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The lymph ends its journey in the thoracic duct or right lymphatic duct, which drain into the blood circulation. [10] Several research groups have hypothesized that chronic inflammation is a key regulator in the development of lymphedema. Th cells, particularly Th2 differentiation, play a crucial role in the pathophysiology of lymphedema.
Primary lymphedema is a form of lymphedema which is not directly attributable to another medical condition. It can be divided into three forms, depending upon age of onset: congenital lymphedema, lymphedema praecox, and lymphedema tarda. [1] Congenital lymphedema presents at birth. Lymphedema praecox presents from ages 1 to 35.
Lymphedema praecox [2] is a condition characterized by swelling of the soft tissues in which an excessive amount of lymph has accumulated, and generally develops in females between the ages of nine and twenty-five. This is the most common form of primary lymphedema, accounting for about 80% of the patients.
Lymphedema is a buildup of lymph in the interstitial space as a result of an obstruction in the lymphatic system, which can cause edema, inflammation, and fibrosis in the tissues. Lymphedema can be primary, when it occurs alone, or secondary, when it occurs as a result of another disease like filariasis or cancer.
Angiosarcoma is found to occur in 0.07% to 0.45% of people who survive at least 5 years after a radical mastectomy.Although the majority of Stewart-Treves syndrome-related angiosarcomas are caused by post-mastectomy lymphedema, angiosarcoma development has been linked to persistent lymphedema of any origin.
Hennekam syndrome, also known as intestinal lymphagiectasia–lymphedema–mental retardation syndrome, [1] is an autosomal recessive disorder consisting of intestinal lymphangiectasia, facial anomalies, peripheral lymphedema, and mild to moderate levels of growth and intellectual disability.
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