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PubMed1986

Coagulation and immunology.

One of the most vital functions of the vertebrates is to maintain hemostasis through coagulation and fibrinolysis. This is achieved by the interaction of vascular walls with blood components such as cells and proteins (coagulation factors, immunoglobulins, and complement). Deficiency of coagulation factors results in bleeding disorders. The immune system, in response to foreign proteins or defective self proteins, produces antibodies triggering an Ag-Ab interaction with the related host of different reactions including abnormal coagulation leading to hemorrhagic diathesis.

Antigen-Antibody Complex↗
PubMed2001

Cerebral Sinovenous Thrombosis.

Cranial sinovenous disorders comprise a disparate group of illnesses affecting one or more intracranial venous sinuses and cerebral veins, alone or in combination, due to a variety of causes. As medical knowledge advances, fewer and fewer patients have an "idiopathic" diagnosis, with causes clarified in an ever-increasing number of patients. These not only include the long-known puerperal, marantic, infective, and traumatic causes, but in recent years, also a variety of congenital and acquired coagulation disorders, such as protein S, protein C, and antithrombin III deficiency. Certain sinuses are preferentially involved with certain causative entities; for example, cavernous and lateral sinuses are more frequently occluded in relation to infectious processes, either directly or as a parameningeal focus, whereas the superior sagittal sinus is most often occluded by trauma, tumor, or coagulopathy. The optimal treatment of sinovenous occlusion depends on establishing the cause with alacrity, because delays in diagnosis may lead to life-threatening hyperpyrexia, elevations in intracranial pressure, venous infarctions, seizures, coma, and death. However, because up to a third of patients with nonseptic occlusions may survive untreated, with few residua, controversy persists regarding optimal management. There has been a dearth of randomized, prospective treatment trials in this group of disorders. The little data that exist suggest that rapid control of infection, seizure prophylaxis, and anticoagulation must be achieved early so as to prevent progression of thrombosis and intracranial venous hypertension. In recent years, direct retrograde venous thrombolysis has become increasingly available, and has produced such remarkable results that it is likely soon to become the primary treatment of choice for the nontraumatic or nontumoral occlusions.

Journal Article↗
PubMedDate not supplied

Thrombosis and coagulation abnormalities associated with cancer.

Abnormalities of hemostasis and malignancy have been recognized since the 19th century. Thrombosis and hypercoagulability are reported in as many as 60 percent of patients with malignancies. Decreased levels of protein coagulation factors, circulating anticoagulants and platelet numbers, and function changes are reported. The purpose of this work is to report a case of portal thrombosis in a patient with a myeloproliferative disorder and to review protein coagulation and platelet abnormalities associated with malignancies. The clinical laboratory assessment of these abnormalities is reviewed. The patient was a 59-year-old woman who was referred to the Vanderbilt University Medical Center with a diagnosis of septic portal vein thrombosis. After evaluation, it turned out that she had a myeloproliferative disorder and portal vein thrombosis secondary to that. Hypercoagulative states have been reported with a variety of carcinomas and other neoplasms. They may or may not be associated with acquired or genetic deficiencies of antithrombin III, protein C and/or S. Factors I, V, VIII:C, IX, and XI have all been reported as being elevated and implicated in hypercoagulability in patients with neoplasms. Increased platelet turnover and decreased survival have been noted in patients with disseminated tumors. Thromboses with lysis of the thrombus may be monitored by increased levels of fibrin degradation products, D-dimer, fibrinopeptides A and B, and platelet factor IV among others. There are frequently decreases in coagulation inhibitors including antithrombin III, protein C and protein S. These changes lead to a state of low-grade disseminated intravascular coagulopathy where thrombus formation is a more frequent occurrence than is hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Disorders↗
PubMed1983

[Effect of prostaglandin F 2 alpha on the functional state of the tissue component of blood coagulation and fibrinolysis in albino rats with disorders of protein metabolism].

Experiments were made on 80 white rats to examine hemostatic and fibrinolytic properties of the liver, kidney, small intestine and skeletal muscle tissue and subcellular fractions (nuclei, mitochondria, nuclear supernatant liquid containing lysosomes, ribosomes, microsomes and with no mitochondria) during prostaglandin F2 alpha administration in the presence of upset protein metabolism induced by experimental toxic hepatitis and protein deficiency. It was shown that intravenous injection of prostaglandin F2 alpha leads to an increase in hemostatic properties and reduction of fibrinolytic activity of all the test tissues with the exception of gastric wall tissue which showed a different line of changes. Variation of hemostatic properties of whole tissues was followed by appropriate changes in hemocoagulation potential of subcellular fractions.

Animals↗
PubMed1990

Molecular biology of proteins involved in blood coagulation.

Normal hemostasis in humans requires the interaction of a large number of plasma glycoproteins with blood platelets and vascular endothelial cells. Many of the plasma glycoproteins which participate in blood coagulation are zymogens of enzymes that interact in a stepwise manner in a series of reactions. In the last years most of these glycoproteins have been purified from human plasma by standard techniques. Some of them are used as therapeutics for restoring coagulation disorders. The knowledge about the plasma proteins involved in blood coagulation was greatly increased after cloning and sequencing of the respective complementary DNAs. Furthermore, recombinant DNA technology is used for the alternative production of several coagulation factors. It is the aim of this article to give an overview about the molecular biology of the enzymes and cofactors involved in blood coagulation.

Blood Coagulation↗
PubMed1975

The K-test (trypsin clotting time) in coumarin treated patients and in congenital deficiencies and abnormalities of the prothrombin complex.

The behavior of K-test (Trypsin clotting time) has been studied in 38 patients on long-term coumarin therapy and in 19 patients with congenital coagulation disorders of the prothrombin complex. All coumarin treated patients showed a clear prolongation of the test. The results obtained were compared with the standard prothrombin time, the Hepato-Quick-test (P-P test) and the Factor II + X test values, observed in the same patients. A good correlation was observed in each instance. The highest correlation was observed between K-test and the Factor II + X test (r=+0,78;t=7,80;p less than 0.001). All congenital coagulation disorders of the prothrombin complex yielded a prolonged K-test value but for Factor VII deficiency. In three patients with this latter condition a perfectly normal value was obtained. The K-test together with the prothrombin time may be useful in the differential diagnosis of factor VII deficiency from factor X deficiency and from the factor X Friuli abnormality.

Blood Coagulation Disorders↗