Hemostatic Disorders and the Liver

2021 ◽  
pp. 269-283
Author(s):  
Ton Lisman
Keyword(s):  
Hemostatic Disorders

The Animal Models for Hemorrhage and Thrombosis in the Neonate

1987 ◽  
Vol 57 (01) ◽  
pp. 118-122 ◽  
Author(s):  
C Thomas Kisker
Keyword(s):  
Animal Models ◽  
Normal Development ◽  
Relevant Information ◽  
Relevant Model ◽  
Current Information ◽  
Single Animal ◽  
Hemostatic Disorders ◽  
Thrombotic Diseases

SummaryAnimal models have added significantly to our understanding of adult hemorrhagic and thrombotic diseases. Few models, however, have been developed for studies of the hemostatic disorders in the fetus and newborn. This report reviews the current information on animal models of fetal and neonatal hemostasis. The requirements of a relevant model are addressed and previous studies using fetal and neonatal animal models are reviewed. A recommendation of a single animal for all studies of fetal and neonatal hemostasis is not possible. However, the lamb has been the most frequently studied and appears to provide relevant information regarding normal development and the factors which may adversely influence hemostasis in the fetus and newborn.

Impairment of Platelet Aggregation by Echis colorata Venom Mediated by L-Amino Acid Oxidase or H2O2

1982 ◽  
Vol 48 (03) ◽  
pp. 277-282 ◽  
Author(s):  
I Nathan ◽  
A Dvilansky ◽  
T Yirmiyahu ◽  
M Aharon ◽  
A Livne
Keyword(s):  
Hydrogen Peroxide ◽  
Amino Acid ◽  
Platelet Aggregation ◽  
Snake Venom ◽  
Oxidase Activity ◽  
Enzyme Preparation ◽  
Acid Oxidase ◽  
Crude Venom ◽  
Amino Acid Oxidase ◽  
Hemostatic Disorders

SummaryEchis colorata bites cause impairment of platelet aggregation and hemostatic disorders. The mechanism by which the snake venom inhibits platelet aggregation was studied. Upon fractionation, aggregation impairment activity and L-amino acid oxidase activity were similarly separated from the crude venom, unlike other venom enzymes. Preparations of L-amino acid oxidase from E.colorata and from Crotalus adamanteus replaced effectively the crude E.colorata venom in impairment of platelet aggregation. Furthermore, different treatments known to inhibit L-amino acid oxidase reduced in parallel the oxidase activity and the impairment potency of both the venom and the enzyme preparation. H2O2 mimicked characteristically the impairment effects of L-amino acid oxidase and the venom. Catalase completely abolished the impairment effects of the enzyme and the venom. It is concluded that hydrogen peroxide formed by the venom L-amino acid oxidase plays a role in affecting platelet aggregation and thus could contribute to the extended bleeding typical to persons bitten by E.colorata.

scholarly journals Personalized Approaches to the Treatment of Hemostatic Disorders

2021 ◽  
Vol 47 (02) ◽  
pp. 117-119
Author(s):  
Roger J.S. Preston ◽  
Jamie M. O'Sullivan
Keyword(s):  
Hemostatic Disorders

A novel coagulation inhibitor fromSchistosoma japonicum

Parasitology ◽  
2015 ◽  
Vol 142 (14) ◽  
pp. 1663-1672 ◽  
Author(s):  
SHIWANTHI L. RANASINGHE ◽  
KATJA FISCHER ◽  
GEOFFREY N. GOBERT ◽  
DONALD P. MCMANUS
Keyword(s):  
Human Blood ◽  
Neutrophil Elastase ◽  
Molecular Mechanisms ◽  
Genomic Sequence ◽  
Proteolytic Enzymes ◽  
Venous Blood ◽  
Coagulation Factors ◽  
Intestinal Wall ◽  
Hemostatic Disorders

SUMMARYLittle is known about the molecular mechanisms whereby the human blood flukeSchistosoma japonicumis able to survive in the host venous blood system. Protease inhibitors are likely released by the parasite enabling it to avoid attack by host proteolytic enzymes and coagulation factors. Interrogation of theS. japonicumgenomic sequence identified a gene,SjKI-1, homologous to that encoding a single domain Kunitz protein (Sjp_0020270) which we expressed in recombinant form inEscherichia coliand purified.SjKI-1is highly transcribed in adult worms and eggs but its expression was very low in cercariae and schistosomula.In situimmunolocalization with anti-SjKI-1 rabbit antibodies showed the protein was present in eggs trapped in the infected mouse intestinal wall. In functional assays, SjKI-1 inhibited trypsin in the picomolar range and chymotrypsin, neutrophil elastase, FXa and plasma kallikrein in the nanomolar range. Furthermore, SjKI-1, at a concentration of 7·5µm, prolonged 2-fold activated partial thromboplastin time of human blood coagulation. We also demonstrate that SjKI-1 has the ability to bind Ca++. We present, therefore, characterization of the first Kunitz protein fromS. japonicumwhich we show has an anti-coagulant properties. In addition, its inhibition of neutrophil elastase indicates SjKI-1 have an anti-inflammatory role. Having anti-thrombotic properties, SjKI-1 may point the way towards novel treatment for hemostatic disorders.

Hemostatic Disorders and Platelet Nucleotide Release in Myeloproliferative Disease

1979 ◽  
Author(s):  
A.B. Hagedorn ◽  
E.J.W. Bowie ◽  
C.A. Owen
Keyword(s):  
Platelet Aggregation ◽  
Postoperative Bleeding ◽  
Myeloproliferative Disorders ◽  
Myeloproliferative Disease ◽  
Myeloid Metaplasia ◽  
Normal Platelet ◽  
Agnogenic Myeloid Metaplasia ◽  
Nucleotide Release ◽  
The One ◽  
Hemostatic Disorders

Since patients with myeloproliferative disorders may have bleeding tendencies, the surgeon, in particular, is anxious for an hemostatic evaluation if splenectomy is contemplated. It is known that platelet aggregation, particularly with epinephrine, tends to be reduced in these patients. The nucleotide content of their platelets may be deficient. Furthermore, megakaryocytic fine structure is often abnormal. We have studied, In detail, 9 patients with hemostatic disorders. Diagnoses included polycythemia vera, agnogenic myeloid metaplasia, evolving myeloproliferative disease and erythroleukemia. Ages ranged from 36 to 75 years. Bleeding tendencies, including bruising, operative or postoperative bleeding, melena, hematuria, and hemarthrosis, characterized 8 of the 9 patients; the one exception had normal platelet ADP and elevated ATP. All had abnormal platelet aggregation, but the extent of the abnormality could not be related to the ADP and ATP contents of the platelet.ADP (normal 26.7 ± 6.5 nmol/109 platelets) was reduced in 7. ATP (normal 38.6 ± 7.6 nmol/109 platelets) was reduced in 1, elevated in 2 and normal in the other 6. In no patient were both values normal. Nucleotide release induced by collagen activation was measured in 6 of the patients. In all 6 it was deficient whether platelet ADP were normal (1 case) or depressed (5) and whether platelet ADP were elevated (1) or decreased (3).

Molecular Diagnostics in Hemostatic Disorders

2009 ◽  
Vol 29 (2) ◽  
pp. 367-390 ◽  
Author(s):  
Peter L. Perrotta ◽  
Annika M. Svensson
Keyword(s):  
Molecular Diagnostics ◽  
Hemostatic Disorders

scholarly journals Use of recombinant activated factor VII

Medicina ◽  
2009 ◽  
Vol 45 (3) ◽  
pp. 248
Author(s):  
Dagmara Reingardienė ◽  
Robertas Lažauskas
Keyword(s):  
Prothrombin Time ◽  
Liver Diseases ◽  
Hemophilia A ◽  
Tissue Injury ◽  
Factor Vii ◽  
Recombinant Activated Factor Vii ◽  
Congenital Deficiency ◽  
Activated Factor Vii ◽  
Life Threatening ◽  
Hemostatic Disorders

Recombinant activated factor VII (rFVIIa) has been used in the treatment of various congenital and acquired hemostatic disorders for more than 10 years. Hemostasis is initiated by the FVIIa bound to tissue factor (TF), which constitutes only approximately 1% of total amount of the FVII protein existing in the blood. rFVII becomes activated only after the binding to the TF, released at the site of tissue injury. The efficiency of rFVIIa in the treatment of such life-threatening hemorrhagic states like hemophilia reaches up to 76–84%. rFVIIa is successfully used in the treatment of congenital deficiency of factor VII. It normalizes prothrombin time in the patients with the liver diseases and in cases of overdose of indirect anticoagulants. It is also useful for patients suffering from thrombocytopenia, thrombocyte function disorders, hemophilia A and B with development of inhibitors. rFVIIa allows overcoming uncontrollable hemorrhages, etc. It is supposed that rFVIIa is becoming a universal hemostatic drug.

scholarly journals Masked arterial hypertension: prevalence, pathophysiological determinants and clinical significance

2019 ◽  
pp. 92-98 ◽  
Author(s):  
В. I. Geltser ◽  
V. N. Kotelnikov ◽  
О. О. Vetrova ◽  
R. S. Karpov
Keyword(s):  
Arterial Hypertension ◽  
Cardiovascular Complications ◽  
Hypertension Prevalence ◽  
Rational Pharmacotherapy ◽  
Maximum Reduction ◽  
Target Organs ◽  
Rf Exposure ◽  
Increased Risk ◽  
Water Salt ◽  
Hemostatic Disorders

In most modern studies, masked arterial hypertension (MAH) is characterized as a poorly diagnosed, latent clinical condition predisposing to subclinical damage to target organs and an increased risk of cardiovascular complications. The prevalence of MAH among the population depends on gender, age, anthropometric and socioeconomic factors, profession, race and other characteristics. The most important risk factors (RF) of MAH and its pathophysiological determinants include genetic polymorphism, subclinical non-specific inflammation, hemostatic disorders, obesity, metabolic syndrome, water-salt imbalance, dyslipidemia, hyperuricemia. A defined value has latent dysfunction of the mechanisms that provide circulatory homeostasis, the detection of which is possible by the hemodynamic response to psycho-emotional, hypoxic, hypocapnic, orthostatic effects. Aggressiveness of RF exposure and the consequences of their implementation are evaluated by the rate of development of cardiovascular events and mortality, which indicate an unfavorable prognosis of “uncontrolled” MAH. The maximum reduction of the RF effects and rational pharmacotherapy can significantly improve its clinical prospects.

scholarly journals Mechanisms of Development of Hemostatic Disorders after Liver Resection

2010 ◽  
Vol 6 (3) ◽  
pp. 61
Author(s):  
S. A. Shaposhnikov ◽  
S. V. Sinkov ◽  
K. F. Ivanov ◽  
I. B. Zabolotskikh
Keyword(s):  
Liver Resection ◽  
Mechanisms Of Development ◽  
Hemostatic Disorders
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