Lymphangitis carcinomatosa is inflammation of the lymph vessels (lymphangitis) caused by a malignancy. Breast, lung, stomach, pancreas, and prostate cancers are the most common tumors that result in lymphangitis. Lymphangitis carcinomatosa was first described by pathologist Gabriel Andral in 1829 in a patient with uterine cancer. Lymphangitis carcinomatosa may show the presence of Kerley B lines on chest X-ray. Lymphangitis carcinomatosa most often affects people 40–49 years of age.Lymphangitis carcinomatosa may be caused by the following malignancies as suggested by the mnemonic: "Certain Cancers Spread By Plugging The Lymphatics" (cervical cancer, colon cancer, stomach cancer, breast cancer/bronchiogenic carcinoma, pancreatic cancer, thyroid cancer, laryngeal cancer)

Pathology
In most cases, lymphangitis carcinomatosis is caused by the dissemination of a tumor with its cells along the lymphatics. However, in about 20 percent of cases, the inflammation of the lymphatic tubules (lymphangitis) is caused by a tumor that blocks the drainage of the lymph duct. In the lung, this is often caused by a centrally located mass, near the hilum of the lung that blocks lymphatic drainage. Prognosis
Previously, the finding of lymphangitis carcinomatosis meant about a six-month life expectancy. However, improved treatment has improved survival in patients with lymphangitis carcinomatosis, with patients often surviving three or more years with treatment. History
Lymphangitis carcinomatosa was first described by pathologist Gabriel Andral in 1829 in a patient with uterine cancer. See also
Lymphangitis

References


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More specifically, calcium overload and excessive production of reactive oxygen species in the first few minutes after reperfusion set off a cascade of biochemical changes that result in the opening of the so-called mitochondrial permeability transition pore (MPT pore) in the mitochondrial membrane of cardiac cells.The opening of the MPT pore leads to the inrush of water into the mitochondria, resulting in mitochondrial dysfunction and collapse. Upon collapse, the calcium is then released to overwhelm the next mitochondria in a cascading series of events that cause mitochondrial energy production supporting the cell to be reduced or stopped completely. The cessation of energy production results in cellular death. Protecting mitochondria is a viable cardioprotective strategy.In 2008, an editorial in the New England Journal of Medicine called for more studies to determine if cyclosporin can become a treatment to ameliorate reperfusion injury by protecting mitochondria. To that end, in 2011 the researchers involved in the original 2008 NEJM study initiated a phase III clinical study of reperfusion injury in 1000 myocardial infarction patients in centers throughout Europe. Results of that study were announced in 2015 and indicated that "intravenous cyclosporine did not result in better clinical outcomes than those with placebo and did not prevent adverse left ventricular remodeling at 1 year." This same process of mitochondrial destruction through the opening of the MPT pore is implicated in making traumatic brain injuries much worse. TRO40303
TRO40303 is a new cardioprotective compound that was shown to inhibit the MPT pore and reduce infarct size after ischemia-reperfusion.