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)

Cytogenetic and ultrastructural findings were important diagnostic indicators of hypergranular promyelocytic leukemia (APL) in a patient whose bone marrow morphology appeared, by light microscopy, to be similar to that in acute myeloblastic leukemia (AML) with maturation. Peripheral blood smears and bone marrow specimens examined by light microscopy showed few cells with the numerous coarse, azurophilic granules typical of APL. Cytogenetic analyses, with several banding techniques, of cells from bone marrow and unstimulated peripheral blood revealed the 15;17 translocation, which has been observed only in APL. A reinterpretation of the reciprocal translocation, based on R banding, suggests that the breakpoints are distal to q24 in No. 15 and at or near the junction of q21 and q22 in No. 17. In addition, the patient had disseminated intravascular coagulation. The characteristic morphology of granules seen in APL was observed in this case only when transmission electron microscopy was used, since the granules were quite small. Since treatment for AML differs from that for APL, identification of the 15;17 translocation and ultrastructural evidence of granules represent valuable diagnostic aids for APL.
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PMID:Hypergranular promyelocytic leukemia (APL): cytogenetic and ultrastructural specificity. 27 86

Disseminated intravascular coagulation (DIC) commonly occurs in patients with acute promyelocytic leukemia (APL, FAB-M3) but may also be seen in other subtypes of AML. DIC in patients with AML has been attributed to procoagulants released from granular fractions of leukemic blast cells. The present study was designed (i) to evaluate thrombin activity in patients with AML by measuring plasma levels of fibrinopeptide A (FPA) prior to chemotherapy, and (ii) to examine whether a relationship between FPA levels and the number of peripheral blast cells exists. Plasma levels of FPA were determined using a commercially available RIA kit. To remove fibrinogen and the majority of elastase-induced fibrinopeptides (A alpha 1-21) known to crossreact with the FPA (A alpha 1-16) antiserum used in this assay, plasma samples were treated with bentonite prior to further processing. The study was conducted on 5 patients with APL and on 22 patients with other subtypes of AML. Peripheral blast cell counts at initial diagnosis ranged from 2100 to 56,000/microliters in patients with APL and from 1900 to 151,000/microliters in patients with other AML subtypes. The mean (+/- 1 SEM) pretreatment plasma level of FPA was significantly higher (p = 0.021) in the 5 patients with APL (38.2 +/- 8.3 ng/ml) than in patients with other AML subtypes (8.1 +/- 0.7 ng/ml). No relationship was found between peripheral blast cell counts and the corresponding FPA levels in the total group of 27 patients. However, when considering the 5 patients with APL separately, a significant correlation was observed between peripheral blast cell number and FPA plasma levels (r = 0.88, p = 0.050). This study confirms that thrombin generation is considerably greater in patients with acute promyelocytic leukemia than in other subtypes of AML. We conclude that type and number of circulating blast cells and their related capacity to express procoagulant activities appear to be major determinants of excessive fibrinogen degradation in AML.
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PMID:Relationship of thrombin generation to peripheral blast cell count in patients with acute myeloblastic leukemia (AML). 236 38

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

A 34-year old female was admitted to our clinic because of fever and general fatigue on March 26, 1987. On admission, peripheral blood (PB) revealed pancytopenia. Bone marrow smears revealed 9. 0% of promyelocytic cells with or without Auer rods. Diagnosis of RAEB in transformation was made. Chromosome study of the bone marrow cells showed t(15; 17) in 3 out of 20 cells analysed. After 3 months, the leukemic cells were observed in PB and increased in number. Then the patient showed bleeding tendency and fibrin degradation products (FDP) increased up to 40 micrograms/ml. And the leukemic cells were over 30% in PB at the end of July, 1987. The diagnosis of APL with DIC was made. To our knowledge, this is the first case of APL with a history of MDS with t(15; 17).
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PMID:[Acute promyelocytic leukemia with a history of RAEB in transformation and the 15/17 translocation]. 271 1

I studied the karyotype in 66 patients (38 children and 28 adults) with ANLL, who were diagnosed on the basis of the FAB classification. Clonal chromosome abnormalities were found in 45 of the 66 patients. Six patients had AML (M1), and 23 including 8 with t (8; 21), had AML (M2). All 10 patients but one with APL (M3) had t (15; 17). Twelve patients had AMMOL (M4); 7 of these had a normal karyotype, and another had t (11; 19). Fourteen patients had AMOL (M5); 4 of these had t (9; 11), and 4 others had 11q rearrangements not involving chromosome 9. Only one patient had EL (M6), whose karyotype was normal. As t (8; 21) and t (15; 17) are uniquely associated with AML (M2) and APL (M3), respectively, t (9; 11) is seen only kn AMOL The other 11q rearrangements are more common in AMOL, but are also seen in AMMOL. To examine correlation of karyotype with prognosis, the 66 patients were classified into 6 groups; 8 with t (8; 21), 9 with t (15; 17), 4 with t (9; 11), 5 with other 11q rearrangements, 19 with other abnormalities, and 21 with normal diploidy. All the patients with t (8; 21) entered remission, and their median survival (16 months) was longer than that of any other group of patients. The patients with normal diploidy, those with the 11q rearrangements, or those with other abnormalities had a little shorter survival than those with t (8; 21). All 9 patients with t (15; 17) had DIC, and 4 of these died during induction therapy. Their median survival was only 6 months. All patients with t (9; 11) died during induction therapy; 3 of these had extremely high WBC counts and DIC at diagnosis. The patients were also classified into 3 groups, i. e. NN (20 patients), AN (21 patients) and AA (19 patients), on the basis of the frequency of abnormal mitotic cells in the bone marrow. The NN patients or the AN patients had longer survival times than the AA patients (p less than 0.05). My study demonstrated that the karyotype is correlated with morphology of leukemic cells and with survival.
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PMID:[Chromosome aberrations and clinical features of childhood and adult acute nonlymphocytic leukemia]. 666 86

Procoagulant activity of gastric cancer tissues and leukocytes obtained from various types of leukemia have been studied with special reference to TTP. The following results were obtained. Homogenates of APL leukocytes and gastric cancer tissues contained strong procoagulant activities, most of which have been identified as TTP since the activities were neutralized by a specific antibody against purified human placenta TTP, inactivated by the removal of phospholipid with heptane-butanol mixture, and inactivated by the addition of phospholipase C. The delipidated homogenates regained procoagulant activities by relipidation procedures. These results also confirmed that TTP from APL leukocytes and gastric cancer tissues have the same lipoprotein properties as those of TTP in normal tissues. Though slight proteolytic activity and fibrinolytic activity were demonstrated in the homogenate of gastric cancer tissues, it was noted that the TTP activity was different from these two activities by partial purification of TTP from gastric cancer tissues. The TTP activity of 9 homogenates of gastric cancer tissues was 301 +/- 289 (mean +/- SD) units per mg protein, being higher in homogenates of mucinous adenocarcinoma and signet-ring cell carcinoma than in those of tubular and poorly differentiated adenocarcinoma. The mean TTP activity of leukocyte homogenates from 14 patients with APL and one out of 4 patients with CML in blastic crisis was 81 +/- 76 units/10(7) cells. The TTP activity of the homogenates of leukocytes from 7 out of 18 patients with AML and another patient with CML in blastic crisis ranged from one to six units/10(7) cells with a mean of 3.3 +/- 1.2. The TTP activity of leukocyte homogenates from the other 11 cases of AML, two cases of CML in blastic crisis, 6 cases of CML, and one case each of ALL and CLL were less than one unit/10(7) cells. In leukemic patients, all cases with a value of more than 202 for the product of units of TTP activity per 10(7) cells and differential count (%) of leukemic cells in the bone marrow smear (MU value) were accompanied by DIC. The MU value of leukemic patients correlated well to the plasma fibrinogen and serum FDP levels. All patients with a MU value of more than 277 died of DIC when a sufficient amount of heparin was not administered. On the other hand, no DIC developed in any of the patients with a MU value of less than 90.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of tissue thromboplastin in the development of DIC accompanying neoplastic diseases. 666 48

This study was made to know the significance of fibrinopeptide A(FPA) as an indicator for coagulative analysis in thrombotic diseases. In normal control subjects (n=21), values of FPA by the radioimmunoassay were 0.5 +/- 1.4 ng/ml (mean +/- SD). In animal models, using Lyoplastin (tissue thromboplastin, n=5) or Ancrod (n=5) to piglets, plasma FPA levels elevated rapidly as a reflection of fibrin formation, and these changes of FPA were found to be most rapid and sensitive among the indicators for coagulation and fibrinolysis. In patients with thrombosis (n=32), elevated FPA levels (14.7 +/- 13.8 ng/ml) and beta-thromboglobulin (beta-TG)(86.1 +/- 65.6 ng/ml) were found. FPA levels in these patients positively correlated to beta-TG (r=0.5539, P less than 0.05) and inversely to fibrinogen (fbg) (r= -0.3622, P less than 0.05). In patients with acute myelocytic leukemia (AML, n=112), acute promyelocytic leukemia (APL, n=18) and acute lymphocytic leukemia (ALL, n=15), mean FPA levels in patients with active signs and symptoms were significantly higher (AML: 13.5 ng/ml, APL: 20.8 ng/ml, ALL: 12.4 ng/ml) than those examined during remission states (AML: 7.7 ng/ml, P less than 0.02, APL: 3.9 ng/ml, P less than 0.01, ALL: 2.7 ng/ml, P less than 0.01). FPA levels in patients with APL inversely correlated to fbg (r= -0.6399, P less than 0.01). In patients with lung cancer (n=75), mean FPA level in advanced stage (17.7 ng/ml, n=67) were significantly higher than those examined in early stage 6.5 ng/ml, n=8, P less than 0.001). In patients with acute disseminated intravascular coagulation (n=12), prolonged prothrombin time and activated partial thromboplastin time, severely reduced fbg and platelets, and remarkably elevated fibrin degradation product were found. Elevated FPA and beta-TG levels were also found (FPA: 23.5 +/- 15.0 ng/ml, beta-TG: 100.0 +/- 63.0 ng/ml). In five patients with thrombotic diseases who were treated successfully with 12500 IU of heparin per 12 hours (subcutaneous injection), plasma FPA levels were reduced to near normal levels quicker than changes of other indicators. These clinical and experimental data suggested that FPA was an useful indicator for active coagulation process.
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PMID:[Significance of fibrinopeptide A as an indicator for coagulative analysis in thrombotic diseases]. 695 68

From January 1986 to April 1991, 100 consecutive patients with APL received oral ATRA at a dose of 60-100 mg/d alone or in combination with chemotherapy. In 84 cases treated with ATRA, 74 (88.1%) achieved CR; in the 16 cases treated with combined therapy, the CR Rate was 75%. Among the 50 patients followed up for a median of 36 months, 10 used ATRA (Group B) as continuation therapy, 10 chemotherapy (Group C), and 30 cases ATRA and chemotherapy alternatively (Group A). The mean survival was 8, 9, 21 months, respectively. For the 29 cases who died, the overall 3-year survival rate was higher in the group A (46.7%) than in the group B and C. ATRA did not provoke or aggravate DIC, nor did it cause bone marrow hypoplasia. The main side effects were dryness of the lip or skin, headache, nausea or vomiting and liver dysfunction. Severe scrotum exfoliative dermatitis with ulceration was seen in one case. In vitro induction of differentiation, GM-CFU, L-CFU assay and cytogenetic studies were performed. The results were discussed together with clinical observation regarding the mechanism of action of ATRA on APL. ATRA used as an inducer of differentiation is an alternative effective drug in the induction of remission in de novo APL as well as in cases in relapse.
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PMID:[Treatment of acute promyelocytic leukemia (APL) with all-trans retinoic acid (ATRA): a report of five-year experience]. 822 22

A 46-year-old white male presented with a two-week history of a flu-like illness and bleeding gums. A diagnosis of acute promyelocytic leukemia was made on bone marrow examination with accompanying DIC. All cytogenetically abnormal cells (28/30 at intake and 30/30 at two weeks post-induction) represented a single clone with apparent deletion of 1(p22) and 3(p25), and with a large, derivative chromosome 17. By conventional G- and C- banded analysis, the monocentric der(17) appeared to be disrupted distal to the typical (17q21) APL breakpoint, chromosome 15 did not demonstrate gross rearrangement, and the source of the additional material on the der(17) was unknown. Fluorescence in situ hybridization (FISH) with t(15;17), RAR alpha, and 17qter probes and with chromosome 1, 15, and 17 paints demonstrated that the der(17) consisted of a complex rearrangement with duplication of both RAR alpha and PML, insertion of chromosome 1 sequences, and double insertion of chromosome 15 sequences. The fusion of RAR alpha and PML consistent with APL appears to have occurred at the distal juxtaposition of these sequences in the derivative chromosome.
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PMID:Complex t(1;15;17) in acute promyelocytic leukemia with duplication of RAR alpha and PML sequences. 868 11

The study was aimed to detect expression rate of survivin gene in APL cell and to explore the relationship between its expression and clinical manifestation. PML/RARalpha and survivin mRNA expression were analyzed by using reverse transcriptase polymerase chain reaction (RT-PCR) technique. The results showed: (1) the survivin gene expression was detected in NB4 cell line. By treatment with ATRA, survivin mRNA expression in NB4 cell gradually decreased along with time delay and almost could not be detected at the 72th hour. (2) the positive and negative rate of survivin mRNA expression was 67% and 33% respectively, while in all 36 cases of de novo and relapse APL patients, the PML/RAR(alpha) fusion gene expression was positive. In 22 cases at remission stage, the PML/RARalpha fusion gene expression was negative, and the positive and negative rate of survivin mRNA expression was 36% and 64% respectively. The survivin mRNA expression positive rates in the de novo group, relapse group and PML/RARalpha fusion gene L-type positive group were obviously higher than those in remission period group (P < 0.05) and were significantly lower than those in acute leukemia group (P < 0.05, < 0.001). (3) whether the survivin mRNA expression was positive or negative in 36 cases of de novo and relapse APL patients, all the 36 cases could obtain complete remission. 4 APL patients with positive expression of survivin mRNA had DIC and serious infection (one patient died). The clinical symptom showed slight skin or mucosa bleeding, fever and asthenic in the patients with negative expression of survivin mRNA. When 2 APL patients with positive expression of survivin mRNA had been treated with ATRA, induction differentiation sign in their peripheral blood and bone marrow figures was not obvious. It is concluded that the survivin gene positive expression rate is lower in acute promyelocytic leukemia than that in any other types of leukemia and is related to clinical manifestation.
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PMID:[Expression of survivin gene in NB4 cell line and cells of acute promyelocytic leukemia and its anti-apoptosis and clinical significance]. 1663 9


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