Background: Designing a skin flap that perfectly covers the anatomical and dynamic territories is challenging. Tissues capturing territories beyond may be insufficiently perfused, and these hypoperfused areas can lead to partial flap necrosis. Indocyanine green angiography (ICGA) is an effective tool for identifying hypoperfused areas. This retrospective study proposes a standardized strategy for managing the hypoperfused area identified by ICGA in pre-expanded extended lower trapezius myocutaneous (e-LTMC) flaps.
Methods: Patients who underwent pre-expanded e-LTMC flap surgery with perfusion assessment using ICGA between June 2016 and January 2022 were identified. A standardized protocol was applied, and patients were divided into four groups according to different management options for hypoperfused areas detected by ICGA. Preoperative and operative variables of interest and postoperative outcomes, including flap necrosis and flap survival length, were collected and analyzed.
Results: Sixty-nine flaps were included in the study. No total flap necrosis was observed. Partial necrosis occurred in 10 flaps. Significant differences were observed in the incidence of full-thickness necrosis between the management groups. The incidence of flap necrosis in cases where management relied on ICGA findings was significantly lower than that of cases where management did not rely on ICGA findings. There were no differences in the relative survival length of the flap between cases with and without intervention for the hypoperfused areas.
Conclusion: The proposed standard strategy effectively reduced the necrosis rate of the pre-expanded e-LTMC flap, thus it is sensible to act on the ICGA findings. Prophylactic resection of the hypoperfused area should be recommended. Where resection may lead to poor reconstructive outcomes, flap trimming or a second flap should be the preferred option.
Keloids, benign fibroproliferative cutaneous lesions, are characterized by abnormal growth and reprogramming of the metabolism of keloid fibroblasts (KFb). However, the underlying mechanisms of this kind of metabolic abnormality have not been identified. Our study aimed to investigate the molecules involved in aerobic glycolysis and its exact regulatory mechanisms in KFb. We discovered that polypyrimidine tract binding (PTB) was significantly upregulated in keloid tissues. siRNA silencing of PTB decreased the mRNA levels and protein expression levels of key glycolytic enzymes and corrected the dysregulation of glucose uptake and lactate production. In addition, mechanistic studies demonstrated that PTB promoted a change from pyruvate kinase muscle 1 (PKM1) to PKM2, and silencing PKM2 substantially reduced the PTB-induced increase in the flow of glycolysis. Moreover, PTB and PKM2 could also regulate the key enzymes in the tricarboxylic acid (TCA) cycle. Assays of cell function demonstrated that PTB promoted the proliferation and migration of KFb in vitro, and this phenomenon could be interrupted by PKM2 silencing. In conclusion, our findings indicate that PTB regulates aerobic glycolysis and the cell functions of KFb via alternative splicing of PKM.
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