NIH conference. XXXX with dysproteinemia.

@entity1 @entity3329 @entity1910 @entity882 @entity706 @entity281 @entity4754 @entity5714 @entity9233
@entity9233 with dysproteinemia is a disorder characterized by a sudden onset of constitutional symptoms and @entity3329 . @entity1 often have @entity4754 , autoantibodies, @entity1910 , @entity882 , or @entity5714 . Diagnosis requires a lymph node biopsy that shows architectural effacement, absence of germinal centers, arborization of postcapillary venules, and a polymorphous infiltrate that includes immunoblasts. Early in the disease, activated T cells in blood and lymph nodes stimulate B cells to proliferate and produce antibody. However, late in the disease, immune suppression may result from increased suppressor function. Clonal rearrangements, which are seen in all @entity1 with regard to either the T-cell receptor beta-chain gene or immunoglobulin genes, have been followed by @entity706 in some @entity1 . Thus, this disorder stands partway between benign lymphoid proliferation and clonal lymphoid transformation. The prognosis of this disorder is poor; 75% of @entity1 die within 2 years or develop a @entity706 . The rest usually go into a sustained remission. Current treatment with corticosteroid and immunosuppressive agents is unsatisfactory, especially because of late immunosuppression and predisposition to @entity281 .
