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)

We studied the clinical, morphological, and immunologic characteristics of 11 patients with 11q translocation-associated acute leukemia. There were three patients with t(9;11)(p22;q23), one with a variant of the t(9;11), three with t(11;19)(q23;p13), two with t(1;11)(p32;q23), one with t(10;11)(p15;q22or23), and one with t(11;17) (q23;q25). The breakpoints in chromosome 11 clustered in band q23. The morphological feature was FAB-M5 in two patients, FAB-M2 in one, FAB-L1 in six, and lymphoblastic lymphoma in one. The remaining patient underwent morphological changes from FAB-L1 seen at the time of diagnosis to M5b at relapse. Immunologic marker studies in ten patients revealed that one had T cell type; another pre-B cell type; three CALLA- Ia- non-T, non-B type; two CAL-LA- Ia+ non-T, non-B type; two monocytic type (positive Fc-receptor); and the remaining one underwent phenotypic changes from CALLA+ Ia+ non-T, non-B type to monocytic type. The patients were usually young; five were under 1 year and two were 9 and 13 years. Hyperleukocytosis was observed in eight of the ten patients with acute leukemia, and two of the eight died of intracranial hemorrhage within two days of admission, associated with disseminated intravascular coagulation. These findings indicate that leukemia with the 11q23 translocation share certain characteristics in common, irrespective of the recipient chromosome, even though the latter may have some influence on the morphological and immunologic phenotype. Our data provide a hypothesis that multipotent stem cells are involved in the genesis of the 11q translocation-associated leukemia.
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PMID:Clinical and hematologic characteristics in acute leukemia with 11q23 translocations. 394 33

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.
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PMID:[M3 variant leukemia: clinical and diagnostic features]. 816 87

Acute promyelocytic leukemia (APL) is a type of acute leukemia showing unique clinical, morphological and cytogenetic features. A skin infiltration by APL cells is an extremely rare occasion, but there have been several case reports of leukemia cutis in APL, in which all-trans retinoic acid (ATRA) may have induced the skin infiltration. However, no immunohistochemical analyses of the APL cells in the skin have been done to date. A 30-year-old woman with APL developed multiple reddish purple nodules on the extremities in her second complete remission. Histological findings revealed a dense infiltration of medium to large atypical cells, which were positive for myeloperoxidase, throughout the dermis. Despite the conventional chemotherapy and ATRA therapy she died from disseminated intravascular coagulation during her third relapse. Leukemic cells in the peripheral blood before the treatment with ATRA revealed CD3-/CD4-/CD5-/CD7-/CD8-/CD10-/CD13++/CD14-/CD19 -/ CD20-/CD33++/CD38++/CD41-/Ia-, but they expressed CD3-/CD4-/CD5-/CD7++/ CD8-/CD10-/CD13++/CD14-/CD19-/CD20-/CD33++ /CD38++/CD41+/Ia+ after the treatment. We suggest that the alternation of the surface molecules on the tumor cells is closely associated with the skin infiltration of APL cells.
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PMID:Skin infiltration in acute promyelocytic leukemia. 909 68

Herein is presented a case of carcinosarcoma of the pancreas in an 82-year-old woman, analyzed on immunohistochemistry and K-ras sequence. The tumor, which arose in the pancreas head, was removed on pancreaticoduodenectomy. The patient died, however, of disseminated intravascular coagulation syndrome from postoperative sepsis 13 days later. Microscopically, the tumor consisted of malignant epithelial (well-differentiated adenocarcinoma cells) and mesenchymal (spindle-shaped tumor cells) components. The adenocarcinoma cells had positive immunostaining for cytokeratin AE1/AE3, cytokeratin 7, epithelial membrane antigen (EMA), CEA and carbohydrate antigen 19-9 (CA 19-9), while focal staining of these proteins was observed in the sarcomatous cells. In contrast, the sarcomatous cells had diffuse immunostaining for vimentin, CD10 and p53, while these proteins were not expressed in the ductal adenocarcinoma cells. These findings support the dual characteristics of a carcinosarcoma. DNA sequencing of the present case indicated point mutations of K-ras in both codons 12 and 34 on exon 2. The latter mutation is likely to correlate with the sarcomatous characteristics of this tumor. The tumor cells had specific and diffuse positive staining for CD10 and p53, with features characteristic of rapid growth.
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PMID:Immunohistochemistry and K-ras sequence of pancreatic carcinosarcoma. 1880 Oct 90

Acinetobacter baumannii is an important nosocomial pathogen that displays high antibiotic resistance. It causes a variety of infections including pneumonias and sepsis which may result in disseminated intravascular coagulation. In this work, we identify and characterize a novel secreted, zinc-dependent, metallo-endopeptidase CpaA (coagulation targeting metallo-endopeptidase of Acinetobacter baumannii) which deregulates human blood coagulation in vitro and thus is likely to contribute to A. baumannii virulence. Three quarters of the clinical isolates tested (n = 16) had the cpaA gene; however, it was absent from two type strains, A. baumannii ATCC 17978 and A. baumannii ATCC 19606. The CpaA protein was purified from one clinical isolate and was able to cleave purified factor (F) V and fibrinogen and reduce the coagulation activity of FV in human plasma. CpaA-treated plasma showed reduced clotting activity in contact pathway-activated partial thromboplastin time (aPTT) assays, but increased clotting activity in tissue factor pathway prothrombin time (PT) assays. A significant portion of clinically relevant A. baumannii isolates secrete a protease which targets and deregulates the coagulation system.
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PMID:CpaA a novel protease from Acinetobacter baumannii clinical isolates deregulates blood coagulation. 2491 20