Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute monocytic leukaemia (AMoL) was diagnosed in 99 adults, aged 18-85 years (median 56) over a period of 10 years. Sixty-five patients had extramedullary leukaemia, 13 had clinical signs of leucostasis, and 19 had disseminated intravascular coagulation. Four patients died before receiving any treatment, 12 received supportive care only and seven received low dose AraC, but only one of them responded. Seventy-six patients received intensive chemotherapy, 72 of them with an anthracycline-AraC based regimen, with or without an epipodophyllotoxin. Fifteen patients died within 7 d of diagnosis, due to leucostasis in nine cases. Predictive factors for early death were advanced age, leucostasis, fever, leucocytes above 100 x 10(9)/l, and renal failure. Fifty (66%) of the patients treated intensively reached complete remission (CR). Advanced age, fever and complex cytogenetic abnormalities were significantly associated with a lower CR rate. Median actuarial disease-free survival was 20.5 months, and was not significantly influenced by any pretreatment parameter. Five patients relapsed in the central nervous system (CNS), in spite of systematic CNS prophylaxis. No differences in CR rates were seen with the three anthracycline-AraC based regimens used in our patients. Significant differences in disease-free survival were seen between them, however, suggesting that early consolidation chemotherapy and, more hypothetically, epipodophyllotoxin agents could prolong remission duration in AMoL.
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PMID:Acute monocytic leukaemia in adults: treatment and prognosis in 99 cases. 237 23

A 26-year-old woman was admitted to our hospital for lumbago on November 29, 1995. The white blood cell count was 6,500/microliter with 26.5% myeloblasts and the bone marrow was hyperplastic due to myeloblasts. Myeloblasts were negative for myeloperoxidase and positive for alpha-naphthyl butylate esterase, CD11a (89%), CD11b (38%), CD11c (92%), CD33 (91%) and HLA-DR (58%). Chromosomal abnormalities were recognized: 46, XX, t(9;11) (p22;q23), 45, XX, -7, t(9;11) (p22;q23) and 47, XX, +19, t(9;11) (p22;q23). Acute myeloblastic leukemia (M5a) was diagnosed. Disseminated intravascular coagulation was also present. The patient received induction therapy and achieved remission on January 9, 1996, but myeloblasts increased to 3.6% in bone marrow despite consolidation therapy. Low doses of cytarabine (AraC) and etoposide were instituted on March 7, granulocyte colony-stimulating factor (G-CSF) was started on March 15, and pronounced skin infiltration developed on March 18. The patient received reinduction therapy from April 16 and administration of G-CSF was combined for 2 days, and a marked increment of myeloblasts in the peripheral blood was observed. After discontinuation of G-CSF, myeloblasts decreased and skin infiltration disappeared. However, the patient died of cerebral infiltration on June 30. The response of myeloblasts to G-CSF by in vitro liquid culture was noteworthy. The present case stresses the requirement for great caution to be exercised in the use of G-CSF in patients receiving low dose AraC.
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PMID:[Acute myeloblastic leukemia showing pronounced skin infiltration during administration of low-dose cytarabine and etoposide with granulocyte colony-stimulating factor]. 936 68

Superior sagittal sinus thrombosis (SSST) is a very rare but life-threatening complication in leukemia patients. SSST is very rare in acute myeloid leukemia (AML). In leukemia patients, several risk factors for SSST have been reported such as administration of L-asparaginase, disseminated intravascular coagulation, congenital thrombophilia, meningeal leukemia, and intrathecal chemotherapy (IT). Lumbar puncture itself and corticosteroid administration have also been acknowledged as risk factors. We describe herein our clinical experience with SSST in a 29-year-old Japanese man suffering from AML with t(8;21)(q22;q22), who presented with abrupt onset of loss of consciousness, left hemiplegia, and seizure soon after IT and high-dose cytarabine (HD-AraC) with dexamethasone for post remission consolidation. Despite the presence of intracranial hemorrhage (ICH) due to SSST rupture, we conducted anticoagulant therapy with heparin. Although ICH worsened temporarily, his clinical condition gradually improved with resolution of the SSST, and he eventually became fully ambulatory. There were no deficiencies of natural anticoagulants. Three additional cycles of HD-AraC without IT therapy were conducted, but no neurological complications recurred with the concomitant use of warfarin. He was discharged free of neurological deficits. In our case, there is a possibility that IT and the administration of corticosteroids along with HD-AraC triggered SSST.
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PMID:[Superior sagittal sinus thrombosis after intrathecal chemotherapy and intravenous high-dose cytarabine in an acute myeloid leukemia case with t(8;21)(q22;q22)]. 2716 54

Idarubicin (IDR), cytarabine (AraC), and tamibarotene (Am80) are effective for treatment of acute myeloid leukemia (AML). In acute leukemia, the incidence of venous thromboembolism or disseminated intravascular coagulation is associated with induction chemotherapy. Procoagulant effects of IDR, AraC, and Am80 were investigated in a vascular endothelial cell line EAhy926 and AML cell lines HL60 (AML M2), NB4 (AML M3, APL), and U937 (AML M5), focusing on tissue factor (TF), phosphatidylserine (PS), and thrombomodulin (TM). IDR induced procoagulant activity on the surface of vascular endothelial and AML cell lines. Expression of TF antigen, TM antigen, and PS were induced by IDR on the surface of each cell line, whereas expression of TF and TM mRNAs were unchanged. Conversely, Am80 decreased TF exposure and procoagulant activity, and increased TM exposure on NB4 cells. In NB4 cells, we observed downregulation of TF mRNA and upregulation of TM mRNA. These data suggest IDR may induce procoagulant activity in vessels by apoptosis through PS exposure and/or TF expression on vascular endothelial and AML cell lines. Am80 may suppress blood coagulation through downregulation of TF expression and induction of TM expression. Our methods could be useful to investigate changes in procoagulant activity induced by antineoplastic drugs.
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PMID:Cell-based evaluation of changes in coagulation activity induced by antineoplastic drugs for the treatment of acute myeloid leukemia. 2840 95