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

We developed an assay for the factor XIa-alpha 1 antitrypsin complex (F.XIa-alpha 1AT complex) in plasma. The purified factor XI (F.XI) activated with beta-XIIa and treated with alpha 1 antitrypsin (alpha 1 AT) served as the standard complex. The assay is an enzyme-linked differential antibody immunosorbent assay. The complex level of tested plasma was measured with peroxidase-labeled anti-alpha 1AT Fab' after the addition of 10-fold diluted test plasma (200 microliter) to the anti-F.XI monoclonal antibody beads. To eliminate the effects of plasma, the standard F.XIa-alpha 1AT complex was diluted with F.XI-deficient plasma (10-fold diluted) which did not contain the complex. Purified F.XI (0.08 micrograms/assay, i.e. 100%) was added to the standard F.XIa-alpha 1AT complex, because the absorbance of the standard complex containing F.XI (0.016-0.12 micrograms/assay, i.e. 20-150%) was a little lower than that of the complex alone. The recovery of the F.XIa-alpha 1AT complex added was over 90%. Neither F.XI nor alpha 1AT alone had the color development. The complex level of 25 normal individuals was below the detectable limit (less than 0.18 ng/assay), whereas the 30 patients with disseminated intravascular coagulation (DIC) had a high level complex (0.18-4.2 ng/assay). This assay may be helpful for the diagnosis of DIC.
 ...
PMID:Factor XIa-alpha 1 antitrypsin complex--elevation in the patients with DIC. 349 61

An autopsy case of systemic mastocytosis without cutaneous involvement in a 76-year-old woman was described. The patient presented with general malaise, chest and epigastric discomfort, flushing of the face and progressive hepatosplenomegaly, and she terminated in hemorrhagic complications of DIC within 2 months. There was neither rash nor urticaria pigmentosa recognizable in the entire course. The diagnosis was made by the histologic identification of abnormal aggregates of mast cells in a bone marrow aspirate. These mast cell granules were chloroacetate esterase-positive, peroxidase-negative, and electronmicroscopically they were composed of fine granular materials containing variable numbers of lamellar structures. At autopsy, diffuse infiltration of the mast cells was found in the liver, spleen, bone marrow, lymph nodes, lungs, kidneys, stomach, and adrenal glands.
 ...
PMID:Systemic mastocytosis without cutaneous involvement. 355 89

We have developed a variation of the solid-phase enzyme-linked immunosorbent assay (ELISA) to enable measurement of the activity and antigen levels of protein C (PC) in human plasma. With this assay it is possible to do both tests with the same sample and same microtiter plate coated with anti-PC monoclonal antibody (MCA)JTC-4, which inhibited neither activation of PC nor activity of activated PC (APC). Even in patients undergoing heparin treatment for severe disseminated intravascular coagulation, there were no detectable differences between amidolytic activity and antigen levels of PC in patients' plasma. In addition, there was a strong correlation between the immunologic levels of PC in patients' plasma determined both by polyclonal ELISA using peroxidase-labeled immunopurified antiprotein C-IgG and those found with MCA ELISA using peroxidase-labeled MCAJTC-5, which does not bind to APC. In contrast, when oral anticoagulation therapy was started, immunologic levels of plasma PC estimated by peroxidase-labeled MCAJTC-1, a MCA that recognizes a gamma-carboxyglutamic acid domain-related conformational change of PC induced by metal ions, decreased more rapidly than did either the PC level determined by polyclonal ELISA or the percent prothrombin time. This suggested that comparison of MCAJTC-1-recognized PC levels and prothrombin time may be necessary at the beginning of oral anticoagulation therapy to treat patients safely.
 ...
PMID:Level of protein C determined by combined assays during disseminated intravascular coagulation and oral anticoagulation. 358 May 75

Giant granules formation was investigated in myeloblasts of a patient with acute myelogenous leukemia by means of the combined techniques of peroxidase cytochemistry both in light and electron microscopy. Several pathologic features were noted: first an abnormal packaging of peroxidase in the peripheral area in large azurophilic granulations, second the progressive enlargement of huge vacuolar inclusions resulting from the interaction and fusion of large azurophilic granules with each other, with normal-sized primary granules and with cytoplasmic components. Microcrystalline structure could not be found in giant vacuoles no in vacuolar inclusions resembling Auer bodies. This last finding could explain that no disseminated intravascular coagulation was observed in our patient.
 ...
PMID:Acute myeloid leukemia with giant inclusions: cytochemical and ultrastructural study. 642 81

A 28-year-old man developed AML 18 months after a diagnosis of non-Hodgkin's lymphoma, diffuse small cell type, clinical stage IIA. Induction therapy for the lymphoma consisted 60Co 4000 rads bilaterally to the cervical areas and 2000 rads to the right cervical area. Complete remission was attained. Nineteen courses of combination chemotherapy with Vincristine (VCR), 6-meraptopurine (6 MP), cyclophosphamide (CY) and predonisolone (pred) was added (Total dose: VCR; 26.5 mg, 6 MP; 3320 mg, CY; 3350 mg, pred; 4310 mg). Seven days after the final chemotherapeutic treatment he developed AML with DIC. Leukemic cells were peroxidase and specific esterase (naphthol AS-D chloroacetate) positive. Induction therapy for the AML consisting of DCMP (Daunomycin, Cytosine arabinosid, 6 MP and pred) and VCR (vindesine, CY and pred) was unsuccessful. The patient died of cranial hemorrhage 3 month after the diagnosis of acute leukemia. Autopsy revealed no recurrence of non-Hodgkin's lymphoma in the lymph nodes, bone marrow, spleen and liver. Seven other cases reported in the Japanese literature are reviewed.
 ...
PMID:[Post therapeutic myeloblastic leukemia in non-Hodgkin's lymphoma]. 659 32

Thrombocytopenia occurs frequently in newborn infants with sepsis, but the exact mechanism remains obscure in those infants who do not have evidence of disseminated intravascular coagulation. Since recent work has suggested a possible immune mechanism for thrombocytopenia observed in adults with sepsis, we have investigated the role of platelet-associated immunoglobulin in severe neonatal infections. To detect PAIgG we use a method employing protein A and peroxidase-antiperoxidase as a labeled antibody. PAIgG was quantitated by phase contrast microscopy and expressed as a reactive index. Our control group included 16 normal newborn infants whose mean RI was 0.65 +/- 0.01 SE. In addition to the control group, five infants with nonimmune thrombocytopenia were included; their mean RI was 0.66 +/- 0.01 SE. Seventeen newborn infants with severe infections were assayed for PAIgG. Eight of nine infants with bacterial infections had increased RI, with a mean of 1.16 +/- 0.03 SE (P less than 0.01). Six of the eight infants with viral infections had elevated RI, with a mean of 1.23 +/- 0.03 SE (P less than 0.01). These findings suggest that an immune mechanism may be involved in the thrombocytopenia of severe neonatal infection.
 ...
PMID:Immune thrombocytopenia in severe neonatal infections. 705 22

Intravenous administration of bacterial endotoxin (lipopolysaccharide: LPS) induces shock and disseminated intravascular coagulation in rats. Our report here shows that LPS-administered rats (10 mg/100 g) develop tissue injuries and functional disorders in multiple vital organs. In the present study, we investigated changes in tissue antioxidant enzyme activities, neutrophil sequestration, and lipid peroxides in multiple organs (lung, stomach, small intestine for antioxidant enzyme activities and neutrophil sequestration; lung, stomach, small intestine, liver, abdominal aorta for lipid peroxides) of LPS-treated rats. LPS-treated animals morphologically revealed pulmonary interstitial edema, alveolar hemorrhage, and mucosal hemorrhage in the small intestine 45 min after LPS administration. Blood samples withdrawn from LPS-treated animals exhibited increases in serum amylase, blood urea nitrogen, creatinine, and transaminase levels up to 180 min post-LPS infusion. LPS-treated animals showed a significant increase in tissue myeloperoxidase (MPO) activities of the lung, but not of the small intestine and stomach 45 min after LPS infusion. Thiobarbituric acid reactive substances (TBARS) in the lung, small intestine, stomach, liver, and abdominal aorta significantly increased at 45 min post-LPS-infusion. Tissue superoxide dismutase (SOD) activities of the LPS-treated animals demonstrated a significant decrease in the lung, which suffered from severe insults and neutrophil sequestration; no significant change in the small intestine, which suffered from morphological insults without neutrophil sequestration, and a significant increase in the stomach, which showed no histological impairment, at 180 min post-LPS administration. Glutathione peroxidase (GSH-PX) activities of the lung and small intestine showed no significant change in LPS-treated rats, while those of the stomach revealed a marked increase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Changes in tissue antioxidant enzyme activities and lipid peroxides in endotoxin-induced multiple organ failure. 814 10

Acute promyelocytic leukemia represents 5-10% of acute myeloid leukemia cases (AML) recorded in the literature, occurring more frequently in young adults. It has a special clinical and biological behaviour when compared to the other forms of AML, being characterized by a particular morphology of blast cells (M3 in FAB classification), translocation of chromosomes 15;17, and disseminated intravascular coagulation at diagnosis or after the onset of chemotherapy. Within this AML subgroup there are 2 morphological subsets called the hypergranular promyelocytic leukemia and the hypogranular or variant form. We have studied clinical and laboratory aspects of 19 cases of AML M3 out of 217 AML cases, and observed a high incidence of failure to recognize the M3 variant form, although its diagnosis has been mainly based on cytomorphology. Only 4 out of 8 cases of the variant form received in our laboratory were correctly diagnosed, being the other 4 cases wrongly identified as the myelomonocytic subset of AML (M4). Immunophenotyping with monoclonal antibodies using CD2 and CD7 as T cell markers, CD10 and CD19 as B cell markers and CD33, CD13, CD14, CD15 and anti MPO as myeloid markers is a complementary diagnostic tool that permits solving difficult cases. It is important to classify AML correctly because of the special therapeutic and prognostic features of AML M3, which differently from other AML forms, has been successfully treated with cellular differentiating agents.
 ...
PMID:[M3 variant leukemia: clinical and diagnostic features]. 816 87

We report on a 3 year old girl with acute promyelocytic leukemia (APL) with cerebral infarction due to disseminated intravascular coagulation (DIC) at initial presentation. She was hospitalized because of unconsciousness and petechiae on the chest wall and extremities. Cerebral ischemia and infarction were found on computed tomography scan and magnetic resonance imaging. Peripheral blood content was hemoglobin 7.3 g/dL, white blood cells 1.0 x 10(3) cells/microL (31% blasts) and platelet count was 12 x 10(3) cells/microL. Fragmented erythrocytes were frequently observed on May-Giemsa stained blood smears. Bone marrow aspirates showed normal cellularity, with 60.4% blasts, containing faggot cells. The blasts were positive for peroxidase. Therapy was begun; however, the patient died 1 week after admission.
 ...
PMID:Cerebral infarction in acute promyelocytic leukemia at initial presentation. 877 58

A 60-year-old Japanese woman was admitted to our hospital because of fatigue, weight loss and abdominal distension. Myelofibrosis was diagnosed, based on anemia, huge hepatosplenomegaly, leukoerythroblastosis and bone marrow fibrosis. Following treatment with ranimustine, anemia and splenomegaly improved. Seven months after initial therapy of ranimustine, however, polycythemia (RBC 7.39 x 10(6)/microliter; Hb 19.1 g/dl, Ht 65.9%) developed gradually, then RBC decreased to normal level following venesection (total 1,200 ml). After 32 months, blastic transformation occurred. The blasts were negative for myeloperoxidase. By flow cytometric analysis, the cells were positive for CD2, CD13, CD33 and HLA DR. Thus, AML (M0) was diagnosed. Despite of treatment with multicytotoxic agents, she died of DIC 36 months after the initial diagnosis of myelofibrosis. The progression from myelofibrosis to polycythemia is rare and only 15 cases have been reported so far. In addition, although a chromosomal abnormality, 46, XX, t(3; 12) (q25; p11), was present at the time of first diagnosis of myelofibrosis, the development of an additional abnormality, del(11) (q-), might be related to the transformation to AML.
 ...
PMID:[A case of myelofibrosis that developed polycythemia vera following treatment with ranimustine and then acute myelogenous leukemia (M0)]. 882 83


<< Previous 1 2 3 4 Next >>