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)

The nursing management of patients with rare leukemias involves physiologic, psychologic, and ethical activities. Specific nursing interventions aimed at supporting bone marrow suppressed patients have been addressed in the literature and other reports in this issue. The potential for oncologic emergencies in these rare leukemias is great. These include disseminated intravascular coagulation (DIC), cerebral and pulmonary leukostasis, sepsis, and acute renal failure. Recognition that patients are at risk for these acute events prepares nurses for their assessment, diagnosis, and plans of care. Eleven high-incidence problems for cancer patients have been described, and all can be applied to these patients. Emotionally, patients and their families rely on nurses to assist them in coping with a new diagnosis of cancer, and/or dealing with the chronic nature of their disease. Open communication, firmly based on a thorough knowledge of the particular disease and treatment, will promote trust and a sense of comfort as the patient begins treatment. Finally, it is important for all nurses caring for cancer patients to identify their personal feelings and biases. In the current environment where clinical investigation is a part of everyday care, the nurse must be comfortable with the research process and the participation of human subjects in clinical trials. Nurses play a role in the development of clinical trials and the process of informed consent, and in the management of patients involved in clinical trials. Over the last 5 years, we have witnessed a dramatic increase in the number of therapies available for one particular rare leukemia (hairy cell leukemia). This has resulted in significant improvements in patient outcomes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uncommon leukemias: implications for clinical practice. 240 28

An unusual case of Q fever in a 62-year-old female is described. The patient presented with severe pneumonia and developed renal failure, disseminated intravascular coagulation and pancytopenia which recurred after antibiotics were discontinued. Subsequently hairy cell leukemia was diagnosed and evolved favorably under treatment with doxycycline and alpha-interferon. A review of the literature confirms that renal failure and disseminated intravascular coagulation do not appear to be associated with Coxiella burnetti infections, nor has the association of Q fever and hairy cell leukemia been previously described.
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PMID:[Unusual manifestations of Q fever disclosing hairy cell leukemia]. 292 42

Disseminated intravascular coagulation (DIC) was produced by an infusion of a prothrombin activator (Echis carinatus venom; 30 minutes; 0.5 NIH thrombin equivalent U/kg) in mongrel dogs (Echis group, n = 7). Fibrinogen declined to below measurable levels (less than 25 mg/dl), and fibrin-fibrinogen degradation products appeared (53 +/- 8 micrograms/ml) at end venom infusion in the Echis group. These alterations were not seen when an irreversible thrombin inhibitor, D-phenylalanyl-L-prolyl-L-arginine-L-chloromethyl ketone (PPACK) (57 nmol/kg/min for 120 minutes), was given alone (PPACK group, n = 5) or in association with venom (Echis + PPACK group, n = 5). Factor II activity (1% +/- 1%) in the Echis and Echis + PPACK groups was significantly below the PPACK (55% +/- 9%) and the control (79% +/- 2%) levels at 120 minutes. In contrast, factor VIII coagulant (factor VIII:C) activity in the Echis group (1% +/- 1%) remained significantly below that in the Echis + PPACK (68% +/- 8%), PPACK (78% +/- 10%), and control (91% +/- 9%) groups at this interval. No change in factors X (91% +/- 7% to 81% +/- 7%, P not significant) and VII (64% +/- 10% to 48% +/- 11%, P not significant) activities were observed. Hemolysis was observed only in the Echis group, whereas thrombocytopenia and leukopenia were noted in both the Echis and the Echis + PPACK groups. These data show that large amounts of E. carinatus venom produce rapid DIC in vivo, because of the activation of prothrombin. In contrast, the decline in factor VIII:C activity appeared to be the result of the liberated thrombin. PPACK antagonized all of the venom-released thrombin without any major deleterious clotting abnormalities. This inhibitor appears to prevent thrombin-mediated DIC in vivo. In contrast, heparin was found to be an unreliable antagonist of the venom-released thrombin in vitro. PPACK also inhibited the marked hemolysis usually observed after venom. In addition, we found that the esterolytic (N-benzoyl-L-prolyl-L-phenylalanyl-L-arginine-p-nitroanilide HCL) activity of E. carinatus venom degrades fibrinogen in vitro.
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PMID:Disseminated intravascular coagulation following Echis carinatus venom in dogs: effects of a synthetic thrombin inhibitor. 308 70

A case in which prescription medications induced heat intolerance which led to heat stroke is presented. A subject who suffered from depression and was treated with fluoxetine HCL (prozac) and lithium carbonate was engaged in mild intermittent work for 4 hours under hot/dry climatic conditions (Ta = 37 degrees C, rh = 15%). The subject lost consciousness, was hyperthermic and suffered from disseminated intravascular coagulation. A year later residual cerebellar symptoms were still evident and severe atrophy of the cerebellar tissue was demonstrated in a CT scan. It is suggested that drug-induced heat intolerance was the predisposing factor that reduced the patient ability to sustain exercise-heat stress, and under the favorable environmental circumstances led to excessive heat accumulation which ultimately caused heat stroke. This is the first description, to our knowledge, of heat intolerance of a patient treated by a combination of fluoxetine and lithium carbonate.
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PMID:Heat intolerance induced by antidepressants. 910 Sep 34

A 25-year-old male, who had returned from the Republic of Mali in Africa, was admitted to our hospital because of a 3-day history of high fever, on the first of October 1996. He was diagnosed as Plasmodium falciparum malaria by peripheral blood smear. From the admission day he was treated with quinine HCL, 1,500 mg per day, and sulfamethoxazole 2,400 mg trimethoprim 480 mg per day, but on October 2nd blood examination showed 35% parasite density and he was given mefloquine. However he was complicated with DIC on October 3rd, ARDS on October 5th. By anti-coagulant therapy and methylprednisolone pulse therapy he became afebrile and respiratory function improved rapidly. ARDS should be emphasized as a severe complication of imported severe malaria.
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PMID:[Acute respiratory distress syndrome complicating imported Plasmodium falciparum malaria]. 954 90

Hairy cell leukemia (HCL) is an indolent B-cell neoplasm, strongly expressing CD20. Despite initial very high response rates following cladribine, many patients (pts) ultimately relapse. Having relapsed after prior treatment with cladribine, 24 HCL pts (21 male, 3 female) with a median age of 53.5 years were treated with rituximab at 375 mg/m2 intravenously weekly for 4 weeks. Of the pts, 3 (13%) achieved complete remissions and 3 (13%), partial responses. Thus, 6 (25%) of 24 pts achieved a response following rituximab. At a median follow-up of 14.6 months, 2 responders have relapsed; median time to relapse was not yet reached. The only grade III or IV toxicities demonstrated were culture-negative febrile neutropenia, transient and reversible disseminated intravascular coagulation related to rituximab administration, and a diverticular abscess, each in single patients. Of 18 nonresponders, 9 pts subsequently received other treatments; 5 pts were retreated with cladribine, 3 underwent splenectomy, and 1 received pentostatin. Follow-up data are available on 7 of these 9 patients; all 7 patients achieved improvements in hematologic parameters. Rituximab, administered at this dose and schedule, has only modest single-agent activity in cladribine-failed HCL patients when compared with other agents active in this disease.
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PMID:Phase 2 study of rituximab in the treatment of cladribine-failed patients with hairy cell leukemia. 1266 46