title: [Therapeutic effectiveness of thalidomide to multiple myeloma and its mechanism].
abstract: OBJECTIVE
  To observe the effective mechanism and side effects of thalidomide to multiple myeloma (MM).
  
  
  METHODS
  Ten cases of MM were studied, of which 3 were previously untreated and 7 refractory or relapsed. Bone marrow microvascular density (MVD) was detected by factor-VIII related antigen and CD(34) immunohistological staining and serum concentration of vascular endothelial growth factor (VEGF) before and after treatment was determined by ELISA. The initial dosage of thalidomide was 100 approximately 200 mg/d with a weekly escalation of 50 mg/d to 450 approximately 650 mg/d. The therapeutic effectiveness is classified into partial remission, improvement and uneffective according to the decrease of serum M protein and bone marrow myeloma cells. Anemia, renal function and blood electrolytes were also observed.
  
  
  RESULTS
  Before treatment, MVD was 73.32 +/- 28.80 and 32.30 +/- 12.50 in MM and control group, respectively, (P < 0.01). MVD in MM group decreased to 56.12 +/- 19.34 after treatment, and was of significant difference (P < 0.05) as compared to the pretreatment value. However, there was still a significant difference as compared to control (56.12 +/- 19.34 vs 32.30 +/- 12.50, P < 0.01). The concentration of VEGF significantly decreased after treatment [from (178.23 +/- 26.56) ng/L to (78.48 +/- 19.98) ng/L, P < 0.01)]. The total effective rate was 70%. There were no serious side effects.
  
  
  CONCLUSIONS
  MVD and VEGF concentration were decreased obviously by thalidomide treatment. The dosage of 450 approximately 650 mg/d might be effective in refractory or initial MM.
authors.affiliation: Department of Hematology, Dongying Hospital, Dongying 257091, China.
authors.forename: Minglin
authors.initials: M
authors.lastname: Wang
authors.forename: Yuefen
authors.initials: Y
authors.lastname: Liu
authors.forename: Yinggang
authors.initials: Y
authors.lastname: Li
authors.forename: Hongguang
authors.initials: H
authors.lastname: Wu
mesh_terms: D000368:Aged; D020533:Angiogenesis Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D018952:Antigens, CD34 / Q000032:analysis; D001853:Bone Marrow / Q000098:blood supply / Q000187:drug effects; D003248:Constipation / Q000139:chemically induced; D016228:Endothelial Growth Factors / Q000097:blood; D005221:Fatigue / Q000139:chemically induced; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood; D008222:Lymphokines / Q000097:blood / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009101:Multiple Myeloma / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D009325:Nausea / Q000139:chemically induced; D012893:Sleep Wake Disorders / Q000139:chemically induced; D013792:Thalidomide / Q000009:adverse effects / Q000627:therapeutic use*; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D020533:Angiogenesis Inhibitors; D018952:Antigens, CD34; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014841:von Willebrand Factor; D013792:Thalidomide