Reading about this disorder really seems alot like cfs, dysfunctional cd lymphocytes, b-cells and nk cells. Possible causes: Altered immunity 3.3.1. Inherited syndromes and susceptibility via individual inherited genetic sequences. Several studies have suggested a slight excess of cases occurring in blood relatives. There is a range of rare but well defined and usually simply inherited conditions that have an excess of lymphoproliferative disease as part of the syndrome, for example, ataxia telangiectasia, Wiskott-Aldrich syndrome and common variable immunodeficiency. The potential underlying genetic defects in heterozygotes could represent a major initiating cause of a lymphoproliferative disorder although it would be unlikely to be the only step required to manifest the disease in this population. 3.3.2. Immunodeficiency due to past medical history. There is a higher risk of developing chronic lymphoproliferative disorders in individuals receiving long-term immunosuppressive drug therapy such as transplant recipients and patients with autoimmune diseases. An increased risk is also seen in patients suffering from a variety of autoimmune conditions, for example, rheumatoid arthritis, Sjgrens syndrome and coeliac disease, independent of immunosuppressive treatments. 3.3.3. Infections. Human immunodeficiency virus (HIV), human T-cell lymphotrophic virus type 1 (HTLV-1), human herpes virus-8 (HHV8) and Epstein-Barr virus are all associated with an increased risk of certain types of lymphoproliferative disease, most probably by causing immunosuppression. HTLV is a retrovirus that is endemic in southern Japan and the Caribbean basin. Infection with HTLV-1, especially in early childhood, is strongly related to the development of adult T-cell leukaemia/lymphoma with an estimated cumulative lifetime risk of approximately 5%. HTLV can be transmitted both sexually and by blood transfusion. Unlike HTLV-1, EBV infection is a highly prevalent 5 infection in the adult population (approximately 90% of individuals in developed countries having evidence of previous infection by the age of 40). The association between EBV and lymphoma is well described for both Burkitts lymphoma and immunodeficiency-associated lymphoma. Nearly all cases of endemic Burkitts lymphoma (in Africa) can be shown to contain EBV viral genomic DNA, but the frequency is less than 20% in sporadic cases in developed countries. Natural killer (NK) cell lymphoma is an aggressive and refractory form of lymphoma which is strongly associated with EBV and although rare in the west has a relatively high incidence in south-east Asia. In addition, the Gram negative bacterium, Helicobacter pylori, is associated with the development of gastric non-Hodgkins lymphoma (NHL) of B-cell origin arising from the mucosa-associated lymphoid tissue (MALT). Prognosis: 4.1. It is impossible to generalise regarding the outcome of chronic lymphoproliferative disorders due to the heterogeneity of the group and the different behaviour of each disease entity. Furthermore, within each entity there is a wide variation in potential outcomes, although it can be stated that in the majority of cases survival is measured in terms of years rather than months. 4.2. Many patients do not require any treatment when first diagnosed, with an expectant or watch and wait approach employed. In very indolent disease patients may never require treatment for their lymphoproliferative disease and remain asymptomatic during their lifetime. The aims of treatment are to control symptoms or other effects of the tumours. 4.3. Chronic lymphoproliferative disorders are incurable using conventional treatments and tend to run an indolent course with treatment being required when there is symptomatic disease progression. Treatment modalities include chemotherapy and radiotherapy with varying degrees of response and remission. Newer agents, such as monoclonal antibodies, can improve the response rates for some tumours and achieve responses in patients refractory to other forms of chemotherapy. 4.4. The only potential curative treatment for these disorders is through allogeneic haemopoietic stem cell transplantation. However, this approach is only suitable for the minority of younger and fitter patients and is associated with a high mortality and morbidity. Therefore, it is still considered as an experimental treatment in chronic lymphoproliferative disorders and should only be performed in the setting of a well designed clinical trial in younger patients with aggressive or poorer risk disease. http://www.veterans-uk.info/publications/chronic_lymphoproliferative_disorders.pdf It all sounds familiar, mmm cfs/me and this document is from the UK. cheers!!!