New application of direct lymphangiography in the diagnosis and treatment of chylothorax after lung cancer surgery: a case series.

BACKGROUND: Chylothorax is caused by accumulation of chylous fluid in the thoracic cavity following injury to the thoracic duct or its tributaries. It is a rare but relatively severe complication of lung cancer surgery, especially after lung resection and mediastinal lymph node dissection. If chylothorax is not treated promptly and effectively, it may result in relatively high mortality rate. Although the majority of patients with chylothorax secondary to lung cancer surgery can be treated with conservative measures, there are still some patients who fail to respond to conservative treatment or suffer from recurrent episodes. This study aims to explore the causes of postoperative chylothorax and how targeted treatment can help achieve better outcomes. METHODS: Four cases of chylothorax secondary to lung cancer surgery are reported in which patients underwent direct lymphangiography (DLG) after failed conservative treatment. RESULTS: Thoracic duct obstruction was found in all patients on DLG, as well as dilated intrathoracic part of the thoracic duct. Thoracic duct reconstruction was performed to successfully treat 3 of the 4 patients. CONCLUSIONS: DLG is of great value in the diagnosis of chylothorax secondary to lung cancer surgery, for which thoracic duct reconstruction proves to be an effective procedure. DLG provides a new objective basis for the diagnosis and treatment of chylothorax. It is our best wish to help more patients with chylothorax secondary to lung cancer surgery.

Vaccine of RANKL mutant conjugated with KLH effectively stabilizing bone metabolism and preventing trabecular microstructural degeneration in osteoporotic rats.

Receptor activator of nuclear factor kappa-B ligand (RANKL) is one of the key factors regulating the maturation of osteoclasts and an important target for osteoporosis treatment. A monoclonal antibody against RANKL showed effective therapeutic activity against osteoporosis by inhibiting bone resorption by osteoclasts. However, being an exogenous protein, its efficacy decreases after long-term use, and its discontinuation increases the risk of vertebral fractures. Here, we aimed to design an active immunotherapeutic agent to induce a T-cell dependent primary response. The agent, a mutant RANKL vaccine (mRv), was produced by cross-linking mutant RANKL, lacking the ability to stimulate osteoclast maturation, with the carrier protein keyhole limpet hemocyanin, a neo-antigen with a large molecular mass. Subcutaneous injection of mRv stimulated rats with ovariectomy-induced osteoporosis to produce high titers of anti-RANKL antibodies. The mutant RANKL vaccine decreased serum CTX-1 and BALP levels and inhibited the microstructural degeneration of trabecular bone in osteoporotic rats. mRv overcame immune system tolerance, stimulated rats to produce therapeutic antibodies, stabilized bone metabolism, and inhibited trabecular microstructural degeneration. These findings confirm the potential of the mutant RANKL vaccine to be developed into an effective preventive and therapeutic agent for osteoporosis.