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A late defect in wound healing associated with recurrent spontaneous pneumothoraces: a presumptive role for abnormal collagenase activity

 

作者: William J. Lindblad,   James E. Kolb,   Louise C. Flood,   Karen A. Holbrook,   I. Kelman Cohen,   Claude C. Roland,   James Hoehn,   Timothy Judge,   Martin F. McKneally,  

 

期刊: Wound Repair and Regeneration  (WILEY Available online 1995)
卷期: Volume 3, issue 1  

页码: 15-24

 

ISSN:1067-1927

 

年代: 1995

 

DOI:10.1046/j.1524-475X.1995.30107.x

 

出版商: Blackwell Science

 

数据来源: WILEY

 

摘要:

This case report concerns an individual with a defect in wound healing which resulted in recurring, bilateral pneumothoraces during the late postoperative period. This patient had no history of systemic disease or wound healing abnormalities before his recurrent wound disruption. Physical examination and routine biochemical studies failed to identify any causative agent for the multiple wound dehiscences in the patient. Histologic examination of scar tissue showed collagen fiber bundles with a diameter 50% less than that of normal fibrils. Elastic fibers were barely visible, and the scar tissue included a large number of inflammatory cells. A significant finding was an elevated and aberrant expression of collagenase by a fibroblast cell line established from a skin biopsy specimen. This enhanced level of collagenase expression could be inhibited by treatment of the cells with diphenylhydantoin, an inhibitor of collagenase biosynthesis. After initiation of diphenylhydantoin therapy, the patient's scar formation normalized with the recurrent pneumothoraces. These findings support the conclusion that an abnormal expression of collagenase resulted in enhanced degradation of collagen in the patient's wounds, thereby leading to wound dehiscence.

 

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