Lymphedema is a chronic disease that results in swelling and decreased function due to abnormal lymphatic fluid clearance and chronic inflammation. In Western countries, lymphedema most commonly develops following an iatrogenic injury to the lymphatic system during cancer treatment. It is estimated that as many as 10 million patients suffer from lymphedema in the United States alone. Current treatments for lymphedema are palliative in nature, relying on compression garments and physical therapy to decrease interstitial fluid accumulation in the affected extremity. However, recent discoveries have increased the hopes of therapeutic interventions that may promote lymphatic regeneration and function. The purpose of this review is to summarize current experimental pharmacological strategies in the treatment of lymphedema.

Purpose of Review This review aims to summarize the current knowledge regarding the pharmacological interventions studied in both experimental and clinical trials for secondary lymphedema. Recent Findings Lymphedema is a progressive disease that results in tissue swelling, pain, and functional disability. The most common cause of secondary lymphedema in developed countries is an iatrogenic injury to the lymphatic system during cancer treatment. Despite its high incidence and severe sequelae, lymphedema is usually treated with palliative options such as compression and physical therapy. However, recent studies on the pathophysiology of lymphedema have explored pharmacological treatments in preclinical and early phase clinical trials. Summary Many potential treatment options for lymphedema have been explored throughout the past two decades including systemic agents and topical approaches to decrease the potential toxicity of systemic treatment. Treatment strategies including lymphangiogenic factors, anti-inflammatory agents, and anti-fibrotic therapies may be used independently or in conjunction with surgical approaches.

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ensure that cells were not dislodged from the vessel surface, perfusion was started at 2.92 dyne/cm 2 and increased daily by 0.66 dyne/cm 2 . RESULTS:We designed sacrificial loops with a 750um diameter. Some sacrificial materials previously published quickly dissolve following contact with liquid and cannot be sterilized with ethanol. The PVA properties allowed its submersion in 70% ethanol for 15 minutes without appreciable material degradation or structure loss. ECs incubated with an 8% PVA mixture over 72h did not experience significant cytotoxicity. Immunofluorescence demonstrated an elaborate blood vessel shape in the 3D printed structure robustly lined with complete SMC and EC layers. As early as 2 days after perfusion, ECs aligned and elongated matching perfusion direction comparable to physiologic flow changes. CONCLUSIONS:To engineer larger tissue flaps with better nutrient perfusion, we explored the role of a perfused lab-fabricated vessel utilizing PVA as a sacrificial material in complex 3D shapes microns in diameter. PVA is beneficial over other loop materials, like Pluronic F127 or needles, because it can be sterilized, has good biocompatibility, high 3D-printability, and flexible mechanical properties.

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