Treatment Optimization of Post-pneumonectomy Pleural Empyema.

INTRODUCTION: Pleural empyema after pneumonectomy still poses a serious postoperative complication. A bronchopleural fistula is often detected. Despite various therapeutic options developed during the last five decades it remains a major surgical challenge. RESULTS: There is no widely accepted treatment for post-pneumonectomy pleural empyema (PPE) and the management depends mostly on the presence or absence of broncho-pleural fistula (BPF) and the patient's general condition. In the absence of BPF, the role of surgery is still not clear because of its high morbidity and impossibility to prevent recurrences. In the earlier period, the definitive treatment consisted of open window thoracostomy followed by obliteration of the pleural cavity with antibiotic solution at the time of chest wall closure. Subsequently, the proposed different methods and modifications improved the outcome. There is an association between hospital volume and operative mortality after the lung resection. Hospital volume and the surgeon's specialty have more influence on the outcome than the individual surgeon's volume. CONCLUSIONS: Treatment management of PPE should be individualized. Definitive treatment options comprise aggressive surgery that is not possible in quite a high proportion of impaired patients. Hospital volume, surgeon's volume and surgeon's specialty may influence the prognosis.

Epidemiology, Etiology and Prevention of Postpneumonectomy Pleural Empyema.

BACKGROUND: Pleural empyema after pneumonectomy still poses a serious postoperative complication. A broncho-pleural fistula is often detected. Despite various therapeutic options developed over the last five decades it remains a major surgical challenge. MATERIALS AND METHODS: A literature search in MEDLINE database was carried out (accessed through PubMed), by using a combination of the following key-words and MeSH terms: pneumonectomy, postoperative, complications, broncho-pleural fistula, empyema, prevention. The following areas of intervention were identified: epidemiology, etiology, prevention. RESULTS: Pleural empyema in a post-pneumonectomy cavity occurs in up to 16% of patients with a mortality of more than 10%. It is associated with broncho-pleural fistula in up to 80% of them, usually in the early postoperative months. Operative mortality could reach 50% in case of broncho-pleural fistula. Unfavourable prognostic factors are: benign disease, COPD, right-sided surgery, neoadjuvant and adjuvant therapy, time of chest tube removal, long bronchial stump and mechanical ventilation. Bronchial stump protection with vascularised flaps is of utmost importance in the prevention of complications. CONCLUSION: Postpneumonectomy pleural empyema is a common complication with high mortality. The existing evidence confirms the role of bronchopleural fistula prevention in the prevention of life-threatening complications.

Epidermal growth factor receptor gene copy number changes in lung cancer.

OBJECTIVE: The objective of this study was to assess the implication of copy number changes of epidermal growth factor receptor (EGFR) in lung cancer pathogenesis. MATERIALS AND METHODS: We used the highly reliable method of FISH, applied on tissue microarray (TMA), containing 306 lung tumors of different histological types, grades and tumor stage, in order to analyze the correlations between gene copy number changes and tumor phenotype. RESULTS: The frequency of EGFR copy number changes was 22.2%-2.8% amplifications and 19.4% gains. EGFR gains occurred more commonly in the squamous cell cancers (23.5%) than in adenocarcinomas (11.8%). Amplifications of EGFR were found only in the squamous cell cancers. Regarding cancer phenotype, there was a statistically significant correlation between EGFR copy number changes and histological grade (p = 0.001). No statistically significant relation could be observed with the metastatic spread of the tumors (lymphogenic and haematogenic) (p = 0.082 and p = 0.1, respectively). In our study EGFR could not be determined as a prognostic factor of survival (p = 0.6115). CONCLUSION: EGFR copy number changes could supplement the clinical significance of EGFR as a marker related to its pathogenesis and targeted therapy.

Thymic epithelial cells of human patients affected by myasthenia gravis overexpress IGF-I immunoreactivity.

Accumulating evidence shows that several kinds of thymic cells express insulin-like growth factor-I (IGF-I), which is known to play an important role in T cell ontogeny under both physiological and pathological conditions. Still, little is known about the mechanisms of IGF-I involvement in the pathological transformation of the thymocyte microenvironment. The present study focuses on a comparative analysis of the IGF-I immunoreactivity of thymic epithelial cells (EC) from human patients with hyperplasia-associated myasthenia gravis (MG) versus physiological thymic tissue from healthy controls using immunohistochemistry and immunoelectron microscopy. We show that myasthenic EC overexpress IGF-I in comparison to EC from control subjects. The IGF-I immunoreactivity in the medullary and cortical EC from MG patients was stronger than in the normal gland. The increased expression of IGF-I and more frequent distribution of IGF-I and IGF-I-receptor (IGF-IR) immunopositive EC correlated with modulation in the immunoreactivity of double (IGF-I/IGF-IR) positive EC. Our data provide new immunocytochemial evidence for alterations of IGF-I and IGF-IR immunoreactivity in EC from pathological thymi. The persisting expression of IGF-I and IGF-IR most likely indicates that the myasthenic thymus is still capable of governing IGF-I signaling pathways, which are involved in the local regulation of T cell development and plasticity.

Structural and ultrastructural localization of NGF and NGF receptors in the thymus of subjects affected by myasthenia gravis.

We have previously reported that the thymus of patients affected by myasthenia gravis (MG) is characterized by an elevated level of nerve growth factor (NGF), an endogenous polypeptide which plays a marked role in the cell biology of nervous and immune system. A consistent number of studies has shown altered expression of NGF in diseases associated with inflammatory and/or autoimmune responses. To evaluate the biochemical and molecular mechanisms implicated in NGF action in human myasthenic thymus, it is important to identify the cellular and structural organization of NGF receptors. To address this question, we investigated, both at light and electron microscopic levels, the cellular distribution of immunoreactivity for NGF and its low-affinity receptors, (p75) and its high-affinity receptor (TrkA) in the thymus of patients with MG. The present investigation shows that NGF and NGF receptors are overexpressed in the thymic cells of patients with MG compared to control subjects.