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1.
Ann Plast Surg ; 92(6): 703-710, 2024 Jun 01.
Article in English | MEDLINE | ID: mdl-38768024

ABSTRACT

INTRODUCTION: Breast reconstruction with the deep inferior epigastric perforator (DIEP) flap is the current gold-standard autologous option. The profunda artery perforator (PAP) and lumbar artery perforator (LAP) flaps have more recently been described as alternatives for patients who are not candidates for a DIEP flap. The aim of this study was to review the survival and complication rates of PAP and LAP flaps, using the DIEP flap as a benchmark. METHODS: A literature search was conducted using PubMed, MEDLINE, Embase, BIOSIS, Web of Science, and Cochrane databases. Papers were screened by title and abstract, and full texts reviewed by three independent blinded reviewers. Quality was assessed using MINORS criteria. RESULTS: Sixty-three studies were included, for a total of 745 PAP, 62 stacked PAP, 187 LAP, and 23,748 DIEP flap breast reconstructions. The PAP (98.3%) had comparable success rate to DIEP (98.4%), and the stacked PAP (88.7%) and LAP (92.5%) success rate was significantly lower (P < 0.0001). The PAP and LAP groups both had a low incidence of fat necrosis. However, the revision rate for the LAP group was 16.1% whereas the PAP group was 3.3%. Donor site wound dehiscence rate was 2.9 in the LAP group and 9.1% in the PAP group. CONCLUSIONS: Profunda artery perforator and DIEP flaps demonstrate very high rates of overall survival. The LAP flap has a lower survival rate. This review highlights the survival and complication rates of these alternative flaps, which may help clinicians in guiding autologous reconstruction technique when a DIEP flap is unavailable.


Subject(s)
Mammaplasty , Perforator Flap , Humans , Mammaplasty/methods , Perforator Flap/blood supply , Perforator Flap/transplantation , Female , Graft Survival , Postoperative Complications/epidemiology , Epigastric Arteries/transplantation
2.
J Invest Dermatol ; 141(6): 1482-1492.e4, 2021 06.
Article in English | MEDLINE | ID: mdl-33242499

ABSTRACT

Systemic sclerosis a chronic, fibrotic disorder associated with high disease-specific mortality and morbidity. Cutaneous manifestations include dermal thickening and obliteration of dermal adipose tissue. Accumulation of low-molecular-weight hyaluronan, which signals through the receptor for hyaluronan-mediated motility, RHAMM, leads to progressive fibrosis and is correlated with increased severity of systemic sclerosis. The purpose of this study is to test the efficacy of two function-blocking RHAMM peptides, NPI-110 and NPI-106, in reducing skin fibrosis in a bleomycin-induced mouse model of systemic sclerosis. NPI-110 reduced visible measures of fibrosis (dermal thickness and collagen production, deposition, and organization) and profibrotic gene expression (Tgfb1, c-Myc, Col1a1, Col3a1). NPI-110 treatment also increased the expression of the antifibrotic adipokines perilipin and adiponectin. Both RHAMM peptides strongly reduced dermal RHAMM expression, predicting that dermal fibroblasts are peptide targets. Transcriptome and cell culture analyses using Rhamm-/- and Rhamm-rescued dermal fibroblasts reveal a TGFß1/RHAMM/MYC signaling axis that promotes fibrogenic gene expression and myofibroblast differentiation. RHAMM function‒blocking peptides suppress this signaling and prevent TGFß1-induced myofibroblast differentiation. These results suggest that inhibiting RHAMM signaling will offer a treatment method for cutaneous fibrosis in systemic sclerosis.


Subject(s)
Adipokines/metabolism , Extracellular Matrix Proteins/antagonists & inhibitors , Hyaluronan Receptors/antagonists & inhibitors , Peptides/pharmacology , Scleroderma, Systemic/drug therapy , Skin/pathology , Animals , Bleomycin/administration & dosage , Bleomycin/toxicity , Cell Differentiation/drug effects , Disease Models, Animal , Extracellular Matrix Proteins/genetics , Extracellular Matrix Proteins/metabolism , Female , Fibrosis , Humans , Hyaluronan Receptors/genetics , Hyaluronan Receptors/metabolism , Mice , Mice, Knockout , Peptides/therapeutic use , Proto-Oncogene Proteins c-myc/metabolism , Scleroderma, Systemic/chemically induced , Scleroderma, Systemic/pathology , Signal Transduction/drug effects , Skin/drug effects , Transforming Growth Factor beta1/metabolism
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