The Role of Hageman Factor in Disseminated Intravascular Coagulation Induced by Septicemia, Neoplasia, or Liver Disease

1971 ◽  
Vol 26 (02) ◽  
pp. 325-331 ◽  
Author(s):  
J. W Mason ◽  
R. W Colman
Keyword(s):  
Liver Disease ◽  
Disseminated Intravascular Coagulation ◽  
Plasma Kallikrein ◽  
Severe Liver ◽  
Gram Negative ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Gram Negative Bacteremia ◽  
Severe Liver Disease

SummaryThe human plasma kallikrein system was assayed in patients with disseminated intravascular coagulation (DIC) induced by gram negative bacteremia, neoplasia and severe liver disease. Only the patients with gram negative septicemia showed activation of plasma kallikrein with concomitant depletion of kallikreinogen and kallikrein inhibition. Since the activation of kallikrein is a function of activated Hageman factor, it is suggested that in DIC associated with gram negative septicemia, Hageman factor activation may be involved in the DIC. In DIC associated with neoplasia or liver disease lack of Hageman factor activation should be considered.

Role of transjugular liver biopsy in the diagnostic and therapeutic management of patients with severe liver disease

2008 ◽  
Vol 113 (7) ◽  
pp. 1008-1017 ◽  
Author(s):  
A. A. Esposito ◽  
A. Nicolini ◽  
D. Meregaglia ◽  
A. Sangiovanni ◽  
P. Biondetti
Keyword(s):  
Liver Disease ◽  
Liver Biopsy ◽  
Therapeutic Management ◽  
Severe Liver ◽  
Transjugular Liver Biopsy ◽  
Severe Liver Disease

Disseminated Intravascular Coagulation: Experience in a Major Cancer Center

1975 ◽  
Author(s):  
Hamid Al-Mondhiry
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Cancer Center ◽  
Vascular Tumors ◽  
Thrombin Time ◽  
Severe Liver ◽  
Liver Impairment ◽  
Intravascular Coagulation ◽  
Number Of Patients ◽  
Severe Liver Disease ◽  
Precipitating Factor

Disseminated intravascular coagulation (DIC) developed in 89 patients seen at Memorial Sloan-Kettering Cancer Center between 1971 and 1974. Criteria for the diagnosis of DIC wore: 1. Hypofibrinogenemia or > 50% reduction in plasma fibrinogen on serial determinations. 2. Prolonged thrombin time and/or elevated titer of fibrinogen-related material in the serum. 3. Thrombocytopenia not due to drugs or disease. Patients with severe liver disease or uremia were excluded. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors (12 genitourinary, 10 lung, 9 breast, 8 gastrointestinal, 7 miscellaneous), 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gramnegative sepsis (20 patients), mild liver impairment (31 patients), and mucin secreting tumors (4 patients), were also noted. Four patients with vascular tumors, two with leukemia, and one with vasculitis had markedly shortened fibrinogen survival. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies.Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

Disseminated intravascular coagulation syndrome

2020 ◽  
pp. 22-40
Author(s):  
A. Kulikov
Keyword(s):  
Clinical Practice ◽  
Disseminated Intravascular Coagulation ◽  
Blood Cells ◽  
Physical State ◽  
Clinical Manifestations ◽  
Vascular Wall ◽  
Stages Of Development ◽  
Intravascular Coagulation ◽  
Hemostatic Disorder

Presented material reveals main links in the pathogenesis of hemostatic disorder. In particular, attention is paid to the role of the lungs, liver and other organs in the development of this process. Role of vascular wall and blood cells in regulation of the physical state of blood is described in detail. The most frequent factors leading to hypercoagulation are indicated. Difference between hypercoagulation and thrombophilia is shown. The latter is found in clinical practice quite often, but at the same time, it is poorly diagnosed. Such a terrible complication of hemostatic disorder as disseminated intravascular coagulation is described. Its classification, stages of development, clinical manifestations are offered to the readers.

Severe liver disease is caused by HBV rather than HCV in children with hematological malignancies

2003 ◽  
Vol 4 (5) ◽  
pp. 321-327 ◽  
Author(s):  
Manal H El-Sayed ◽  
Magdy M Mohamed ◽  
Amr Karim ◽  
Anna-Maria Maina ◽  
Filippo Oliveri ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hematological Malignancies ◽  
Severe Liver ◽  
Severe Liver Disease

Extra Lactate Dehydrogenase Isoenzyme Band in Serum of Patients with Severe Liver Disease

1971 ◽  
Vol 17 (9) ◽  
pp. 882-885 ◽  
Author(s):  
T Lubrano ◽  
A A Dietz ◽  
H M Rubinstein
Keyword(s):  
Liver Disease ◽  
Lactate Dehydrogenase ◽  
Serum Bilirubin ◽  
High Serum ◽  
Severe Liver ◽  
Additional Band ◽  
Dehydrogenase Isoenzyme ◽  
Severe Liver Disease ◽  
Isoenzyme Patterns ◽  
High Serum Bilirubin

Abstract In a study of lactate dehydrogenase isoenzyme patterns in the sera of patients with severe liver disease, who were primarily selected because of an abnormally high serum bilirubin, 42 of 76 patients had an additional band (LDH-T) between isoenzymes 4 and 5 on acrylamide gel. Thirty of the 42 patients died during followup, 24 within a month of recognition of the extra band.

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