title: Oral eicosapentaenoic acid for complications of bone marrow transplantation.
abstract: The 'systemic inflammatory response syndrome' (SIRS) may represent the underlying cause of complications after bone marrow transplantation (BMT). This study was conducted to determine whether blocking the etiologic factors of SIRS could improve the complications of BMT. Sixteen consecutive patients with unrelated donors were allocated alternately to two groups. Seven patients received 1.8 g/day of eicosapentaenoic acid (EPA) orally from 3 weeks before to about 180 days after transplantation, while nine patients did not. These two groups were compared with respect to complications, survival, and various cytokines and factors causing vascular endothelial damage. All seven patients receiving EPA survived and only two had grade III graft-versus-host disease (GVHD). Among the nine patients not receiving EPA, three had grade III or IV GVHD. In addition, thrombotic microangiopathy developed in four patients and cytomegalovirus disease occurred in four. Five patients died in this group. The levels of leukotriene B(4), thromboxane A(2), and prostaglandin I(2) were significantly lower in patients receiving EPA than in those not receiving it (all P < 0.01). Cytokines such as tumor necrosis factor-alpha, interferon-gamma, and interleukin-10 were also significantly decreased by EPA (P < 0.05), as were factors causing vascular endothelial damage such as thrombomodulin and plasminogen activator inhibitor-1 (P < 0.05). The survival rate was significantly higher in the group given EPA (P < 0.01). EPA significantly reduced the complications of BMT, indicating that these complications may be manifestations of the systemic inflammatory response syndrome.
authors.affiliation: Second Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takatsuka
authors.forename: Y
authors.initials: Y
authors.lastname: Takemoto
authors.forename: N
authors.initials: N
authors.lastname: Iwata
authors.forename: A
authors.initials: A
authors.lastname: Suehiro
authors.forename: T
authors.initials: T
authors.lastname: Hamano
authors.forename: T
authors.initials: T
authors.lastname: Okamoto
authors.forename: A
authors.initials: A
authors.lastname: Kanamaru
authors.forename: E
authors.initials: E
authors.lastname: Kakishita
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000284:Administration, Oral; D000328:Adult; D000741:Anemia, Aplastic / Q000628:therapy; D016026:Bone Marrow Transplantation / Q000009:adverse effects*; D016207:Cytokines / Q000097:blood*; D003586:Cytomegalovirus Infections / Q000209:etiology; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D006086:Graft vs Host Disease / Q000209:etiology; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D007378:Interleukins / Q000097:blood; D007938:Leukemia / Q000628:therapy; D015993:Life Tables; D017563:Lung Diseases, Interstitial / Q000209:etiology; D008297:Male; D016019:Survival Analysis; D018746:Systemic Inflammatory Response Syndrome / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D014184:Transplantation, Homologous; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014652:Vascular Diseases / Q000209:etiology
chemical_list: D016207:Cytokines; D007166:Immunosuppressive Agents; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D015121:6-Ketoprostaglandin F1 alpha; D007371:Interferon-gamma; D015118:Eicosapentaenoic Acid