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)

A 21-year-old male patient with non-Hodgkin lymphoma of the "convoluted' T cell type and marked involvement of skin and central nervous system presented in the early stages of the disease with subconjunctival bleeding of the eyeballs and massive serious retinal detachment near the optic disc in both eyes. In addition, there was a severe disseminated intravascular coagulation (DIC) caused by the lymphoma. It appears that the non-haemorrhagic retinal detachment on both sides is due to a neoplastic lymphocellular infiltration with high affinity of this malignant lymphoma to the central nervous system. Treatment of the underlying disease and of DIC with rapid onset of total remission lead to resorption of the conjunctival haemorrhages and fast reduction of the retinal detachment.
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PMID:[Transient retinal detachment and hyposphagma in a patient with non-Hodgkin lymphoma of the T cell type (author's transl)]. 697 25

Three nonsplenectomized patients were infected with Babesia microti. One had fever, abdominal pain suggesting gallbladder disease, and evidence of disseminated intravascular coagulation; another was considered to have lymphoma, partly because two smears for Babesia before admission were negative. All three patients were treated with pentamidine isethionate and improved clinically. Parasites were no longer seen on smears after 5 days of therapy, but Babesia could still be recovered by hamster inoculation 5 weeks after therapy in one of the patients tested, underscoring the need for this test to properly evaluate eradication of the organism. In one patient, pentamidine was stopped after 7 days because of increased creatinine concentration, and this amount of drug appeared adequate to control the parasitemia. Pain at drug injection sites was a major side effect in all three patients. Pentamidine appears to be useful in controlling clinical manifestations of babesiosis and decreasing parasitemia, but it does not eradicate the organism.
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PMID:Response of babesiosis to pentamidine therapy. 719 15

Multiple extremity gangrene developed in five patients as a complication of dopamine therapy. The clinical conditions were (1) penetrating chest trauma requiring pneumonectomy with postoperative sepsis, (2) cardiac arrest with aspiration pneumonia, (3) lymphoma with sepsis, (4) Klebsiella pneumonia, and (5) myocardial infarction. The development of acrocyanosis leading to gangrene occurred at dopamine dosages of 5.1 to 10.2 micrograms/kg/min. The alpha-adrenergic vasoconstriction effects of dopamine would not be expected from the doses employed in these patients. Thus, other factors beside pure alpha vasoconstriction are responsible for tissue necrosis after the use of dopamine. We believe that the embolic complications of disseminated intravascular coagulation and hypovolemia are serious risk factors in the development of dopamine gangrene. Peripheral vasoconstriction from dopamine, even at low doses, may set the stage for thrombotic complications of disseminated intravascular coagulation and lead to tissue damage. In laboratory models of disseminated intravascular coagulation, an alpha-adrenergic drug is required to produce peripheral ischemic tissue damage. Treatment of tissue ischemia related to dopamine depends on early recognition of acrocyanosis. Phentolamine, an alpha blocker, has been recommended for treating dopamine ischemia, either through local instillation into ischemic tissues or intravenous infusion. We recommend a high index of suspicion for, and early treatment of, underlying consumptive coagulopathy in all patients requiring dopamine.
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PMID:Dopamine gangrene. Association with disseminated intravascular coagulation. 730 16

Four cases of fulminant pneumococcal septicemia in splenectomized patients are reported. Three had undergone splenectomy for trauma 42, 28 and 14 years prior to the septicemia. The fourth had been splenectomized for suspected lymphoma 3 years earlier. In 3 out of 4 patients the symptomatology was so rapidly progressive that a physician was consulted within 12 hours. Two patients hospitalized after a second consultation and 20 hours after the first symptoms had evidence of septic shock, disseminated intravascular coagulation and hypoglycemia, and died within a few hours despite early antibiotherapy. Diplococci were seen in peripheral smears of these 2 patients and in the buffy coat of the 3 cases in which this was carried out. These four cases reemphasize the fact that during their entire life splenectomized patients are at risk for development of overwhelming septicemia even when the splenectomy was performed because of trauma. Therefore, such patients should be aware of this risk, should be treated promptly with antibiotics in the event of a febrile episode, and should be vaccinated against pneumococci and possibly other encapsulated bacteria such as Haemophilus influenzae and Neisseria meningitidis.
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PMID:[Fulminant pneumococcal septicemia in splenectomized patients]. 731 55

A patient is presented in whom celiac disease was complicated by the development of chronic nongranulomatous ulcers in the small and large intestine. In addition, he had nodular lymphoid hyperplasia in the bowel wall and mesenteric lymphoadenopathy. The terminal illness was characterized by disseminated intravascular coagulation. It is postulated that the lymphoid hyperplasia was secondary to excessive stimulation of the reticuloendothelial system by nongluten antigens and may be a precursor of the development of lymphoma in celiac disease. Nongluten antigens such as bacteria or endotoxins were probably responsible for the consumptive coagulopathy.
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PMID:Celiac disease complicated by chronic nongranulomatous ulcerative enterocolitis, nodular lymphoid hyperplasia, and disseminated intravascular coagulation. 746 Jul 9

A 73-year-old man was admitted to our hospital with nasal hemorrhage and high grade fever on Aug, 1992. Physical examination revealed a tumor in the nasopharyngeal cavity, generalized skin eruptions and three tumors on different subcutaneous lesions, splenomegaly 2 cm below the costal margin, and the enlargement of the right cervical and axillary lymph nodes. Biopsy of the nasopharyngeal and cutaneous tumor disclosed non-Hodgkin's lymphoma (WF: Diffuse small cleaved). Peripheral blood examination showed a WBC of 4,800/microliters with 10% blastoid cells. Bone marrow examination showed 60% blastoid cells which frequently appeared a hand mirror configuration had no azurophilic granules in the cytoplasm. Flow cytometic analysis of these cells in the bone marrow showed that they expressed CD56 (NKH-1) and Ia but not expressed T-cell antigens as well as B-cell antigens and myeloid cell antigens. Phenotype of subcutaneous tumor biopsy cells was similar to that of blastoid cells in the bone marrow. T-cell receptor gene (TCR beta and gamma) rearrangements in blastoid cells were not found. The patient was treated with local radiotherapy to nasopharyngeal and skin tumors, followed by chemotherapy. The patient died of complication with pulmonary bleeding due to DIC. These results suggested that this nasopharyngeal lymphoma derived from NK cell.
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PMID:[Primary nasopharyngeal lymphoma with CD3- and CD56+ phenotype]. 753 74

Ten percent (214/2,059) of all dogs with cancer at North Carolina State University Veterinary Teaching Hospital had thrombocytopenia. The thrombocytopenia was associated with infectious/inflammatory etiologies in 4%, miscellaneous disorders (therapy, bone marrow failure, disseminated intravascular coagulation) in 35%, and neoplasia without identifiable secondary factors in 61% of cancer-bearing dogs. Classifying these dogs by tumor groups revealed the following proportionate ratios: lymphoid, 29%; carcinoma, 28%; sarcoma, 20%; hemic neoplasia, 7%; multiple, 5%; unclassified, 3%; benign, 3%; brain, 3%; and endocrine, 3%. Dogs with hemangiosarcoma, lymphoma, and melanoma were at increased risk of developing thrombocytopenia. Cytotoxic therapy was the major factor increasing the risk of thrombocytopenia in dogs with melanoma. Golden Retrievers were the only breed recognized with a predisposition to develop thrombocytopenia. If thrombocytopenia is identified in a dog with cancer, we recommend thorough evaluation of the coagulation system before surgery or therapy, and careful consideration of the risks and potential benefits of myelosuppressive or L-asparaginase therapy.
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PMID:Thrombocytopenia associated with neoplasia in dogs. 788 25

Patients with acute promyelocytic leukemia (APL) are at high risk for the development of life-threatening thrombotic and hemorrhagic complications, particularly during induction chemotherapy. This propensity has been attributed to the release of tissue factor (TF)-like procoagulants from the leukemic cells leading to disseminated intravascular coagulation (DIC). However, recent data suggest that the pathogenesis of the coagulopathy is more complicated and may involve activation of the generalized proteolytic cascade resulting in either clotting and/or excessive fibrinolysis. Furthermore, controversy exists regarding the mechanism(s) responsible for the activation of either clotting or fibrinolysis. The malignant promyelocyte may act directly to activate coagulation and/or fibrinolysis. Alternatively, reactive inflammatory cells, which express procoagulant and/or profibrinolytic activities may play an essential role. A third possibility may involve endothelial cell expression of mediators with procoagulant/profibrinolytic properties. Putative profibrinolytic mechanisms include the release of urokinase-type and tissue-type plasminogen activators, decreases in plasminogen activator inhibitor-1 and 2, and decreases in alpha-2 plasmin inhibitor. Putative procoagulant mechanisms include the release of tissue factor, Cancer Procoagulant, or cytokines such as interleukin-1, tumor necrosis factor and vascular permeability factor. Putative anticoagulant mediators include annexins, a group of proteins in human tissue which bind phospholipids and have anticoagulant activity, which have been reported in patients with APL. The current treatment of APL is rapidly evolving because of the efficacy of all-trans retinoic acid (ATRA). All-trans retinoic acid promotes terminal differentiation of leukemic promyelocytes leading to complete remission in the majority of patients with APL with rapid resolution of the coagulopathy. Although the mechanism by which this occurs has not been established, preliminary data suggest that ATRA blocks the downregulation of the thrombomodulin gene and the up-regulation of the tissue factor gene induced by tumor necrosis factor. Since APL is a relatively uncommon disorder, the collaboration of cooperative oncology groups will be important to study patients receiving ATRA or conventional chemotherapy to further elucidate the mechanism(s) of the coagulopathy.
Leuk Lymphoma 1993 Sep
PMID:New insights into the pathogenesis of coagulation dysfunction in acute promyelocytic leukemia. 822 Jan 53

A patient with acute leukemia is presented in whom the leukemic cells, as seen by light microscopy were typical promyelocytes. The cells had normal or slightly invaginated nuclei with typical cytoplasmic granules and the diagnosis was confirmed by cytochemistry. The clinical course was rapid and the patient died of disseminated intravascular coagulation and urosepsis within a few days of diagnosis. However, electron microscopic examination showed cells with extremely convoluted and lobulated nuclei with nuclear pockets and cytoplasmic bridges as well as the complete absence of cytoplasmic granules in the majority of the cells. Furthermore, the urine lysozyme (muramidase) was elevated. These findings suggest that the leukemia in this patient may be classified as a hypogranular variant of acute promyelocytic leukemia (APL), with monocytoid ultrastructural appearances.
Leuk Lymphoma 1993 Mar
PMID:Ultrastructural observations on a variant of acute promyelocytic leukemia. 834 79

Patients with leukemia, lymphoma, or multiple myeloma are prone to critical illness because of the diffuse nature of their disease and the disruption of protective mechanisms. Despite high morbidity rates, a number of these patients have an excellent probability of long-term remission if supported through a crisis. Complications that cause critical illness can be categorized as related to disease or those caused by therapy. Those with unique features or management strategies for the hematologic malignancy patient and are included in this discussion include: leukostasis, disseminated intravascular coagulation, tumor lysis syndrome, respiratory failure, and typhlitis. A case study of an acutely ill, newly diagnosed patient with several of these oncologic emergencies is used to exemplify typical clinical finds and management strategies.
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PMID:Critical care of the patient with hematologic malignancy. 869 16


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