Role of Mitomycin C in Preventing Capsular Contracture in Implant-Based Reconstructive Breast Surgery

2017 ◽  
Vol 139 (4) ◽  
pp. 819-826 ◽  
Author(s):  
Maurizio Bruno Nava ◽  
Nicola Rocco ◽  
Giuseppe Catanuto ◽  
Joanna Frangou ◽  
Corrado Rispoli ◽  
...  
2000 ◽  
Vol 15 (5) ◽  
pp. 377-382 ◽  
Author(s):  
E. Bäz ◽  
H. Madjar ◽  
C. Reuss ◽  
M. Vetter ◽  
B. Hackelöer ◽  
...  

Ophthalmology ◽  
1998 ◽  
Vol 105 (4) ◽  
pp. 740-745 ◽  
Author(s):  
Dong H Shin ◽  
Yong Y Kim ◽  
Nilesh Sheth ◽  
Jianming Ren ◽  
Mahir Shah ◽  
...  

Author(s):  
Andrei Pașca ◽  
Eduard-Alexandru Bonci ◽  
Codruța Chiuzan ◽  
Nicoleta Monica Jiboc ◽  
Vlad Alexandru Gâta ◽  
...  

Abstract Background Capsular Contracture (CC) is the most common long-term complication of breast surgery with prosthesis. Leukotriene Receptor Antagonists (LRAs) have been tested as a potential treatment; however, mixed results have been observed. Objectives This study presents a meta-analysis to clarify the treatment and prophylactic capabilities of LRAs in the management of CC. Methods A systematic literature search in the most popular English databases was performed to identify relevant primary publications. We included all studies that evaluated the treatment and preventive capabilities of LRAs using the Baker scale assessment. Results Six eligible studies were included based on predefined inclusion and exclusion criteria, totalling 2276 breasts, out of which 775 did not receive LRAs and 1501 did. Final pooled results showed that LRAs could help manage CC with a Risk Difference (RD) of -0.38 with the corresponding 95% Confidence Interval (CI) between -0.69 and -0.08, showing statistical significance at a Z value of 2.48, p=0.01. Subgroup analysis based on the type of drug used showed that only montelukast yielded statistical significance (RD=-0.27, 95% CI between -0.51 and -0.03, Z=2.20, p=0.03). Zafirlukast did not seem to influence CC. Further subgroup analysis based on treatment timing showed that prophylaxis was ineffective and only treatment for ongoing CC yielded statistical significance. Conclusions The current meta-analysis proved that LRAs could be used in the management of CC. Only treatment for the ongoing CC showed statistical significance. Montelukast seemed to be more efficient with a safer profile for adverse effects, while zafirlukast yielded no statistical significance.


2011 ◽  
Vol 27 (2) ◽  
pp. 101-105 ◽  
Author(s):  
Ahmed M. Omar ◽  
Mohamed A. Mansour ◽  
Hisham H. Abdelwahab ◽  
Ossama H. Aboushanab

2011 ◽  
Vol 151 (3) ◽  
pp. 488-493 ◽  
Author(s):  
Ahmad Kheirkhah ◽  
Ali Izadi ◽  
Mohammad Yaser Kiarudi ◽  
Rahman Nazari ◽  
Hesam Hashemian ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Yin Zhang ◽  
Qinge Wang ◽  
Yuping Xu ◽  
Jing Sun ◽  
Yanbo Ding ◽  
...  

Benign esophageal strictures (BESs) frequently results from esophageal fibrosis. The transformation of fibroblasts into fibrocyte is an important cause of fibrosis. The treatment of fibrosis is challenging. Some previous studies have indicated the antifibrotic effect of mitomycin C (MMC). However, the mechanism of action of MMC and its optimal dose for treatment remains unclear. In the present study, the role of MMC in fighting fibrosis and its mechanism was investigated. Human esophageal fibroblast cells (HEFs)were treated without or with MMC, at 2, 5, 10 μg/ml, combining with mimic lncRNA-ATB, miR-200b inhibitor, rapamycin (RAPA), and 3-Methyladenine (3-MA). The cell viability, and cell apoptosis were evaluated. In addition, expression of apoptosis related proteins (caspase8 and caspase3), autophagy related proteins (LC3II and ATG5) and fibrosis related proteins (α-SMA collagen-1 and TGF-β) were also evaluated. Furthermore, autophagosome was observed by transmission electron microscope. Results showed that the expression of lncRNA-ATB was down-regulated and miR-200b was up-regulated after treated with MMC. And MMC induced cell apoptosis and inhibited cell autophagy. On the other hand, RAPA, mimic lncRNA-ATB and miR-200b inhibitor reduced fibrogenic effect of MMC on HEFs. Collectively, this study suggests that MMC inhibited esophageal fibrosis by regulating cell apoptosis and autophagy via downregulating lncRNA-ATB and upregulating miR-200b.


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