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)

Hematologic alterations unrelated to neoplastic bone marrow involvement include polycythemia, anemia, leukocytosis, leukopenia, thrombocytosis, thrombocytopenia and coagulopathies. Serum globulin levels may be increased or decreased, depending on the type of neoplasm. Plasma fibrinogen and fibrin degradation product concentrations are usually elevated in cancer patients, whereas cancer patients with DIC have low plasma fibrinogen concentrations. Hypercalcemia can be a sequel of osseous metastases. Neoplasia may cause the nephrotic syndrome in some patients. Effusions should be examined microscopically for signs of malignancy. Elevated serum enzyme levels are not specific in neoplastic disease.
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PMID:Laboratory aspects of cancer. 650 15

Still's disease is characterized by arthritis, fever, rash, lymphoid hypertrophy, leukocytosis, and anemia, often in association with thrombocytosis. We describe a patient with Still's disease and thrombocytopenia secondary to disseminated intravascular coagulation (DIC). Fifteen definite cases of DIC complicating Still's disease have been reported in the English literature. Most developed this complication while receiving high doses of salicylates in association with hepatic dysfunction. In a few, the coagulopathy has been associated with gold therapy. Our patient is only the second reported to develop DIC in the absence of drug therapy and the fourth reported to die from this complication. The clinical features of these 16 patients are summarized and proposed mechanisms of pathogenesis are reviewed.
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PMID:Disseminated intravascular coagulation in Still's disease. 789 78

Thrombocytosis is always noted in patients with Kawasaki disease (KD). Here we present a case of KD with an unusual finding of thrombocytopenia. A 3 months old female baby was admitted to our hospital presenting with the classical symptoms and signs of KD. However, initially she also had thrombocytopenia and disseminated intravascular coagulation. She was treated successfully with a single high dose of intravenous immunoglobulin. (2 gm/kg). Thrombocytosis was found on the 10th day of illness, and treatment with low dose aspirin was administered for 3 months. No coronary aneurysm was found on cardiac echography. She was found to be well on a follow-up of 8 months.
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PMID:Kawasaki disease presenting with disseminated intravascular coagulation: report of one case. 808 58

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

A case of pure red cell aplasia (PRCA) with various complications polyarthritis, angitis, acute renal failure and DIC was successfully treated with steroid pulse therapy was described. A 55-year-old woman was hospitalized with a 9-month of intermittent but progressive joint pain, morning stiffness, general fatigue, and fever. Her initial laboratory evaluation revealed a hemoglobin of 4.4 g/dl and absence of reticulocyte. Her bone marrow aspirate showed no erythroblast which was compatible with a diagnosis of PRCA. Marked leukocytosis and thrombocytosis, positive antinuclear antigen, elevation of gammaglobulin and C-reactive protein and the presence of polyarthritis and angitis which was confirmed by renal angiography, indicated an underlying autoimmune disorders. Steroid pulse therapy was administered at 500 mg/day for 3 days, resulting in the complete response in both red cell aplasia and above findings. PRCA is known to be associated with systemic lupus erythematosus and rheumatoid arthritis very rarely, but this case did not fulfill the criteria of known collagen diseases, and there is no previous report representing PRCA with various complications such as polyarthritis, angitis and acute renal failure. This case may help us to understand more about the relationship between PRCA and autoimmune disorders.
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PMID:[Pure red cell aplasia complicated with polyarthritis, angitis, and acute renal failure]. 825 11

A young primigravida presented with postpartum haemorrhage with no apparent cause following a low forceps delivery. She was extremely pale with gross hepatosplenomegaly. Hysterectomy was performed following three episodes of disseminated intravascular coagulation. Investigations revealed an extremely high platelet count with poor aggregatory function. A diagnosis of primary thrombocythaemia was made.
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PMID:Primary thrombocythaemia presenting as postpartum haemorrhage: a case report. 859 Mar 57

Any oral and maxillo-facial surgical treatment, however urgent it may be, must not include pathological states in which the patient's life may be particularly at risk as, for example, with Disseminated Intravascular Coagulation (DIC) or throm-botic thrombocytopenic purpura. In this article the authors present the result of studies carried out on the nosology of thrombocytopathy from an odontostomatological point of view. Thrombocytopathy can be divided into two groups: the first including the pathologies with a predominant defective number of thrombocytes (i.e.: thrombocytopenia, thrombocythemia, thrombocyto-sis), the second including forms with predominant qualitative defects (commonly known as thrombocytopathies). The authors, after having presented in short the physiopathologic functions of thrombocytes, illustrate the clinical and therapeutic aspects of the most important thrombocytopathies. Morbus Maculosus Werhofii, Glanzmann's disease, Bernard-Soulier syndrome, thrombocytopathies from defective reaction of release, Thrombocytopathies from defective procoagulant activity of blood plaques, thrombocytopathies in linkage to other genetic anomalies, von Willebrand's pseudodisease and a lot of acquired thrombocytopathies are identified. In the last part the authors illustrate the most opportune clinical steps corresponding to the most important thrombocytopathies. The results obtained suggest the necessity of keeping to the management that was described, Actually a low percentage of accidents occurred only when the above-mentioned clinical processes were completely performed.
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PMID:[Management of patients with coagulation disorder in oral and maxillofacial surgery. I. Management of patients with hypocoagulation caused by primary thrombocytopathy]. 917 18

Thromboembolic (TE) events have been frequently reported in beta-thalassemic patients in association with known risk factors such as diabetes, complex cardiopulmonary abnormalities, hypothyroidism, liver function anomalies, and postsplenectomy thrombocytosis. In a recent survey involving 9 Italian thalassemic centers, we identified 32 patients with TE episodes in a total of 735 subjects, of whom 683 had thalassemia major and 52 thalassemia intermedia, corresponding to 3.95 and 9.61%, respectively. There was a great variation in localization: the main one (16/32) was CNS, with a clinical picture of headache, seizures and hemiparesis. Other localizations were the pulmonary (3 patients), mesenteric (1 patient) and portal (2 patients) sites. There were 6 cases of deep venous thrombosis (2 in the upper limbs, 4 in the lower ones). Intracardiac thrombosis was found in 2 subjects and clinical and laboratory signs of DIC were observed in 2 others during pregnancy. Since our patients with TE events present a statistically significantly higher incidence of associated dysfunction (cardiomyopathy, diabetes, liver function anomalies, hypothyroidism) than those without TE events (50 vs. 13.8%), we suggest close monitoring of those patients who are at higher risk of developing TE events because of the presence of one or more of these predisposing factors.
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PMID:Thromboembolic events in beta thalassemia major: an Italian multicenter study. 985 99

Perturbations of coagulation in cancer patients have been described for a long time. In up to 90% of cancer patients "routine" blood tests are abnormal leading to a hypercoagulable state in these patients. Among these tests are an increase in clotting factors, fibrinogen, fibrinogen/fibrin degradation products, and thrombocytosis. Markers of the activation of coagulation have been developed, and levels of FPA, F1+2, TAT, and D-Dimer have been found higher in cancer patients. More specific procoagulant activities in cancer (CP and TF) have also been described and can be measured but none of them have any predictive value for the occurrence of venous thromboembolism in these patients. Consistent with this hypercoagulable state in cancer is the finding that most cancer patients have reduced plasma levels of inhibitors of coagulation. These complex abnormalities are clinically expressed as thrombosis, low-grade or fulminant DIC which can be assessed by different laboratory tests, and as hemorrhage when the fibrinolysis system is impaired. However, no studies have shown to date a relationship between these abnormalities of the coagulation tests and the clinical expression in any single individual. Because these patients are at high risk for thrombosis in special conditions such as surgery or during chemotherapy, prophylaxis with various forms of heparin are recommended.
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PMID:Laboratory diagnosis of the thrombophilic state in cancer patients. 1035 84

Whole-blood platelet aggregation and adenosine triphosphate secretion were measured in 15 dogs with untreated multicentric lymphoma and 10 normal control dogs to determine if dogs with lymphoma have altered platelet function. Dogs with quantitative platelet disorders (ie, thrombocytopenia or thrombocytosis) or with clinical evidence of a bleeding disorder were excluded from the study. Platelets from affected dogs had significantly greater maximum aggregation than those from control dogs, suggesting that platelets from dogs with lymphoma are hyperactive. Platelet hyperactivity may play a role in the development of hemostatic disorders (eg, disseminated intravascular coagulation) or in tumor metastasis. Further investigation is needed to determine if modification of platelet function in patients with lymphoma affects disease progression or outcome.
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PMID:Platelet aggregation and adenosine triphosphate secretion in dogs with untreated multicentric lymphoma. 1044 22


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