1997
DOI: 10.1016/s0959-8049(96)00296-1
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Pneumothorax following induction chemotherapy for a germ cell tumour

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1997
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Cited by 6 publications
(6 citation statements)
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“…The pathophysiologic mechanisms of pneumothorax in the setting of treating a pulmonary malignancy are not known, but may include fistula formation between the lung parenchyma and pleural space due to necrosis of a subpleural tumor nodule, infarction and necrosis of tumor emboli, over distension and subsequent rupture of alveoli due to tumor progression, and increased intrathoracic pressure following emetogenic chemotherapy. [ 19 21 , 24 , 28 , 29 ] In the case of antiangiogenesis treatment, sorafenib and bevacizumab both work by blocking VEGF signaling either by VEGFR tyrosine kinase inhibitor (sorafenib) or recombinant humanized anti-VEGF monoclonal antibody (bevacizumab), thereby disrupting the vascular architecture of the tumor-burdened tissue. Within this context, one can hypothesize that the use of VEGF blockers in combination with antiproliferative chemotherapy produces pulmonary nodule necrosis secondary to vascular perfusion compromise, subsequent rupture and pathologic pneumothorax formation.…”
Section: Discussionmentioning
confidence: 99%
“…The pathophysiologic mechanisms of pneumothorax in the setting of treating a pulmonary malignancy are not known, but may include fistula formation between the lung parenchyma and pleural space due to necrosis of a subpleural tumor nodule, infarction and necrosis of tumor emboli, over distension and subsequent rupture of alveoli due to tumor progression, and increased intrathoracic pressure following emetogenic chemotherapy. [ 19 21 , 24 , 28 , 29 ] In the case of antiangiogenesis treatment, sorafenib and bevacizumab both work by blocking VEGF signaling either by VEGFR tyrosine kinase inhibitor (sorafenib) or recombinant humanized anti-VEGF monoclonal antibody (bevacizumab), thereby disrupting the vascular architecture of the tumor-burdened tissue. Within this context, one can hypothesize that the use of VEGF blockers in combination with antiproliferative chemotherapy produces pulmonary nodule necrosis secondary to vascular perfusion compromise, subsequent rupture and pathologic pneumothorax formation.…”
Section: Discussionmentioning
confidence: 99%
“…Other speculative contributing mechanisms include increased intrathoracic pressure following emetogenic chemotherapy, especially cisplatin, and the defective repair process induced by adriamycin. 3,8 Our patient was a nonsmoker who had no previous history of spontaneous pneumothorax and, although proof of the relationship between the pneumothorax and the effect of chemotherapy is not conclusive, the lack of any other known case or pertinent history, and the temporal relationship to chemotherapy and to its response make this etiology likely. In fact, the occurrence of recidivant SSP in our patient is strongly considered to be related to the radiologic regression of the metastases resulting from chemotherapy.…”
Section: Discussionmentioning
confidence: 86%
“…These included 7 patients with osteogenic sarcoma, 7 with germinal tumors, 3 with uterine leiomyosarcoma, 2 with endometrial carcinoma, 2 with synovial cell sarcoma, 2 with lymphoma, and 1 each with Wilm's tumor, thymoma, small cell lung cancer, adenocarcinoma from an unknown primary, and breast cancer. [3][4][5][6][7][8] The actual mechanism of the complicating pneumothorax in primary and metastatic lung cancer is not completely understood, but the pathophysiology would depend on the particular tumor involved. For example, in primary lung cancer the SSP may be produced either by the pathological lung abnormalities that occur secondary to smoking, or by progression of the tumor, causing rupture of an ischemic primary lesion into the pleural space.…”
Section: Discussionmentioning
confidence: 99%
“…Specifically, it is thought that some peripheral, subpleural nodules are particularly chemosensitive, leading to rapid lysis and necrosis after treatment with chemotherapy. The eventual rupture of these nodules results in leakage of air into the pleural space, producing a pneumothorax [ 12 , 13 ]. Another mechanism that has been proposed includes the use of emetogenic chemotherapy agents.…”
Section: Discussionmentioning
confidence: 99%