@entity751 in XXXX .

@entity1 @entity1581 @entity548 @entity1582 @entity4754 @entity751 @entity209 @entity8057
@entity4754 increases serum viscosity and is the most common cause of @entity751 . @entity4754 resulting in @entity751 is seen in multiple @entity1582 and Waldenstr  m's @entity8057 . The reasons for elevated viscosity are increased protein content and large molecular size, abnormal polymerization, and abnormal shape of immunoglobulin molecules. Other hematologic and @entity209 seen in @entity1 with @entity1581 also contribute to hyperviscosity. Symptomatic hyperviscosity is much more common in Waldenstr  m's @entity8057 (10 to 30%) than it is in @entity1582 (2 to 6%). Symptoms of hyperviscosity usually appear when the normal serum viscosity of 1.4 to 1.8 cp reaches 4 to 5 cp, corresponding to a serum immunoglobulin M (IgM) level of at least 3 g/dL, an IgG level of 4 g/dL, and an IgA level of 6 g/dL. Symptoms of hyperviscosity include constitutional symptoms; @entity548 ; and ocular, neurological, and cardiovascular manifestations. Immediate therapy of symptomatic hyperviscosity is directed at reduction of blood viscosity by plasmapheresis to control symptoms. Long-term management is directed at control of the underlying disease to prevent production of the monoclonal protein. There may be a small proportion of individuals, usually old or with severely compromised performance status, who undergo plasma exchange as the sole symptomatic therapy of hyperviscosity secondary to @entity1581 .
