Multiple Myeloma Pathophysiology

Pathophysiology of multiple myeloma - multiple myeloma pathogenesis - Multiple myeloma is a malignant tumor of plasma cells that is characterized by the development of bone lesions osteolytic often. Bone damage caused by multiple myeloma is due to the increased activity of osteoclasts that occurs adjacent to multiple myeloma cells. This activity is accompanied by the differentiation and activity of osteoblasts pressed, resulting in the formation of bone most affected and the development of osteolytic lesions terrible. Recently, the biological mechanisms involved in the activation of an imbalance between the osteoclasts and inhibition of osteoblasts caused by multiple myeloma cells is described first. In this article, we will review the underlying pathophysiology of modified bone disproportionate and a potential new strategy for the treatment of bone disease in multiple myeloma.
Multiple Myeloma Pathophysiology

The proliferation of plasma cells malignant create immunoglobulin monoclonal to penetrate and destroy adjacent bones. The pain of the bone, renal failure, hypercalcemia, anemia and frequent infections are reported. The Diagnosis is made by proving the protein M (sometimes present in urine, not in serum) with osteolysis, proteinuria light chains and the plasma cells excess in the bone marrow, which usually requires a biopsy core. It is treated with conventional chemotherapy (usually alkylates, corticosteroid, anthracyclines, or thalidomide) and high dose melphalan, which is supplemented with stem cell transplantation autologous.

The incidence of plasmacytomas is 2-4 / 100,000 population. The ratio of men to women is 1.6: 1, and most patients have> 40 years. In black leather, naturally is 2 × higher than the white. The etiology is not known, but factors of chromosomes and genetics, radiation, and some chemical compounds mentioned.

Multiple Myeloma Pathophysiology

About 55% of the plasmacytomas produce IgG, and about 20% of IgA; In which 40% had proteinuria Bence Jones, namely the freezing of the free on monoclonal κ or λ chain light, while 15-20% of patients just give a light protein Bence-Jones. These patients are more prone to osteolytic changes, hypercalcemia, kidney failure, and amyloidosis. Only 1% of the cases there is in myeloma IgD.

Osteoporosis difuzia or changes osteolytic limited occur, usually in the hip, spine, ribs and skull. Of the lesion this is a consequence of the spread of plasmacytomas into the bone or the effect of cytokines, which are cells of a malignant jammed and stimulate osteoclasts. Bone changes are usually numerous, but sometimes also neoplasm intramedullary single. The wound that is rarely found outside the framework, but it can occur in every tissue, mainly in the upper respiratory tract.
See also: Multiple Myeloma Blood Test Results Explained
Often hypercalcemia and anemia occur. The lack of the kidneys ("kidney myeloma") occurs due to the formation of the cylinder much in the tubules of the kidney, atrophic epithelium, and interstices fibrosis.

The spread of bacterial infections is a consequence of the production of immunoglobulins that is not enough, but also other factors. Amyloidosis secondary (page 1311) occurs in 10% of patients with myeloma, especially in proteinuria Bence Jones.

The Clinical Picture

Gum disease continuous (a special on the back and chest), renal failure and bacterial infections in a row is a cause of restlessness. Pathological fractures are frequent, and the collapse of the vertebrae can cause compression of the case of the spinal cord and paraplegia. Sometimes, symptoms of anemia, which is the only causative treatment, adopted, and in cases, rare syndrome hypervisors grow (see page 1128). Peripheral neuropathy, carpal tunnel syndrome, abnormal bleeding and signs of hypercalcemia (e.g. polyuria, polydipsia) is not common. As a rule, lymphadenopathy or hepatosplenomegaly not found.
See also: Multiple Myeloma Foundation: MMRF