Some facts about this disease: Malignant ataxia of claret cells Peak accident amid 60-70 years Rare beneath the age of 30 Males are afflicted added than females. Pathogenesis: -The tissues are infiltrated by proliferating cells. -One blazon of aberrant immunoglobulins (paraprotein) usually IgG or IgA. -This paraprotein may account auto-immune manifestations. -The paraprotein may covering the platelets and agglomeration factors. -Production of abridged immunoglobulins (light alternation only) by plas. beef which are excreted in urine (Bence-Jones protein). -Diminished assembly of accustomed immunoglobulins increases infections. Clinical picture: i- Skeletal: Bone aches and dissection fractures Multiple osteolytic lesions in the skull and osteoclast stimulation ii- Neurological: Compression of analgesic bond by vertebral lesion Infiltration of roots, fretfulness and anatomy by claret cells. iii- Renal Failure: due to: Bence-Jones proteins: precipitated in kidneys Nephrocalcinosis: acquired by hypercalcaemia Hyperuricaemia: due to abolition of claret cells Amyloidosis of kidneys Pyelonephritis: due to susceptibility to infections iv- Anemia: due to: BM (bone marrow) backup by claret cells BM inhibition by chemotherapy and radiotherapy Haemolysis acquired by paraprotein Renal impairment v- Bleeding Tendency due to: Coating of agglomeration factors by paraprotein