Less commonly, FL presents as extra-nodal masses in the skin, thyroid gland, salivary gland, breast, testicles. spleen, liver, and/or lung. Regardless of the type of presentation, FL is usually (~80% of cases) at an advanced stage at diagnosis as indicated by involvement of the bone marrow (50% to 70% of cases), multiple lymph nodes in different parts of the body, and/or other tissues. A minority (<33%) of FL patients present with B symptoms, i.e. recurrent unexplained fevers, recurrent night sweats, and/or weight loss ≥10% in the past 6 months. Generally, the disease has an indolent and prolonged course with a median life expectancy of 15–20 years: a large percentage of patients die from other causes than their FL disease. However, each year, including the early years after diagnosis, some 2-3% of FL cases transform to t-FL; Median survival has been ~4.5 years after the onset of this transformation.There are less common subtypes of FL that differ not only in their presentation but also in their histopathology, genetic abnormalities, and course. These subtypes, which are now (i.e. primary gastrointestinal tract FL) or may in the future (pediatric-type FL) be considered distinctive diseases, are:

Duodenal-type follicular lymphoma
Duodenal-type follicular lymphoma (DFL) was initially considered to be a type of Primary gastrointestinal tract (GI tract) follicular lymphoma (PGTFL), i.e. a follicular lymphoma in which GI tract lesions were prominent parts of the disease.
Familial cutaneous collagenoma is an autosomal dominant genetic disorder characterized by the presence of multiple symmetric nodules on the trunk and upper arms in multiple members of the same family. The nodules are flesh-colored, asymptomatic, and they start appearing during adolescent years.It has been described in 10 families worldwide.These nodules are caused by an overgrowth of collagen fibers with an accompanying decreased number of elastic fibers.In some cases, this condition is associated with anomalies in other parts of the body. Genetics
In a 2-generation Israeli Jewish family (whose affected members were two biological cousins), Hershkovitz et al. found a heterozygous mutation in the LEMD3 gene in both cousins and in the unaffected father of one of them. Possibly related complications
In 1968, Henderson et al. described 3 American brothers with the condition, and found that each one of them had health complications: the first brother suffered from idiopathic cardiomyopathy, the second suffered from iris atrophy of the left eye with accompanying severe high-frequency deafness, and the third suffered from recurrent vasculitis. == References ==