The aim of the study was to compare device life of more recent indwelling voice prostheses Provox Vega and Blom-Singer Dual Valve to device life of well-known standard devices (Provox 2, Blom-Singer Classic). In a prospective, non-randomised study, device life of Blom-Singer Classic, Blom-Singer Dual Valve, Provox2, Provox Vega and Provox ActiValve voice prostheses was recorded in a group of 102 laryngectomised patients. In total 749 voice prosthesis were included. Average overall life time was 108 days, median 74 days. The prosthesis with the longest dwell time was the Provox ActiValve (median 291 days). Provox Vega had longer device life compared with Provox2 (median 92 days vs 66 days; p = 0.006) and compared with Blom-Singer Classic (median 92 days vs 69 days; p = 0.004). In conclusion, device lifetimes of Provox Vega and ActiValve were better than those of Provox2 and the Blom-Singer Classic. New voice prostheses, with a defined valve opening pressure (Provox Vega, Provox ActiValve, Blom-Singer Dual Valve) had longer lifetimes than prostheses without a defined opening pressure (Blom-Singer Classic and Provox 2).
Although exposure to asbestos has been shown in previous epidemiological studies to synergistically increase the risk of bronchogenic carcinoma for cigarette smokers, the pathobiological machanism(s) responsible for the cocarcinogenic action of asbestos is not known. Therefore, the effects of asbestos fibers on normal human tracheobronchial epithelium are of interest. Asbestos fibers, ie., amosite, crocidolite and chrysotile (UICC samples) and glass fibers were initially assayed for their cytotoxicity. Bronchial epithelial cells exposed to either asbestos or glass fibers displayed inhibition of cell growth as a function of fiber concentration. When compared to glass fibers, asbestos fibers caused a statistically significant (w0.05) decrease in cell population doubling rate. Chrysotile was approximately 10 times more cytotoxic than either amosite or crocidolite and more than I00 times more cytotoxic than the glass fibers. Epithelial calls were 10 to I 5 times more sensitive to the cytotoxic effects of asbestos fibers than bronchial fibroblasts from the same donor. Using electron microscopy, asbestos fibers were seen to be ingested by epithelial cells. After exposure for 2 h short fibers (< I 2 pn) were found both in the cytoplasm and within phagosomes. High-voltage electron microscopy combined with stereo-microscopy revealed asbestos fibers in the cytoplasmic matrix. A single exposure to amosite asbestos (IWIOOO Wml) was found to induce focal hyperplasia and epidermoid metaplasia with cellular atypia in human tracheobronchial explants. Surface fine structure observations revealed asbestos fibers protruding from these lesions. lntrasytoplasmic and intranuclear fibers of armsite were identified in these focal lesions using X-ray microanalysis in combination with transmission electron microscopy. With increasing time, fibers were also seen deposited within the submucosa of the explants. The preferential cytotoxicity of asbestos for epithelial calk and the metaplastic response of bronchial epithelium may be important in the cacarcinogenic action of asbestor.
The metabolism of carcinogenic N-nitrosamines was studied in normal-appearing bronchial specimens obtained from 4 patients. Explants of bronchi were cultured in a chemically defined medium for 7 days. N-Nitrosamines [N-nitrosodimethylamine (DMN), N-nitrosodiethylamine (DEN), N,N'-dinitrosopiperazine (DNP), N-nitrosopyrrolidine (NPy), and N-nitrosopiperidine (NPd)] labeled with 14C were each then added at 100 mumoles for 24 hours. Measurable CO2 was formed by bronchial explants from: 1) DMN, DEN, and NPy in all 4 patients; 2) DNP in 3 of 4 patients; and 3) NPd in only 1 of 4 patients. In all bronchial specimens, these N-nitrosamines and/or their metabolites bound to bronchial mucosal DNA and protein. Binding levels were higher to protein than to DNA. Binding levels of DNP were as high as those with the two acyclic N-nitrosamines DMN and DEN, but binding levels of NPy and NPd were lower. Human bronchus was shown to metabolize and bind acyclic and cyclic N-nitrosamines found in the environment and in tobacco smoke.
Using a voice prosthesis with a valve containing silver oxide can normalize and even increase the in-situ lifetime in patients with frequent changing procedures caused by fungal growth on the valve. Therefore we recommend the use of this type of voice prosthesis for those patients as reduction of costs and effort results.
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