technically difficult procedure. Whereas those rare forms of localized pleural mesotheliomy are being detected incidentally and can be cured by complete resection, most patients with diffuse malignant mesothelioma present with an advanced stage of disease. Most of these patients survive less than 12 months irrespective of the treatment modality. For diffuse pleural mesothelioma, some favorable prognostic factors were identified: IMIG (International Mesothelioma Interest Group), stages I and II, epithelial type, age under 50, female gender. In IMIG stages I and II, extended pleuropneumonectomy followed by chemo- and/or radiotherapy is recommended. For this subset of patients, a median survival time of between 20 and 30 months is reported. Pleurectomy and decortication are recommended as palliative surgical strategies against pleural effusion. In patients with technically inoperable infiltration of the thoracic wall, irradiation is helpful; sometimes partial remission and relief of pain can be achieved by chemotherapy.
Combined Modality Therapy↗